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  • Epilepsy Severe the corpus callosum (which connects the two hemispheres – along with the anterior commissure) Hemispheric lateralization, an example of wich is language being left brain. Sensory – some information crosses over from one hemisphere to the other.
  • Question for the class: Is it possible to compensate in terms of visual information getting into the brain? Writing and reading are part of right. What ever you see on the left, is what you will pick up with the left.
  • Meninges are a closed system.
  • Ventricles are larger fluid filled layers Hydroceffeless, head gets larger because fluid does not drian.
  • Cross section of spinal collum Central Canal is where epidurals are given (child bearing, surgery) Butterfly structure- called gray matter- lots of cells Gray matter- lots of cells White matter – lots of fibers Remember terms- Dorsal – Top of back Ventral – Most changes are made in gray matter. That is where the action is. White is from one area to another (highways) Gray is sidewalks
  • Anoter picture of spinal colum Note previous slide fits in center of this one Miningies surround the brain and spinal cord *
  • Thracic – chest cavity We are looking at the dorcel surface
  • Three anatomical planes * First (Easy) Horizontal Plane Second Sagital – left vs right Medial and Lateral Coronal Plane Anterior vs Posterior Confusing Explained Ventral – Underneath the eyes Dorsal – Top of head (like the back) Think alagator. Also the spinal cord turns to a 90degree
  • Spinal Colum is spit in half for dorsal and ventral also Think of each plane as a way to slice the brain into sections. Front –Back (Frontal/Coranal) Right – Left (Segital) Top –Bottom (Horizontal Know that within a plane, only two planes can be described.
  • White matter – roads Gray matter – the houses
  • Know why each plane changes and which part of the body everything is. There is a rotation through the head. Go through it as if I was on my belly but my top of the head was facing up. When talking abut if a part is lateral, anterior, ect it must be compared to another structure of the body. For instance, my nose is ventral to my eyes. Dorsal = Back Ventral = Belly
  • Fore brain Prosencephalon – high functions Midbrain – small part of brain, performs visual and auditory functions, generates chemicals used by the brains Hind – life support structures,
  • Prosencehalon has two parts telencephalon – remember the devisions cerebrum- what you see when you see the brain (four loabs) limbic system basal ganglia diencephalon – Included in the brain stem (plus everything below) * Know what each of the words refer to.
  • Folds – gyrans Pre frontal cortex Primary Motor Cortex Primary somatosensoryry cortex Frontal lobe (planning ahead, social good things) response Parietal lobe – space Occipital lobe – Vision Primary Temporal Lobe – Auditory & Memory & Emotions & Vision association (also processed but mixing it with other inputs, higher analysis)
  • Corpus Callosum is sometimes severed in order to help epelepsy pacents
  • Cerebral Cortex=the gray matter.
  • Cerebral cortex – gray matter does not include gray matter like basal ganglia which is surrounded by white matter Dura matter and meninges is located on the absolute outside of the brain.
  • Limbic system holds the hippocampus, amygdala, septum. Not the highest brain function Located below the gray matter
  • Remember – Hippocampus – longterm memories Amygdala – negitive emotions Both are in the tempral lobe DO NOT memorize where all this stuff is, but it may help to have a general idea
  • Limbic system- memory and emotion Basal Ganglia – smooth movement
  • Nucluus/ nuculi refers to the well studied group of cells. Not the individual center of cell.
  • No worry about identify structurs just fyi
  • Thalamus is like a switchboard operator. Hypothalamus – Hypo (below) is essencial for regulated drives (thirst, hunger, sleep, temp, sex, and emotional)
  • Thamamus is a very important part of communication between higher brain structures and lower brain structures (or other higher brain structures)
  • Know Tectum- Tegmentum- importaint brain chemicals made there.
  • Know Mesenciphalon. If it does not work well, you will be in a coma. Cops in the rear view mirror, consumsion of caffine. Spans all three divisions (hind to forebrain)
  • Rhombencephalon- lowest brain structure
  • Make sure not to confuse Cerebellum and cerebrum. Cerebellum – coordinated ballistic movements – socer, basketball, piano, sobriaty tests Has to know the status of every muscule in the body in order to function smothly Pons – “White matter” tracts between cerebellum and cerebrum Medulla = life support - breathing - Heart Rate - Damage will cause death without life support
  • PNS= somatic & autonomic nervous systems
  • These are all Automatic. Symathetic – watching kids dog get run over.
  • Ballence between Sympathetic and Parasympathetic is constaintly going on.
  • Sensory information enter on the dorsal side generaly. Ventral is where it comes out.
  • If nerve damage occurs high in the spinal column everything below is affected.
  • Injurty to C1 often causes death. Trigeneral nerve 5 (V) provides nerve to the head.
  • Axons can branch many times.
  • Pre synaptic nuron – The cell that is sending the message Post synaptic neuron- the cell that is recieveing the message The post synaptic neuron send messages to up to 10000 other cells.
  • Splinter in divergence – oww that hurts, memory of how it happened, problem solving how to get rid of pain.
  • Read pages 30-36 of the carlson text. Remember that a neuron cell is just like any other functioning cell in the body. The diffrence being that it has a system to communicate complex messages to other cells, they also are eletrical excitable.
  • Classification of neuronds is based on how many processes are coming off of cell. There are 5 types.
  • C. Is found normaly in spinal cord. Don’t have to memorize names. Be able to draw a “bipolar cell, unipolar cell” ect. If asked to draw a unipolar cell do not draw a psedo-unipolar cell.
  • If the pot was hot enough, you would drop the pot reflexivly. Know the functional classification of neurons, vs the anatomical classification scheme.
  • Glial cells are importaint support cells. Nourishment, waste management, scar tissue, contribute to the blood brain barrier. (Astrocytes). Macrophages- white blood cells attack tatoo pigments, or coffing when you smoke. Gliosis – scar tissue in brain. Blood brain barrier – unlike other muscles, the brain has a special protection stystem to prevent some particles acess to brain. The brain is protected at high cost. Radial Glial cells help guide cells to the correct place like a spider web. Schwann- less complex, (PNS) Olidodenrocytes – are more complex just like the word. (CNS) Without Mylonation signals would move too slowly and we would be uncoordinated.
  • Astrocytes – Nourishment!!! (Latate They also bring nourishment from capilaries.
  • Makes it moves a lot faster. Myelin sheath helps with regeneraton of axon. Makes it more efficient, by decreasing the energy needs. Electrical impulse jumps from note to node (sultitory conjuntion) The dark parts on each schwan cell are neculus.
  • Myelin is a lipid.
  • Schwnn cell wraps around axon. Schwan cells are in the perfri.
  • Mylanation: A process by which axons are insolated by lipids. This prevents the axon from shorting out.
  • Capillarys- only one red blood cell can travel at a time. Capillary in brain doesn’t allow stuff to leak out. This is the blood brain barrier.
  • Substances that are very large have dificulty getting throught the blood brain barrier. There are energy driven mechinisms that push Amino-acids,glucose that push substances through barrier. CO2 and O2 are able to diffuse through barrier. Anything that is watersolable usualy has a charge to it. Charged molicules have difficulty getting through the barrier. Fat soluble molecules do not have much difficulty passing through the barier. The barrier is lipid based. Transporter protines are what allow non-lipid molicules to be transported through the barrier.
  • A cell is the smallest functional unit of life
  • Cell/plasma membrain
  • Know that proteins are a part of the cell membrane and they are the channels allowing things in and out of the cell membrain They also provide structure. Mitochongria – takes the food and produces energy for the rest of the cell. Energy is in the form of ATP. (ATP is like a watt) Nucleus – has DNA (the blueprint that makes us). We have two strands. When DNA is needed for reproduction, it seperates them out, in the process of transcription, it turns them into mRNA. DNA vs mRNA – DNA bases – A- T- G- C- DNA is also missing one Oxygen atom. mRNA – A- U - Uracil G- C- Translation – mRNA is converted into protenes. Protens are nessisary for all fuctions. Translation happens outside the nuclus. ER- Takes mRNA Rough ER has ribosomes on surface. It is the one that takes in the mRNA. Golgi Apparatus (fed Ex) Lysomsome finds waste products, engolfs them, degrades them, takes it outside the cell membrane. Vacoules- stores lots of stuff (warehouse) Each type of cell has some specialization (above is common to all cells, including neurons)
  • Basic funtion we are trying to understand- How a cell communicates. Communication is sending and receiving information. Axon- Send (Anus) Dentrite- (dental) imput, recive information Know how to lable a neuron. Soma- body of neuron (CPU) The message sent is binary (there is a message sent or there is not) Receptors receive signals from the outside world. Mylan shleef speeds up the rate of conduction. Cranial nerve Neumonic: On Old Olympus Towering Tops A Finn And German Viewed A Hop
  • EXAM: Know lecture notes. Understand how stuff works most questions will be application.
  • Chemical Transmission- allow neurons to communicate. Cell body= Soma=information processed Dentrite (dental=eat=receive= Tree branches) Axon (anus=send= plunger suction cup)
  • Synapse – Axon, Space & Dentrite Presynaptic end (Usualy the Axon) Synaptic Cleft (the space between) Post Synaptic end (Usualy the Dentrite) Different types : Axo-dendritic Pre- Post Axo-axonic Pre- Post
  • Postsynaptic dencity is electrons passing over synapse
  • Know all white text These are between two neurons Axodendritic (axon communicating with dentrite) Axosomatic (axon communicating with soma) Axoaxonic (axon communicating with axon)
  • Gap junctions are one way for a neiboring neuron to act the same way (if cell a is excited, then cell b is also excited because of the gap junction) Chemical – Synapse- - Neurotransmiters (NT) - they are what carry the chemicals from axon to dentrite -This is the Action Potential - Vescules filled with NT travel down axon, fuse with axon wall, realeasing NT into Synapse gap, They then defuse and bind to receptors in dentrite. Cell responds. (IPSP, EPSP) The NT never actualy transfer through dentrite they just attach to protiens.
  • Electrical way to communicate. Cells are actualy linked together through gap in the membrain. Within a cell dentrite- soma- axon communicaion is also electrical. - IPSP Action Potential (AP) - EPSP
  • At rest the inside cell is more negitive At rest the outside of the cell is more positive. Ca+ion (positive) Ani0n (negitive) Ions are charged particals or atoms (either positive or negitive) like charges usually repell eachother. Unlike charges attract eachother. KNOW that resting is -70mV
  • There is slight changes in charge over time.
  • Hyper makes more negitive (valume makes cells more negitive) Valume calmes down the central nerve system
  • Trans membrain protines allow specific salts, ions, and partices to move in and out. Like a toll booth. Some are designed (specialization) that allowes only specific ions though. Hydrophilic Hydrophobic Anytime a channel opens – Potassium would move out. Cell charge decreases. Potassium is the big driving force for change in the cell. 2 Forces – Concentration Gradiatnt is the BIG one and will be on the test Electro static is the other, non importaint
  • Memorize: Distribuition of ions. Sodium NA+ (higher outside then inside) Cloride CL- (higher outside then inside) Potassium K+ (higher inside then outside) Calcium Ca+(higher outside then inside) Neurons are bathed in sodium chloride (salt water) Sodium chloride is much higher in concentraion outside the cell. This is importaint because there are drugs that effect these channels. Valume- bindes to chloride channels and opens them up. With the extra chlorides the cell is more relaxed and less apt to fire an impulse. Force of diffusion = chemical gradiant Cokane, litakane, novakane blocks sodium diffusion, so less pain is felt.
  • If an ion chanel stays open, and equal libriam becomes closer…. Know that K+ is higher inside than outside Na+ lower inside than outside Cl- is higher outside Ca2+ higher outside Reversal potentional is the voltage of the membrain that if achived causes the ion to reverse (if K+ normaly moves inside the cell, once the equalibrim potential (reverseal) is reached, it moves outside the cell)
  • Use the chemical gradiant to determine movement.
  • If the Action potential were long, the cell would die. It will either fire the action potential or not fire. Have to roll the ball over the hill to get it to roll down. Uphill- Sodium entering Downhill- Potassium leaving Relitive refractory period – the ablity of the cell to fire again in relation to the cell membrain Absolute refractory period – the time before a cell can fire again Above -70mv (-69,-50,-10,0) = depolarized (less away from 0) Below -70mv ( -71,-90,-100) = hyperpolarized (more away from 0)
  • Channel has to reset itself before it can open again. Channel has to be open for stuff to go through. If channel is open, movement is happening. Electrical gradiant – like repell, different attract. Chemical gradiant – move from high to low. The 4 ions we care about: K+ - more abundent inside the cell NA+ | CL- more abundent OUTSIDE the cell. CA2+ | More +’s outside then inside thus it is more NEGITIVE inside the cell.
  • Action Potential – sodium influx followed of by pottassium eflux Overshoot (attempt of cell to reach homeostasis over does it a little)
  • Like a wave. Axon the charge travels both ways, Nerve cells do not.
  • Axon hillic is located at the base of the cell body and is where the charge is initiated It takes a little bit of time K+ Wants to stay inside or get inside Na+ Wants to go inside Cl- wants to go inside Ca2+ wants to go inside Chemical vs chemical have different desires for K+ and other ions
  • No sodium or potassium channels under myelin. Myelin cells are faster transmitters than non myelin covered cell. Larger diamiter axons will reach its action poential much quicker than a narrow. Myelin vs non myelin think of hose with holes verses a hose with fewer holes.
  • An unmyelinated has very big problems getting signal without myelin. This is much worse if you LOOSE mylination (MS) than if it never had it. Because the transmiters are only at the nodes of Ranvier on a myelinated nerve.
  • These pumps need energy in the form of ATP inorder to work.
  • This is how the brain knows if it is a light touch or a punch. Frequency (number of times per time period) determines the percieved intensity.
  • Summation = adding up. Temprol = adding up over time Spacial = adding up at same time from different locations.
  • If the temporal relation ship is appropriate (close enough together) The spikes build off eachother and they reach the threashold to fire. Summation of IPSP (5) it goes even lower.
  • Gated = (how it is controlled) Ligand – able to bind with an ion channel to open it (neuro transmiters, chemicals) - ligand is a chemical that binds to a receptor (protien) - can or cannot be a protein. - receptors are always proteins. Usualy found on membaine - Two types of receptors - ionotrophic - NT (ligand) binds to the receptor - ion channel opens and allows ions to pass through - IPSP/ EPSP occurs - metabotropic - NT binds to receptor - because it is not an ion channel, it does not open - secondary messanger is activated (the secondary is already inside, bound to the receptor, but releases when it is activated) - this leads to opening or closing another ion channel or - it goes to the neuclious and causes transcription -metabotrophic is also known as “G- Protin” which activates the secondary messanger. - an example of this is Cyclic-AMP or Ca+ <- very important Voltage – controlled by the voltage potential of the cell. (Sodium and __) (open primarily during hyper or depolorization) - calcium Ca2 chanels allow for the calcium influx at the axon wich causes neurotransmiter release - k+ channels - sodium channels cause the action potential to travel down the axon Ion – Open when they detect the presence of a particular ion (calcium, or K+) Non – not controlled by anything we know of, they just leak. Nurotransmiters are examples of ligands. Ligands get released and end up binding to the receptor (protine) on the dentrite. ** Receptor = protine that binds to a ligand Ligand = Any chemical including a NT that binds to a Receptor **
  • Chemicals have to be made – synthetic pathways
  • If something can effect your nervous system, your body also has a receptor that is something like it.
  • When Ionotrophic open= Ions are going in or out very rapidly (IPSP/ EPSP) When Metabotrophic open = Ion transport may or not happen, NO (IPSP/EPSP), Slow transport because of the greater complexity of the process.
  • Voltage gated calcium channels. Calcium entering the terminal button causes it to Calcium entering the button causes neurotransmitters to release.
  • Inhibitory- hyperpolarization
  • Ionotropic – very fast (insert key and turn and the door opens) Metabotropic – something else has to trigger it. (deadbolt unlocked then turn the door knob)
  • Nicatine
  • Second messanger in order to bind the chemical and open the ion channel
  • Slower acting but longer effects
  • A chemical antagonist interferes with normal function. Agonists – mimics normal chemical transmiters
  • Indirect binds to a different location.
  • Product= chemical Production can be speed up or slowed down. Chemicals can be packaged. Chemicals have to be shipped. Product has to be somewhere where it can be used. There has to be a way to regulate the product distribution. Recyle some of the products.
  • STUDY THIS SLIDE BIG TIME L-Dopa used in alstimers Drugs that simulate autotransmiters – shut doen SSRI’s block the reuptake. Know this and last slide. Drug names are important. Also Ligands- Agogonists- increase the function of a NT Antagonists – oppose a function of a NT When a drug binds to the exact same spot – compeditive antagonist When a drug binds to another area but still disrupts function – non-compeditive antagonist When a drug is similar to the normal NT and produces the same outcome by binding to the same spot- compeditive anogonist When a drug is similar to the normal NT but binds to a different spot – non-compeditive anogonist Know what a precursur will do – it increases the (non compeditive agonist) If the precurser is an enzyme that prevents the degrigation of NT. (non compeditive agonist)
  • Neurotransmitters – Neurohormones – the diffrence is if they are locally released. Hormones circulate throughout bloodstreem. (adrenalen, eppenefrin) Neurotransmiters are made locally.
  • 1-4 classical neurotrasmiters 5. Excitatory 6. Primary blocker 7. Anandamine (THC)
  • Cholinergic (they dropped the acetyl) Adrenergic (adrenaline) Anadr- canabus)
  • Prominent in PNS Causes muscle contracion
  • Ascetocholine – learning memory & dream sleep <- Know
  • Choline is a lipid membraine product.
  • Curare – to take down (kill)
  • Botox works by reducing Ach release (Ach is the same as aseto choline) Black Widow Venom – causes Ach relase (aganistic) Casuses spastic contractions and Tetanus – lock jaw – excess contractions thus no more control of it
  • A Acetylcholinesterase inhibitor BLOCKS ace… Know that it is not an ace….
  • Memorize the names of the transmitors
  • Major pathways that are used
  • Very few nurons left on the right.
  • MAOs decrease dopamine. MAOI’s stop that breakdown wich helps with depression.
  • Know how all this stuff works. Study how aganistic and its oposite works. Cocaine blocks the re-uptake of dopamine. It also pushes it into the synapse.
  • Changing the dose often changes the effect Autoreceptors are used to shut down the receptors if they are overloaded. If the dose gets too high, the receptors get shut down and it now has the oposit effect.
  • Norepinephrine think epinephrine Sympathetic responses
  • Structurally very similar
  • Beta receptors – decrease cardiac output, both in the heart and lungs. Beta 1 only effect the heart and not the lungs.
  • Works thorugh the adranergic system. Phedrine- adranurgic aganists. If your on an MAOI, (which are a antidepressent, saratonin is a mao), this could increase the effects and build off of the effects of the moai
  • Serotonin decreases during dreaming
  • MAO-A breaks down serotonin PCPA blocks serotonin production
  • SRI- Saritonian Reuptake Inhibitors (old type) SSRI – Selective Saritonian Reutake Inhibitors (new type) Prozac Saratonian levels are usualy higher after eating. Saratonin has been used as a hunger suppressor. The side effect is drowsiness. Extacy – capable of destroying serotonin receptors.
  • He will give us drug name and effect. Know if it is a agonist or antagonist
  • NMDA – is blocked at rest. Both ligand and voltage gated unlike the other receptors Caffeine – stimulante the glutimate system. Interferes with regulation. Cafine blocks the adenosine wich allows for more glutamate release. MSG -
  • NMDA are extreemly implicated in learning and memory. If they are blocked, learning becaomes very difficult. Only opened if the cell has been excited (depolarized) Normally blocked by a magnisum molecule. Know the Glutimate and Magnisum. It’s a VOLTAGE and ION depenent . People on PCP really cannot learn.
  • Strychnine – blocks glycine receptors. Excess excitatory drive. Convulsions, contractions, ect.
  • Know GABA a receptor.
  • Groth factors are importaint for the groth of the nervious system Cells are changing along these lines. Chamicals determin wich path they take.
  • Radial glia assist in the migration of Deeper cells develop first then migrate outwords. Transplantation depends upon age – If a progenitor cell was put into a muscle, it would become a muscle cell. Liver- liver cell, ect. In other words- a stem cell or projenitor will/ can become just about anything. It has to be in the environment that it will develop into. Synaptogenisis- with out it, the cell will die. Cholesteral is essencial for nervious formation.
  • Axons follow chemical messages. They regenerate and go back to the place that they use to be. Once the eye fixed itself, it was upsideown and backwards.
  • Tropic -
  • Maluable. Constantly being formed and taken away.
  • PNS can regenerate some as long as the cell body is still alive. CNS regenerates little if at all.
  • Axons will generate branches to synapes in an area where the synapses may have been damaged. Axon 2’s cell was damaged. Axon sees the vancancy, sprouts collateral axon. (this can be good or bad- phantom limb experience)
  • Damage- Add or remove axons Add or remove receptors 6-HydroxyDopamine (dopamine toxin) injected. It selectivly kills nerve cells, Some drugs will directly effect release in the synapse. Unilaeral distruction of dopamine will destruct normal movement. Injection of 6-0hda in left hemisphere. With loss of dopamine, the receptors increase sensitivity to dopamine. Google: optogenenetics Although left side is supersensitive, there is not dopamine that is being released. Blue- -------- 6-OHDA is injected into left hemisphere and it kills dopamine neurons. Because the left hemisphere controls movement, the effect is that the animal moves to the left more then to the right. (results in increase of receptors in that region) <- denervation supersensitivity Later they inject Amphetamine in the right side to increase the release of Dopamine. They release more dopamine. This causes left side to respond more. Later still they inject Apomorphine. This increases the sensitivity of the dopamine receptors. (stimulating DA-r’s) Response is greater to the right side. This is because once you kill off a certon number of neurons, it increases the number of receptors ***Any change you make in your brain, the brain will try to return to its original function. This is placiticity*** A: Stimulating DA release (amphetamine is precurser to DA release): no DA to release on L, R side dopamine B:Sinthetic DA is enjected, extra receptors take in injected DA, L is dominant.
  • Motor nuerons in the PNS control movement because they have an axon with a synapse the connects to a muscle. The synapse is called a neuro muscular junction (NMJ)
  • Know how they differ
  • Sliding filament theory. When a muscle contracts, thin filaments will slide over the thick filaments. Because of this, the Z- lines start coming closer to gether. Causing the muscle to look shorter. Antagonistic muscles work in oposit fashions. Example : Bicept and Tricept It tells one muscle to contract while another to relax.
  • Sliding philiment theory – big are surrounded by small, they slide against eachother.
  • Know two types of filaments
  • The thick and thin filamints, slide across eachother for contraction. Explain
  • Muscle endplate is on the muscle side. It is where the axon from the never connects to the muscle. ACh is at the NMJ. ACh causes the muscle to contract. Ach has both ionotrophic an mesotropic. Muscles have only ionotrophic Ach receptors. The receptors are also called nicotinic receptors. -------- 1 motor neuron controls very few muscle muscle fiber for fine control. Not much control needed for posture. So 1 motor neuron cotrols large emount of muscle fiber. Fine control – lots of neverves for equal number of muscle fibers. Course control – few nerves for large numbers of muscle fibers.
  • Slow Twitch – Red Fast Twitch – White Myoglobin carries oxygen it is found more in red meet. Hemoglobin binds oxygen in the blood. Myoglobin binds oxygen in muscles. Red muscles are able to work longer because they bind oxygen easier. Cramps after a hard run are because you used up all the oxygen that the muscles had. White- short and rapid bursts. But they get tired over a shorter period.
  • Tricept is contracted – arm straitens (bicept is relaxed) Bicept is contrated – arm bends (tricept is relaxed)
  • Reflex changes around 6mo of age. If drunk or asleep or in a car accident – positive babinski indicates CNS nerve damage.
  • There are one or more neurons that can act.
  • Reflex arc – just means there is a loop
  • Black neuron can release GABA to inhibit reflex response to save the food.
  • Gamma – interfusual (inside muscles) Important for maintaing muscle tone and reaction. How long is it?
  • Internal streach receptor. They are like little springs within the muscle. Weat causes arm to move, enabling streach reactor. This helps prevent muscles from tearing.
  • Head flyes up when sleeping, streach receptors wake you up (think in class or church)
  • Essencial to information about the state of any muscle. Intrafusal fiber is like a spring under a small amount of pull. Spring can reset when length is reduced or expanded.
  • Any time a streach reflex is started, the other muscles must be relaxed otherwise you would have jerky movement.
  • Focus on green. It causes contraction of Flexor muscle. Axon branches to antagonist muscle and sends “relax” signal. Contraction (activation) of any mucle naturaly sends inhabition (relax) to antagonist muscle.
  • GTO – are streach receptors inside tendons not muscles. One responsds to muscle lengt One respons to muscle muscle being loose (GTO)
  • Proprioceptors play a vital role in giving feed back on where body parts are in time and space, also if contracted or relaxed.
  • Crossed extensor reflex – to the other side of the body, streighten limb.
  • Cortico- from cortex spinal – to spine 2. Medial group Coordinated movements you are not always aware of.
  • Pyramidal – pyramid like. Bundal of axons in ?= never Bundle of nerves in extracotraneral =Tract
  • Sections a,b,c,d,e are mostly coronal C should have pyramids on top of mouse head, not ears. The orgin of the pathway – They cross over in madula – Fomrs contralateral tract
  • Three different effects.
  • Study this, Missed this part of lecture.
  • Myasthenia Gravis – immunie system destroys Ach-receptors. RX: increase ACH transmission. Apraxias – difficulty making movements
  • Babies can sit up before they can color.
  • All muscle spindles, positions ect all end in the cerebellum.
  • DUI test – really testing the cerebellum
  • Substantia Nigra – damage produces Parkinsons disease - resting tremmors - rigidness -Given L-Dopa to cross bbb and Subthalamic Necleus – deep brain stimulates it.
  • Ideally, you prevent, but after damage “what can we do with the structure”
  • Tic- isolated involentary muscle contraction. Choreas – multiple mucles involentary contracting.
  • Loss of dopamine producing neurons causes Parkinsons. MOA-I are sometimes used. Small brain leasion. Deep Brain Stimulation - problem: it’s a wire in your head. Galeal cells fight it. Know treatment approches.
  • Know the Antomy of the eye and its function.
  • 400-700nm Short wl = violet Long wl =red Be able to list the rainbow Blueray – shorter wavelength means more information on disk Sunsets are red because it travels through space and the atmosphere better.
  • Know equation Shorter the wavelength the more info you can fit in a given period of time. Longer the wavelength = shorter frequency
  • Strong = lots of outputs Weak = not much output If a stimulous is present long enough, the cell adapts untill body gets fatigued.
  • Distrabution of photo receptors in eye are shaped so it can finds food below itself. The photographer is above the owls so the owl sees much better if ti turns it head upside down for things that are above it.
  • KNOW DISORDERS – any dysfunction ect know for test. Make list so not to confuse them. Elasticity of lens changes and less elastic. Then you cannot see up close. Need reading glasses. Accomodation – lense can change shape (fatter or thinner) Fatter when looking for things near – as we grow older, the elasticity decreases and it makes it harder to see Thinner when looking at things far away Presbyopia – loose the ability to see close
  • Best visual acuity is at fovea. Color and details are best at fovia (which has cones) Opdic disk – this is where all the neves and blood vesles leave, cannot see in this area.
  • Image forms at the back of the eye on the retena. - 3 layers of cells - Photo receptors at rear - Bi- polar in middle (semi transparent) Light is unalterd - Ganglion cells at front (semi transparent) Light is unaltered Once photo receptors receive the light, The ganglian cells get the information, and send the information to optic nerves
  • Deminstrate blind spot. Start close, pull away slowly. Cannot see blind spots with both eyes open
  • Cone = Color Rods= black and white Very few rods in fovia, but plentiful everywhere else. Rods are extreemly sensitive to light. Cones are very consentrated in fovia but very few located elswhere. Cones are not very sensitive to light. Cones can be overwhelmed when you go sking, white out but it must be extreem. Cones not overwhelmed easily. Rods can be overwhelmed easily – car’s headlights. They get bleached momentarily. In the event of no light, the photoreceptors inhibit the bipolar cells from fireing. When light is introduced, photo receptors take in light and stops inhibiting the bipolar cells. Bipolar cells send info to ganglian cells, the axons in the ganglian cells go into the optic nerve.
  • Vitamine A is very important for your eyes. Retinal a After rods are bleached, they must undergo a chemical reaction in order to adapt to the dark again.
  • Right bottom is cone Other three are rods Basic diffrence between rods and cones – cones color and detail, rods at night At night there is far less color. When reading or looking at something directly, the image forms at the fovia. Fovia has only cones. As you get away from the fovia, there are almost no cones.
  • Cones are consentrated at fovia, consentration goes down as you move away Rods are all over the eye, but as it gets closer to the fovia, the consentration goes down.
  • Light is absorbed by the pigment epithelium when it is not used by the photo receptors (rod & Cones). Deer and other animals don’t have this and the light is reflected around the eye, this helps with night vision but decreases visual accuity. Bipolar cells are inhibited by photoreceptors under normal situations.
  • Presentation of light will cause an output of the ganglion cells.
  • Presentation of light will cause an output of the ganglion cells.
  • Photo receptors inhibit the bipolar cell. This causes the bipolar cell to depolarize.
  • Thrichromatic Color Theory – three different cones to see entire visible light spectum. Colors mix. We can see colors because the signals for the cones mix.
  • Like HTML different degrees of color at each type of cone produces different color combinations.
  • Humans are usualy Trichomates – unless color blind (then they only have two types of cones.) they flat out don’t have that type of cones.
  • If you stare at red long enough, the red/ green ganglion get over ecited. Then you look away, the cell over compensates and you see green.
  • Two colors are oposit colors of eachother. Cannot see the oposite colors together. Two type of ganglion cells – -one for red/green -excited: Red - Inhibited: Green - blue/yellow - Exced: Blue - Inhibited: yellow
  • Ganglion cells-> optic nerve-> right/left visual field-> optic nerve cross over to send info to contralateral hemasphere at the optic chiasm ->Thalamus -> LGN Thalamus- relay station for sensory inputs.
  • Rods- Go to Magnocellular. 10% Codes - go to Parvocelular 80%
  • They are like channels, they do not mix.
  • What- Where- Parvocellular – inferial tenpral lobe – cones -
  • V5 damage would be like lady who can only see still images.
  • IT- Facial Recognition.
  • Kinesthesia and Proprioception are very importaint in knowing how you look . x
  • TRP receptors respond to chemicals. (menthol)
  • C-fibers also detect hot, spicey food.
  • Glove in a bag. 5 outer pockets but unable to identify it as a glove.
  • Reorganization happens
  • Substance P is released in substantia gelantinossa Opiants block the realease of substance P. Thus no preception of pain. We rub an injery because it destracts us from the pain.
  • Allodynia – like when you burn your toung on a hot drink.
  • Memory: Idea that you have a change in your behavior in response to experience. Its applicible only when it is testable.
  • 1/3 rd of cerebrum is the frontal cortex
  • Working Memory= short term memory. Mental Math, Chess, convesations
  • Know definitions front and backwards. PFC- Pre-Frontal Cortex Spatial Location – where you parked. Hippocampus- forming memories, Memory = Sensory system picks up info-> Short term (working) memory ---(through rehersal)-->Long term memory Relevent information will be retained easier
  • Diffrence between pictures is orgin of production. They both have Wernicke’s->Broca’s->Motor by way of below. Information flows toward the frontal lobe. Working memory.
  • Cingulate Gyrus*
  • Cold colors- less activation. Warm colors- increased activation. Decrease of demand when practiced. Novel – new set of questions re-engages areas. Naïve – anterior singalate is lit up.
  • KNOW William James!! Donarld Hebb Make list of People and what they did. Short term memory- decays within about 30 seconds. You can handle 7 pices of numbers in that time period. New protines need to be created and new pathways created for long term memory. Consolidation- converting easily disruptable memory (phone number). Reconsolidation – dad with beard, dad without beard. Updating memory. When discussing a memory, it becomes slighly disrupted.
  • ECS- Electro shock theapy. Depression treatment. Could cause memory loss. The day leading up to ECS or a little after the treatment. Short term memory loss. Train – learning new knowledge. Shock given as knowledge is learned. Shock is given 1 day after Knolwege is learned. It is remembered a day after the shock. Shock is given 1 day afer, but then shock also given. No memory.
  • HM had epelepsy- (bilateral- both sides)medial tempral lobe rescetion. After he woke up, he was unable to remember. Long Term Memory- Declarative (explicit) – what did you do for dinner? <- event that happened, episodic event What is the capital of France <- memory of fact, Semantic memory nm-declaritive (implicent) Procedural memory- Motor skills- cerebellum Classic conditioning. Priming still worked with H.M. Amnesia- Medial Tempral Lobe is important for making memories, not important for storing new memories over long term. Skill development (double star) was on par with normal people for HM.
  • We remember 9/11 because the amygdala (activates) tells the brain to remember data at all costs. Epinephrine is also released. Without Epinephrine the enhanced memory is not likely. Its just the like a multiplication table.
  • Emotional State = Flashbulb memory- you remember everything about a event. Emotional arousal= epenephrin increse, amygdala, rest of brain
  • HM would not know that he had already learned to do something, he would just think that he was naturaly good at it. Damage to the hippocampus, may not be able to remember that they were primed but they will fill in “den” for garden when shown “garden” earlier.
  • Plaques and tangles are abmormal brain deposits. Abnormal production of beta…, which poke holes in the membrane and the synapse cannot function properly. Plaques are formed to stop the beta…, they are inert but when there is too much, it is bad.
  • Not getting a lot of inputs, so it eventualy dies. A nerve must have synapes to stay alive.
  • Railroad worker. Know the name. People in high school are often very different because PFC is last to develop.
  • Things are not planned out anymore. Making coffee – pour coffee in, stir, add suger. They see a comb in the gutter and start combing their hair. Normal people would leave it or throw it away but wash their hands. Akd Multiple Errands Task – Go to the bank, grocery store, pick up kids.
  • Damage to PFC will just read the words in C.
  • 26 different movements
  • Not told how to sort. First time, you choose color, WRONG. Next you choose by number, WRONG. Lastly you choose by shape, CORRECT. Other people get stuck and have a hard time changing the rule.
  • Subcortical – lower brain structures (cerebelum)
  • Line- time Elevation – length of time response, conditioned stimulus, unconditioned stimulus is activeated.
  • Know terms. Taste adversion. 1 trial of eating a food that makes you vomit will make you avoid the food. 50-100 trials before a response is learned.
  • Over simplification, but it works. Normal auditory imputs wont do much. LTP – long term placticity. It use to be that both stimulases needed to be present. After a while only the tone is nessisary to get you to blink.
  • CS & US overlap END OF LECTURE
  • LTP – strengthen LTD - weaken

Transcript

  • 1.
    • Overview of the Course & Syllabus
    • Studying the Brain and Behavior
      • • Disciplines & Approaches
    • History of Brain Research
      • • Cardiocentric vs. Encephalocentric
      • – Hippocrates, Aristotle, Galen, Descartes
      • • Holism vs. Localization
    • Development of Brain Research
      • • Topographical Organization
      • • Lashley’s Law of Mass Action
      • • Brain Mapping
      • • Dualism vs. Monism
    • Physiological Approach to Consciousness
      • • Blindsight
      • • Split Brains
      • • Unilateral Neglect
    PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 01 (September 08, 2010)
  • 2. Professor : James R. Moyer, Jr., Ph.D. Semester : Fall 2010 Office : Garland 208 Meeting Time : MW 9:00 – 9:50 a.m. Office hrs: MW 10:00 – 10:50 a.m. Meeting Place : ENG 105 Office ph: x3255 Psych Listing : 254–402 lecture Email: [email_address] Course Description This course is designed to provide each student with comprehensive exposure to the nervous system and how it governs various behaviors . The course will also cover relevant anatomical, behavioral, psychological, cellular, imaging, and neurophysiological approaches used to study animal behavior. Upon completion of the course, the student will have a solid foundation regarding the biological basis of behavior upon which to build in more advanced courses of study. Reading Materials The recommended textbook for this course is Carlson, NR (2010). Physiology of Behavior, 10 th Ed. Allyn & Bacon, New York, NY . (Note: there are a variety of texts on reserve in the library as well). Course Syllabus for Physiological Psychology
  • 3. Determination of Your Final Grade Your overall grade will be determined by combining your scores from the following: 1. Discussion Section Attendance (10%) . Discussion sessions will begin Monday, September 13. TA will take attendance. If you cannot make your discussion session, you must make arrangements to attend one of the other 9 discussion sections that week . See page 6 of the syllabus for the weekly discussion session schedule . 2. Weekly Online Quizzes (25%) . There will be 12 open-book/notes quizzes available for you to take online beginning September 13 (each quiz will be available for one week). See page 7 of the syllabus for the quiz schedule. NO make-ups (if you fail to take a quiz you will receive a grade of zero for that quiz). 3. Regular Exams (40%). There will be 2 exams ( multiple-choice, true-false, matching questions ) scheduled during the semester (see dates on syllabus). Exams will be cumulative , which means that there will be some material from the previous exam(s) on each successive exam. 4. Final exam (25%). There will be a cumulative final exam on Tuesday, December 21, 2010 from 10:00 a.m. to 12:00 p.m. in ENG 105 . Any student who does not take the final exam will fail the course. The final grade for the course will be determined based on your final average according to the following scale: A = 93-100%; A- = 90-92%; B+ = 87-89%; B = 83-86%; B- = 80-82%; C+ = 77-79%; C = 73-76%; C- = 70-72%; D+ = 67-69%; D = 63-66%; D- = 60-62%; F = 0-59%. Course Syllabus for Physiological Psychology
  • 4. Make-up, Curving and Extra Credit Make-up exam. Should a student fail to take one of the three scheduled exams during the semester, that student will receive a zero “0” as a grade for that exam. However, at the end of the semester a “one size fits all” cumulative make-up will be offered for students who missed one of the exams (no excuse or reason necessary). The make-up will be held on the study day at 9:00 a.m. on Wednesday, December 15 in ENG 105 . Curving of exams. I will not curve any of the exams. However, all exams will contain some extra credit questions. Thus, it is always possible to score greater than 100% on any exam, including the final. Extra credit. You may receive up to a maximum of 5 extra credit points, which will be added to your final exam score (thus, if you scored an 86% on the final and you did 5 points worth of extra credit, your final exam score would be a 91%). Check bulletin boards in Garland and Pearse for extra credit opportunities. I will also post some extra credit opportunities on the D2L, if an instructor requests an advertisement in class. Course Syllabus for Physiological Psychology
  • 5. Getting Help If you are having difficulties or have questions, please do not hesitate to come in for a visit to discuss any issues pertinent to your academic success. If you are struggling in the class, don’t wait until you’ve taken numerous quizzes or both exams to come for help . One mistake students often make is waiting too long to come to me to discuss their performance in the class, which limits my ability to help the student. Course Syllabus for Physiological Psychology
  • 6. Studying the Brain and Behavior
    • • Neuroscience – multidisciplinary approach to studying the brain
    • • Behavioral Neuroscience – e.g., psychologists using a bottom-up approach
      • • also Physiological Psychology or Biopsychology
    • • Cognitive Neuroscience – e.g., psychologists using a top-down approach
    • • Neuropsychology – e.g., psychologists ( top-down ) studying higher brain functions and their disorders following brain injury or disease
      • • also Clinical Neuropsychology or Experimental Neuropsychology
    • • Computational Neuroscience – utilization of mathematical models to explain
      • how neuronal activity relates to information processing in the brain
  • 7. History of Brain Research CARDIOCENTRIC explanations of behavior prevailed in ancient cultures • argued that the heart controlled thoughts, emotions and behavior • e.g., ancient Egyptians removed and discarded the brain before mummification but preserved the heart for the afterlife ENCEPHALOCENTRIC explanations of behavior emerged from dissections • argued that the brain controlled thoughts and emotions and behavior • Hippocrates (460-377 B.C.) after witnessing many dissections argued that the brain controls behavior • Plato (427-327 B.C.) agreed with Hippocrates • Aristotle (384-322 B.C.) disagreed & argued it “cools the heart” • Galen (130-200 A.D.) later concluded that Aristotle’s role for the brain was “utterly absurd” for two reasons: 1. The brain was too far away to cool the heart and 2. Too many sensory nerves were attached to the brain • René Descartes (1596-1650 A.D.) argued that the pineal gland is the seat of the soul and exerts its actions via pressure changes in the fluid-filled ventricles
  • 8. Holism vs. Localization Controlled experiments involving the brain were quite rare until the 19th century. • Thus, two schools of thought emerged regarding the extent to which specific brain areas govern behaviors. Holism – argued that every area of the brain can control all human functions Localization – argued that human functions are regulated by distinct brain regions • Franz Gall (1757-1828) popularized localization based on his theories that specific brain protuberances (felt via skull) corresponded to specific personality traits “ Phrenology ” • Although not based on experimental evidence, Gall changed how many people thought about the brain and the work of future scientists supported localization of brain function.
  • 9. 1861 – Paul Broca examined patient “Tan” who had a stroke ~20 yrs earlier.
  • 10. 1876 – David Ferrier stimulated the motor cortex of monkeys and demonstrated that the indicated areas controlled movement of specific body parts: 1 and 2 hind limbs 3 tail 4, 5, 6 arm a, b, c, d hands and fingers 7-11 face and mouth 12, 13 eyes, head 14 ear 1870 – Fritsch and Hitzig stimulated the motor cortex of dogs and noted that stimulation near the top caused the hind legs to wiggle whereas stimulation near the bottom caused the jaw to move.
  • 11. TOPOGRAPHICAL ORGANIZATION - Motor Cortex
  • 12. TOPOGRAPHICAL ORGANIZATION - Motor Homunculus
  • 13. TOPOGRAPHICAL ORGANIZATION - Somatosensory Cortex
  • 14. TOPOGRAPHICAL ORGANIZATION - Somatosensory Cortex
  • 15.
    • 1929 – Karl Lashley claimed to have evidence supporting holism
    • He postulated the following:
    • Law of Mass Action
      • • lesion size rather than
      • location is what matters
    • Law of Equipotentiality
      • • restatement of holism
  • 16.
    • 1940s and 50s – Wilder Penfield used a 3-Volt battery attached to a probe, he stimulated different areas of the cortex in awake patients whose brains were exposed (epilepsy surgery).
    • He observed the following:
    • Recall of memories when back of cortex was stimulated
    • Sensations in various body parts in response to topographical stimulation of the somatosensory cortex
    • Penfield’s work inspired the drawings of the homunculi which are used to illustrate topographical organization of the primary motor and somatosensory cortices.
  • 17. PET scans reveal which specific brain regions are activated by a given task
  • 18. PET scans reveal which specific brain regions are activated by a given task Sight Sound Touch Speech
  • 19. PET scans reveal which specific brain regions are activated by a given task Sight Sound Touch Speech
  • 20. PET scans reveal which specific brain regions are activated by a given task Sight Sound Touch Speech
  • 21. PET scans reveal which specific brain regions are activated by a given task Sight Sound Touch Speech
  • 22. WHERE’S THE MIND? Two schools of thought: Dualism – the mind and body (or brain) are separate. e.g., Plato “father of western dualism” e.g., René Descartes Monism – the mind is the result of brain functioning & follows physical laws e.g., Leonardo da Vinci (1452-1519) stated “mind is a product of the brain” e.g., most modern brain scientists
  • 23. Physiological Approaches to Consciousness • Consciousness can be altered by changes in brain chemistry and thus we may hypothesize that it is a physiological function, just like behavior • Consciousness and ability to communicate seem to go hand in hand • Verbal communication allows us to send and receive messages from other people as well as send and receive our own messages (and thus think and be aware of our own existence)
  • 24. Physiological Approach to Consciousness
    • Blindsight – ability of person who cannot see objects in their blind field to accurately reach for them while remaining “unconscious” of perceiving them (e.g., stroke resulting in damage to the visual cortex)
    • Split Brain operation – surgical cutting of the corpus callosum which connects the left and right hemispheres (to ameliorate the severity of epilepsy)
    • Unilateral Neglect – failure to notice things located to a person’s left (e.g., stroke resulting in damage to the right parietal cortex)
    Consciousness is not a general property of all parts of the brain
  • 25. An explanation of the blindsight phenomenon
  • 26. MRIs of human brain showing corpus callosum (cc) corpus callosum
  • 27. Identification of an object by smell in a split-brain patient
  • 28. Identification of an object by sight in a split-brain patient
  • 29. Angular Gyrus Activity and the Out of Body Experience
  • 30. END – Lecture 01
  • 31. ORGANIZATION OF THE NERVOUS SYSTEM • CNS vs. PNS THE CENTRAL NERVOUS SYSTEM I • Meninges, Ventricles, and Cerebrospinal Fluid • The Spinal Cord • Anatomical Coordinates PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 02 (September 13, 2010)
  • 32. Organization of the Nervous System
    • Central Nervous System or CNS
        • • brain
        • • spinal cord
    • Peripheral Nervous System or PNS
        • • outside the spinal cord
  • 33. The Meninges Line and Protect the CNS
    • 3 Layers:
    • dura mater – tough outer layer
    • arachnoid layer – middle vascular layer
      • • serves to return CSF from base of spinal cord back to brain ( and blood stream via arachnoid villi )
    • pia mater – delicate innermost layer
  • 34. Ventricles & Flow of CSF • Lateral ventricle (2) • Third ventricle – aqueduct of Sylvius • Fourth ventricle – central canal
  • 35. Flow of CSF (Choroid Plexus Produces CSF) * * * * * * • CSF flows from choroid plexus (cells that make CSF) • CSF vol ~125 mL, continuously produced with half life ~3 hr • CSF circulates and then returns to blood stream via arachnoid villi or granulations (absorb CSF)
  • 36. Different Views of the Ventricles & Flow of CSF
  • 37. CSF Flows Down Spinal Cord via the Central Canal
  • 38.  
  • 39.
    • 5 Segments of the Spinal Cord
    • Cervical
    • Thoracic
    • Lumbar
    • Sacral
    • Coccygeal
  • 40. Anatomical Planes
  • 41. Anatomical Planes
  • 42. Anatomical Planes
  • 43. Anatomical Directions
  • 44. END – Lecture 02
  • 45.
    • THE CENTRAL NERVOUS SYSTEM II
    • The Brain
      • • Forebrain ( prosencephalon )
        • • Midbrain ( mesencephalon )
        • • Hindbrain ( rhombencephalon )
    PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 03 (September 15, 2010)
  • 46. 3 Major Divisions of the Brain
    • Prosencephalon ( Forebrain )
      • • telencephalon (cerebrum, limbic system, basal ganglia)
      • • diencephalon (thalamus, hypothalamus)
    • Mesencephalon ( Midbrain ) – smallest of the 3 divisions
      • • dorsal portion or tectum (superior & inferior colliculi)
      • • tegmentum (red nucleus, periaqueductal gray, substantia nigra)
        • • ventral portion (tracts connecting forebrain & hindbrain)
    • Rhombencephalon ( Hindbrain )
        • • metencephalon (cerebellum , pons)
        • • myelencephalon (medulla)
    Brain Stem = diencephalon & mesenephalon & rhombencephalon
  • 47.
    • Prosencephalon ( Forebrain ) – thinking, creating, speaking,
    • planning, emotions, etc… ( pretty much all that makes us human )
      • 1. telencephalon
      • • cerebrum
      • • limbic system (hippocampus, amygdala, septum)
      • • basal ganglia
      • 2. diencephalon
      • • thalamus
      • • hypothalamus
  • 48. The Cerebrum Central Sulcus separates frontal ( precentral gyrus ) from parietal ( postcentral gyrus ) Sylvian Fissure or Lateral Sulcus separates the temporal lobe from other lobes Sulci are fissures or grooves; Gyri are raised areas or outward bumps The Four Lobes of the Cerebrum
  • 49. The Major Lobes of the Cerebrum The Cerebrum
  • 50.
    • Frontal lobes
        • • motor cortex , premotor cortex , prefrontal cortex
        • • prefrontal cortex – executive functions, including short-term
        • memory, decision making, prioritizing behaviors
    • Parietal lobes
        • • postcentral gyrus, secondary somatosensory cortex
        • • somatosensory cortex processes sensory information
    • Occipital lobes
        • • visual cortex processes visual information
    • Temporal lobes
        • • auditory cortex, olfactory cortex
        • • amygdala and hippocampus (emotions; learning & memory)
    Lobes of the Cerebrum
  • 51.
    • The Cerebral Hemispheres are Connected by:
    • Corpus Callosum – connects left and right frontal, parietal, occipital
    • Anterior Commissure – connects left and right temporal lobes
            • (e.g., hippocampus, amygdala)
    The Cerebrum The Cerebrum contains: Gray Matter (5-7 layers of neurons) and White Matter (axons) (the cerebral Gray matter is also called the cerebral cortex)
  • 52. Cross Section through the Cerebrum
  • 53. The Cerebrum Anterior Commissure Note that the line from the label “Cerebral Cortex” at the upper left seems to point to white matter. However, the term Cerebral Cortex is generally used to refer to the Gray Matter.
  • 54. Diffusion Tensor Imaging of Corpus Callosum Projections Diffusion Tensor Imaging involves a modified MRI magnet. It enables visualization of bundles of axons (the processes that transmit signals from one cell to another)
  • 55.
    • Prosencephalon ( Forebrain ) – thinking, creating, speaking,
    • planning, emotions (pretty much all that makes us human)
      • 1. telencephalon
      • • cerebrum
      • • limbic system (hippocampus, amygdala, septum)
      • • basal ganglia
      • 2. diencephalon
      • • thalamus
      • • hypothalamus
  • 56. Limbic System – a circuit of structures involved in emotion and memory (Paul MacLean, 1949)
    • Hippocampus
        • • sea horse shaped structure in temporal lobes
        • • important for forming long-term memories
    • Amygdala
        • • important for emotions
        • • produces fear, aggression
        • • Rabies virus attacks the amygdala
    • Septum
        • • stimulation produces pleasure
    • Mamillary Bodies
        • • hypothalamic nuclei interconnected with hippocampus
        • • important for emotion and memory
    Other regions also make up what is called the “limbic system”
  • 57. Schematic of Limbic Structures
  • 58. Superior View of Limbic Structures Side View of Limbic Structures (without any other brain regions)
  • 59.
    • Prosencephalon ( Forebrain ) – thinking, creating, speaking,
    • planning, emotions (pretty much all that makes us human)
      • 1. telencephalon
      • • cerebrum
      • • limbic system (hippocampus, amygdala, septum)
      • • basal ganglia
      • 2. diencephalon
      • • thalamus
      • • hypothalamus
  • 60. Basal Ganglia – a cluster of neuronal structures concerned with the production of movement.
    • Putamen and Globus Pallidus
        • • egg-shaped structure in each hemisphere
    • Caudate
        • • tail-shaped structure
    Basal ganglia structures are implicated in a variety of disorders, including Obsessive-Compulsive Disorder, Parkinson’s disease, and Huntington’s chorea
  • 61. Location of the Basal Ganglia & Thalamus
  • 62.
    • Prosencephalon ( Forebrain ) – thinking, creating, speaking,
    • planning, emotions (pretty much all that makes us human)
      • 1. telencephalon
      • • cerebrum
      • • limbic system (hippocampus, amygdala, septum)
      • • basal ganglia
      • 2. diencephalon
      • • thalamus
      • • hypothalamus
  • 63. Diencephalon – forebrain region that surrounds the 3rd ventricle
    • Thalamus
        • • a large number of nuclei in each hemisphere
        • • look like flattened egg-shaped structures
        • • relays information to and from the cerebrum
    • Hypothalamus
        • • series of nuclei (located below thalamus)
        • • controls activity of the pituitary gland
        • • important for many regulated behaviors including:
        • – eating and drinking
        • – sleeping
        • – temperature control
        • – sexual and emotional
  • 64. Thalamic Connections with the Cortex
  • 65. Thalamic Connections using Diffusion Tensor Imaging
  • 66. Location of the Hypothalamus & Pituitary Gland
  • 67. Location of the Hypothalamus & Pituitary Gland
  • 68. 3 Major Divisions of the Brain
    • Prosencephalon ( Forebrain )
      • • telencephalon (cerebrum, limbic system, basal ganglia)
      • • diencephalon (thalamus, hypothalamus)
    • Mesencephalon ( Midbrain ) – smallest of the 3 divisions
      • • dorsal portion or tectum (superior & inferior colliculi)
      • • tegmentum (red nucleus, periaqueductal gray, substantia nigra)
        • • ventral portion (tracts connecting forebrain & hindbrain)
    • Rhombencephalon ( Hindbrain )
        • • metencephalon (cerebellum, pons)
        • • myelencephalon (medulla)
    Brain Stem = diencephalon & mesenephalon & rhombencephalon
  • 69.
    • Mesencephalon ( Midbrain ) – also contains the reticular formation which runs from hindbrain to forebrain
      • reticular formation
      • • consists of many nuclei & a diffuse network of interconnected neurons (reticular = little net)
      • • important in arousal (alerts forebrain to important stimuli)
      • • damage results in a coma
  • 70. 3 Major Divisions of the Brain
    • Prosencephalon ( Forebrain )
      • • telencephalon (cerebrum, limbic system, basal ganglia)
      • • diencephalon (thalamus, hypothalamus)
    • Mesencephalon ( Midbrain ) – smallest of the 3 divisions
      • • dorsal portion or tectum (superior & inferior colliculi)
      • • tegmentum (red nucleus, periaqueductal gray, substantia nigra)
        • • ventral portion (tracts connecting forebrain & hindbrain)
    • Rhombencephalon ( Hindbrain )
        • • metencephalon (cerebellum, pons)
        • • myelencephalon (medulla)
    Brain Stem = diencephalon & mesenephalon & rhombencephalon
  • 71.
    • Rhombencephalon ( Hindbrain ) – immediately superior to spinal cord
      • 1. Cerebellum
      • • located dorsal to both medulla and pons
      • • contains a cortex and underlying white matter
      • • coordination of movement
      • • alcohol impairs cerebellar function
      • 2. Pons
      • • located superior to the medulla
      • • composed mostly of white matter tracts
      • • serves as a bridge between cerebral cortex and cerebellum
      • 3. Medulla
      • • located just superior to spinal cord
      • • ascending & descending cortical tracts cross over from left to right
      • • controls many life-support functions ( breathing, HR, coughing, vomiting)
    Metencephalon (cerebellum & pons) ; Myelencephalon (medulla)
  • 72. Midsagittal view of Forebrain, Midbrain, & Hindbrain
  • 73. Parts of the Forebrain, Midbrain, & Hindbrain
  • 74. Human Brainstem
  • 75. END – Lecture 03
  • 76.
    • DIVISIONS OF THE PERIPHERAL NERVOUS SYSTEM
    • Somatic vs. Autonomic
    • Sympathetic vs. Parasympathetic
    • Peripheral Nerves
      • • Cranial nerves
      • • Spinal nerves
    • Organization of the PNS
    PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 04 (September 20, 2010)
  • 77. Divisions of the Peripheral Nervous System
    • Somatic Nervous System
        • • controls skeletal muscles
        • • under voluntary control
    • Autonomic Nervous System
        • • controls smooth and cardiac muscle
        • • NOT under voluntary control
  • 78. Divisions of the Autonomic Nervous System
    • Sympathetic Nervous System
        • • fight-or-flight system
        • • dilates pupils
        • • accelerates heart rate
        • • relaxes bronchi
        • • increases blood flow to muscles
        • • decreases blood flow to stomach & internal organs
    • Parasympathetic Nervous System
        • • energy conservation system
        • • constricts pupils
        • • slows heart rate
        • • constricts bronchi
        • • increases blood flow to stomach & internal organs
  • 79. Divisions of the Autonomic Nervous System
    • Eyes
    • Lungs
    • Heart
    • Stomach, Intestines
    • Blood vessels of internal organs
  • 80. PNS Transmits Information to the Body via 43 Pairs of Nerves • 12 pairs of CRANIAL NERVES – enter & exit the brain through holes in skull • 31 pairs of SPINAL NERVES – enter & exit the spinal cord between vertebrae
  • 81. CRANIAL NERVES (12 pairs, CNs I through XII) • enter & exit the brain through holes ( foramena ) in skull • permit direct communication between brain & PNS • allow for sensory input from head, neck, upper abdomen • allow for motor output from brain to skeletal muscles in head and neck • allow for parasympathetic output to smooth muscles in head, neck, and upper abdomen • CNs I & II go to forebrain (prosencephalon) • CNs III & IV arise from midbrain (mesencephalon) • CNs V–XII enter & exit the hindbrain (rhombencephalon)
  • 82. CRANIAL NERVES (12 pairs) 3 of the cranial nerves serve sensory functions only: • CN I (olfactory nerve) – sensory ; smell • CN II (optic nerve) – sensory ; sight • CN III • CN IV • CN V • CN VI • CN VII • CN VIII (auditory nerve) – sensory ; hearing • CN IX • CN X • CN XI • CN XII
  • 83. Red is motor Blue is Sensory
  • 84. CRANIAL NERVES (12 pairs) 3 of the cranial nerves control eye movement: • CN I (olfactory nerve) – sensory ; smell • CN II (optic nerve) – sensory ; sight • CN III (oculomotor nerve) – motor, eye movement • CN IV (trochlear nerve) – motor, eye movement • CN V • CN VI (abducens nerve) – motor, eye movement • CN VII • CN VIII (auditory nerve) – sensory ; hearing • CN IX • CN X • CN XI • CN XII
  • 85. Red is motor Blue is Sensory
  • 86. CRANIAL NERVES (12 pairs) 2 of the cranial nerves control facial muscles: • CN I (olfactory nerve) – sensory ; smell • CN II (optic nerve) – sensory ; sight • CN III (oculomotor nerve) – motor, eye movement • CN IV (trochlear nerve) – motor, eye movement • CN V (trigeminal nerve) – motor, chewing; sensory, face & head • CN VI (abducens nerve) – motor, eye movement • CN VII (facial nerve) – motor, facial muscles; sensory, taste & face • CN VIII (auditory nerve) – sensory ; hearing • CN IX • CN X • CN XI • CN XII
  • 87. Red is motor Blue is Sensory
  • 88. CRANIAL NERVES (12 pairs) 2 of the cranial nerves control throat and tongue muscles: • CN I (olfactory nerve) – sensory ; smell • CN II (optic nerve) – sensory ; sight • CN III (oculomotor nerve) – motor, eye movement • CN IV (trochlear nerve) – motor, eye movement • CN V (trigeminal nerve) – motor, chewing; sensory, face & head • CN VI (abducens nerve) – motor, eye movement • CN VII (facial nerve) – motor, facial muscles; sensory, taste & face • CN VIII (auditory nerve) – sensory ; hearing • CN IX (glossopharyngeal) – motor, throat & larynx; sensory, taste • CN X • CN XI • CN XII (hypoglossal nerve) – motor, tongue movements
  • 89. Red is motor Blue is Sensory
  • 90. CRANIAL NERVES (12 pairs) 1 cranial nerve wanders to the head, neck, & upper abdomen: • CN I (olfactory nerve) – sensory ; smell • CN II (optic nerve) – sensory ; sight • CN III (oculomotor nerve) – motor, eye movement • CN IV (trochlear nerve) – motor, eye movement • CN V (trigeminal nerve) – motor, chewing; sensory, face & head • CN VI (abducens nerve) – motor, eye movement • CN VII (facial nerve) – motor, facial muscles; sensory, taste & face • CN VIII (auditory nerve) – sensory ; hearing • CN IX (glossopharyngeal) – motor, throat & larynx; sensory, taste • CN X (vagus nerve) – motor, smooth muscles of neck, chest & upper abdomen; sensory, taste, organs of chest & upper abdomen • CN XI • CN XII (hypoglossal nerve) – motor, tongue movements
  • 91. Red is motor Blue is Sensory
  • 92. CRANIAL NERVES (12 pairs) 1 cranial nerve is motor only & innervates neck muscles: • CN I (olfactory nerve) – sensory ; smell (S) • CN II (optic nerve) – sensory ; sight (S) • CN III (oculomotor nerve) – motor, eye movement (M) • CN IV (trochlear nerve) – motor, eye movement (M) • CN V (trigeminal nerve) – motor, chewing; sensory, face & head (B) • CN VI (abducens nerve) – motor, eye movement (M) • CN VII (facial nerve) – motor, facial muscles; sensory, taste & face (B) • CN VIII (auditory nerve) – sensory ; hearing (S) • CN IX (glossopharyngeal) – motor, throat & larynx; sensory, taste (B) • CN X (vagus nerve) – motor, smooth muscles of thoracic & upper abdomen; sensory, taste, organs of chest & upper abdomen (B) • CN XI (accessory nerve) – motor only, skeletal muscles of neck (M) • CN XII (hypoglossal nerve) – motor, tongue movements (M) Mnemonic: S ome S ay M oney M atters B ut M y B rother S ays B ig B rains M atter M ore ( S = sensory; M = motor; B = both)
  • 93. Red is motor Blue is Sensory
  • 94. The Cranial Nerves & Their Functions Bell’s Palsy – facial paralysis caused by an infection of the facial nerve ( CN VII ). Results in paralysis on that side of face (not usually permanent).
  • 95. PNS Transmits Information to the Body via 43 Pairs of Nerves • 12 pairs of CRANIAL NERVES – enter & exit the brain through holes in skull • 31 pairs of SPINAL NERVES – enter & exit the spinal cord between vertebrae
  • 96. Spinal Nerves Exit the Spinal Cord Between Adjacent Vertebra
  • 97. Spinal Nerves Exit the Spinal Cord Between Adjacent Vertebra
  • 98. Spinal Nerves Exit the Spinal Cord Between Adjacent Vertebra
  • 99. Cross Section of Spinal Cord
    • Sensory is Dorsal (signals enter)
    • Motor is Ventral (signals exit the cord)
    • (Bell-Magendie law)
  • 100. SPINAL NERVES (31 pairs) • enter & exit the spinal cord between vertebrae • 8 pairs arise from Cervical region ( C1–C8 ) • 12 pairs arise from Thoracic region ( T1–T12 ) • 5 pairs arise from the Lumbar region ( L1–L5 ) • 5 pairs arise from the Sacral region ( S1–S5 ) • 1 pair arises from the Coccygeal region
    • For a given region, lower numbers are superior (or higher) along the cord.
    • Thus, C1 is superior to C2, etc…
    • (2) In spinal cord damage, the higher the lesion on the spinal cord
    • ( e.g., C is higher than T or L ), the more severe the injury.
  • 101.
    • 5 Segments of the Spinal Cord
    • Cervical
    • Thoracic
    • Lumbar
    • Sacral
    • Coccygeal
  • 102. Dermatome Map • The body area innervated by one spinal nerve Q: Why do you not see C1 on the dermatome map to the right?
  • 103. Sacral–Parasympathetic (anus, genitals, & bladder) Cranial–Parasympathetic (organs, vessels, and muscles, etc…) Thoracic & Lumbar – Sympathetic (organs, vessels, muscles, anus, genitals, bladder, etc…) Distribution of the Autonomic Nervous System
  • 104. • thoracolumbar • craniosacral Distribution of the Autonomic Nervous System
  • 105. END – Lecture 04
  • 106.
    • NEURONS AND GLIAL CELLS
    • Structure of Neurons
        • • Soma
        • • Dendrites
        • • Axons
    • Classifying Neurons
        • • Anatomical
        • • Functional
    • Glial Cells
    • • Types of Glia
    • • Role in Axon Myelination
    PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 05 (September 22, 2010)
  • 107. The Nervous System Two Types of Cells: 1. Neurons – cells of the nervous system 2. Glia – support cells Historically: • 1840 – Schleiden & Schwann proposed cells were basic units of tissue • However, scientists thought that nervous tissue was not made of cells 1860s Golgi – Silver impregnation 1892 Cajal – Neuron doctrine 1906 Golgi & Cajal were awarded the Nobel Prize Camillo Golgi (1843-1926) Ramón y Cajal (1852-1934)
  • 108. 3 Parts of a Neuron
    • Soma or cell body (contains nucleus, etc…)
    • Dendrite (transmits signals toward soma)
        • • some cells have few dendrites
        • • some cells have many dendrites
    • Axon (transmits signals from soma – output)
        • • all cells have one axon
        • • axon can branch many times
  • 109. Example of a Motor Neuron
  • 110. Parts of a Neuron
  • 111. Information Flow Between and Within Neurons 1. Signal enters dendrite or soma 2. Signal travels from soma to axon 3. Signal travels down axon 4. Signal leaves axon and enters dendrite or soma
  • 112. Divergence (e.g., sensory) Convergence (e.g., motor) Information Flow Between Neurons
  • 113. Basic Subcellular Components of Mammalian cells (similar for neurons)
  • 114. Structure of Neurons
  • 115. Major Organelles
    • Nucleus – contains DNA. Gene expression occurs by transcription of DNA into RNA, which is exported out of the cell and used as a template to make proteins.
    • Endoplasmic reticulum – membranous organelle that makes lipids and proteins. There are two varieties observed in cells:
        • Rough ER (studded with ribosomes) - used to make secreted and membrane-bound proteins.
        • Smooth ER (without ribosomes) - used to make lipids.
    • Golgi apparatus – membranous structure that modifies and stores the proteins and lipids made in the endoplasmic reticulum.
    • Mitochondria – fuel powerhouse of the cell. Produces ATP (adenosine triphosphate), which is used as an energy source for chemical reactions.
    • Cell membrane – phospholipid bilayer that surrounds the cell. In neurons, it contains proteins called ion channels that are selectively permeable to various salts or ions (e.g., calcium, sodium, chloride, potassium, etc…).
  • 116. Cell Nucleus and Protein Synthesis Chromosomes contain genetic information, 23 pairs – 22 pairs are autosomal – the final pair are sex chromosomes (XX or XY) – the 23 pair of chromosomes contain ~20,000 to 25,000 genes Genome refers to the sum total of all the genes; same in every cell Nucleic acids are specialized compounds that contain a nitrogenous base, a sugar, and a phosphoric acid • Deoxyribonucleic acid (DNA ) encodes the genetic material of a cell – found in the nucleus (and in mitochondria) • Contains 4 nitrogen bases: Adenine, Guanine, Cytosine, Thymine • Nucleoside is nitrogen base + sugar (2-deoxyribose) • Nucleotide is base-sugar + phosphoric acid • Ribonucleic acid (RNA ) serves as blueprint for proteins – generally found in the cytoplasm as mRNA and ribosomes – also contain 4 nitrogen bases: Adenine, Guanine, Cytosine, Uracil – triplet base pairs encode specific amino acids (e.g., UGG = tryptophan ) – ribosomes read mRNA and add appropriate amino acids to make protein
  • 117. Structure of Neurons
  • 118. Examples of Genetic Alterations that affect Brain Function Fragile-X Syndrome – normally the X chromosome (FMR1 gene has a CGG triad repeated 10-30 times ) – in fragile-X, the CGG triad is repeated hundreds of times – produces mental retardation (disrupted synaptic connections) Mental retardation also results from untreated phenylketonuria (PKU) which is linked to an altered gene on chromosome 12 ( lack of phenylalanine hydroxylase ) Down Syndrome – Results from a trisomy of chromosome 21 (3 copies instead of 2) – leads to faulty brain development and cognitive impairments as well as other skeletal and soft tissue abnormalities
  • 119. Classifying Neurons 1. Based on anatomical or morphological features (Ramón y Cajal) – unipolar (or monopolar) neuron – bipolar neuron – pseudo-unipolar neuron – multipolar neuron 2. Based on functionality (often used to describe neurons in the spinal cord) – motor neuron – sensory neuron – interneuron
  • 120. Anatomical Classifications
  • 121. Example of a Sensory Neuron Note: functionally, this pseudo-unipolar cell contains one axon (on the left) and a sensory process on the right, however this process is functionally an axon (it reliably transmits electrical spikes from the skin to the CNS). Only the sensory endings are technically dendrites. Warning: some people (including your text) refer to pseudo-unipolar cells as unipolar cells, I maintain a separate classification between these, however both are exclusively sensory neurons .
  • 122. Functional Classifications
    • Motor neuron
    • Sensory neuron
    • Interneuron
  • 123. Functional Classifications
    • Motor neuron
    • Sensory neuron
    • Interneuron
    Bell-Magendie law – sensory enters dorsal, motor exits ventral Note:
  • 124. Glial Cells
    • “ glue ” that holds the nervous system together
    • There are 10 times as many glial cells as neurons
      • – about 100 billion neurons (100,000,000,000)
      • – thus, there are at least 1 trillion glia (1,000,000,000,000)
    • Many are much smaller than neurons
  • 125. Roles of Glial Cells in the Nervous System
    • Provide nourishment for neurons
        • Astrocytes surround blood vessels & obtain nutrients
    • Remove waste and dead neurons
        • Astrocytes and Microglia (also function as macrophages )
    • Form scar tissue in the nervous system
        • Astrocytes migrate into empty space
        • Gliosis is the accumulation of glia in brain tissue
    • Direct development of the nervous system
        • Radial glia direct neuronal migration
    • Provide axonal myelination
        • Schwann cells myelinate axons in the PNS
        • Oligodendrocytes myelinate axons in the CNS
    • Contribute to blood-brain barrier (fat-soluble enter easily)
        • Astrocytes form tight junctions with capillary endothelium
  • 126. Glial Cells – Astrocytes
  • 127. Myelination of Axons Schwann Cells (PNS) Oligodendrocytes (CNS) Value of myelination: 1. Speeds axonal transmission (action potential jumps from node of Ranvier to node of Ranvier instead of traveling down entire axon (Saltatory Conduction) 2. Assist in axon regeneration (Schwann cells only)
  • 128. Electron Micrograph of a Schwann Cell Schwann Cells – myelinate only one segment of one axon
  • 129. Comparison of Oligodendrocytes and Schwann Cells
  • 130. Oligodendrocytes myelinate multiple segments of multiple axons
  • 131. Blood-Brain Barrier
  • 132. Blood-Brain Barrier
  • 133. END – Lecture 05
  • 134. Parts of a Cell Slides
    • These slides contain background information the majority of which you are expected to know prior to taking physiological psychology.
    • If this material is not familiar to you, please read pages 30-36 of the Carlson text [if you don’t have the Carlson text, similar material is contained in virtually any physiological psychology text (usually in chapter 2 or 3)
  • 135. Structure of Neurons
  • 136. Major Organelles
    • Nucleus – contains DNA. Gene expression occurs by transcription of DNA into RNA, which is exported out of the cell and used as a template to make proteins.
    • Endoplasmic reticulum – membranous organelle that makes lipids and proteins. There are two varieties observed in cells:
        • Rough ER (studded with ribosomes) - used to make secreted and membrane-bound proteins.
        • Smooth ER (without ribosomes) - used to make lipids.
    • Golgi apparatus – membranous structure that modifies and stores the proteins and lipids made in the endoplasmic reticulum.
    • Mitochondria – fuel powerhouse of the cell. Produces ATP (adenosine triphosphate), which is used as an energy source for chemical reactions.
    • Cell membrane – phospholipid bilayer that surrounds the cell. In neurons, it contains proteins called ion channels that are selectively permeable to various salts or ions (e.g., calcium, sodium, chloride, potassium, etc…).
  • 137. Cell Nucleus and Protein Synthesis Chromosomes contain genetic information, 23 pairs – 22 pairs are autosomal – the final pair are sex chromosomes (XX or XY) – the 23 pair of chromosomes contain ~20,000 to 25,000 genes Genome refers to the sum total of all the genes; same in every cell Nucleic acids are specialized compounds that contain a nitrogenous base, a sugar, and a phosphoric acid • Deoxyribonucleic acid (DNA ) encodes the genetic material of a cell – found in the nucleus (and in mitochondria) • Contains 4 nitrogen bases: Adenine, Guanine, Cytosine, Thymine • Nucleoside is nitrogen base + sugar (2-deoxyribose) • Nucleotide is base-sugar + phosphoric acid • Ribonucleic acid (RNA ) serves as blueprint for proteins – generally found in the cytoplasm as mRNA and ribosomes – also contain 4 nitrogen bases: Adenine, Guanine, Cytosine, Uracil – triplet base pairs encode specific amino acids (e.g., UGG = tryptophan ) – ribosomes read mRNA and add appropriate amino acids to make protein
  • 138. Structure of Neurons
  • 139. Examples of Genetic Alterations that affect Brain Function Fragile-X Syndrome – normally the X chromosome (FMR1 gene has a CGG triad repeated 10-30 times ) – in fragile-X, the CGG triad is repeated hundreds of times – produces mental retardation (disrupted synaptic connections) Mental retardation also results from untreated phenylketonuria (PKU) which is linked to an altered gene on chromosome 12 ( lack of phenylalanine hydroxylase ) Down Syndrome – Results from a trisomy of chromosome 21 (3 copies instead of 2) – leads to faulty brain development and cognitive impairments as well as other skeletal and soft tissue abnormalities
  • 140.
    • How Do Neurons Communicate?
        • • chemical & electrical transmission
    • Chemical Synapse
      • • components of a synapse
      • • types of synapses
      • • neurotransmitters
    • Neuronal Membrane Properties
      • • neuronal cell membrane
      • • membrane potential
      • • distribution of ions
      • • ion channels
      • • depolarization & hyperpolarization
      • • action potential
    • Signal Integration
      • • summation
      • • excitation and inhibition
    PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 06 (September 27, 2010)
  • 141. How Do Neurons Communicate?
    • Chemical Transmission
      • • Releasing chemicals onto another neuron
    • Electrical Transmission
        • • Gap Junctions ( electrical coupling between cells)
        • • Propagating signals within a neuron
        • a) membrane depolarization or hyperpolarization
        • b) action potential propagation
  • 142. Synapse – the junction between two connected neurons (Sherrington, 1906) Synapse is composed of: 1. presynaptic membrane 2. synaptic cleft (<300 Å or 30 nm) 3. postsynaptic membrane Chemical Synapse During an impulse, or action potential, neurotransmitter vesicles fuse with the presynaptic membrane and release neurotransmitters into the synaptic cleft. They then diffuse across the cleft and bind to receptors on the postsynaptic neuronal membrane.
  • 143. Electron Micrograph of an axodendritic synapse
  • 144. EM of axodendritic synapse Mag: 280,000 X
  • 145. Types of Synapses in the Nervous System
    • Axodendritic
      • – onto dendrites (a)
      • – onto spines (b)
    • Axosomatic (c)
    • Axoaxonic (d)
    • Dendrodendritic
    • Neuromuscular junction – axon synapses onto muscle cell
  • 146. How Do Neurons Communicate?
    • Chemical Transmission
      • • Releasing chemicals onto another neuron
    • Electrical Transmission
        • • Gap Junctions ( electrical coupling between cells)
        • • Propagating signals within a neuron
        • a) membrane depolarization or hyperpolarization
        • b) action potential propagation
  • 147. Glial Cells and Neurons can communicate via Gap Junctions Gap junctions – enable electrical coupling between neurons and/or glial cells
  • 148. Resting Membrane Potential (RMP) • Neurons are bathed in a salt solution (the salts dissociate into ions) • Ions are positive (cations) or negative (anions); e.g., NaCl dissociates into Na + & Cl - • Inside cell is more negative • Outside cell is more positive • cell membrane restricts ion movement • RMP is usually ~ -70 mV
  • 149.  
  • 150. Recording Neuronal Activity Much of what we know about the ionic basis of membrane potential and the action potential was learned using the Squid Giant Axon preparation.
  • 151. Recording Neuronal Activity
  • 152. Neuronal Cell Membrane is a Phospholipid Bilayer with Ion Channels Ions (salts) cannot simply diffuse across the cell membrane (they must go through channels) Hydrophilic (attracted to water) & Hydrophobic (repelled from water)
  • 153. High Na + and Cl - outside (low inside) High K + inside (low outside) Distribution of Ions Across the Neuronal Membrane at Rest
  • 154. What is the Equilibrium or Reversal Potential of an Ion?
  • 155. Distribution of Ions Across the Neuronal Membrane at Rest 2 forces at work: chemical and electrical gradients
  • 156. At Rest During Depolarization • Neuron’s RMP is negative at rest • During depolarization, Na + rushes into cell, making inside more positive • If depolarization is strong enough to fire an Action Potential, the inside will become much more positive than the outside Membrane Potential
  • 157. • Small inputs are subthreshold (e.g., 1, 2, 3) • If input is large enough, threshold is reached. • At threshold, an Action Potential is initiated (e.g., 4) Relevant Concepts: • All-or-none law • absolute refractory period • relative refractory period The Action Potential
  • 158. Summary of Ion Channel Activity During an Action Potential
  • 159. Summary of Ion Flow During an Action Potential
    • Na + influx
    • K + efflux
    • Overshoot
  • 160. Conduction of the Action Potential
  • 161. Movement of an Action Potential down an Unmyelinated Axon
  • 162. Action Potential Propagation
    • Na + influx
    • K + efflux
    • Spread of depolarization under the membrane
    • Na + influx …
  • 163. Saltatory Conduction – conserves energy; increases conduction speed (up to 120 m/s or 432 km/hr) Myelination
  • 164. Saltatory Conduction IMPORTANT CONCEPTS: • Distribution of Na + & K + channels • Spread of electrical charge
  • 165. Action Potential Propagation THOUGHT QUESTION: Is it better to have a previously myelinated axon become demyelinated or is it better to have an axon that was never myelinated in the first place? Or do they function the same?
  • 166. The Na-K Pump ( 3 Na + : 2K + ) also called the Na-K ATPase Summary of Action Potential Events 1. During AP, Na + enters 2. After AP begins, K + exits 3. Cell must restore Na + & K + ! Na-K ATPase restores ion balance 1. 3 Na + ions are pumped out 2. 2 K + ions are pumped in
  • 167. Coding of Stimulus Strength
  • 168. 1. Temporal summation 2. Spatial summation How does a neuron integrate or add up inputs it receives?
  • 169. Temporal and Spatial summation
  • 170. Temporal and Spatial summation
  • 171. END – Lecture 06
  • 172. PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 07 (September 29, 2010)
    • Ion Channels
        • • ligand-gated
        • • voltage-gated
        • • ion-gated
        • • non-gated
    • Ion Channels and Action Potentials
    • Neurotransmitter Release at the Terminal Button
    • Presynaptic and Postsynaptic Inhibition
    • Postsynaptic and Presynaptic Receptors
      • • ligand-gated Receptors
      • • G-protein linked Receptors
    • Drug Actions on Neurotransmission
  • 173. Four General Classes of Ion Channels
  • 174. Movement of Sodium Ions with Channel Opening
  • 175. Basic Steps involved in Transmitter Release
  • 176. Before the action potential arrives, the postsynaptic ligand-gated channels are closed After the action potential arrives, neurotransmitter is released, binds and causes postsynaptic ligand-gated channels to open Ligand-Gated Ion Channel A B
  • 177. Schematic of Synaptic Vesicle Release
  • 178. Steps Involved in Neurotransmitter Release
  • 179. Neurotransmitter Release & Reuptake
  • 180. EM of Synaptic Vesicle Release
  • 181. Summary of Steps Involved in Neurotransmitter Release
    • Action Potential Arrives at axon terminal (Na + influx)
    • Neurotransmitter vesicle docks at release site
    • The Na + influx causes depolarization which causes voltage-gated Ca 2+ channels to open
    • The Ca 2+ influx causes fusion pore to open and vesicle membrane to fuse with axonal presynaptic cell membrane
    • Incorporation of vesicle with presynaptic membrane occurs as neurotransmitter is released
    • Vesicle membrane gets added to axon terminal cell membrane
  • 182. Membrane Recycling is Essential
    • Synaptic vesicle fusion
    • Pinocytosis of membrane
    • Cisterna
  • 183.
    • Concentration gradient of Na + (more out than in) means that Na + ions flow INTO the cell (and influx of positive charge is depolarization ); same for Ca 2+ ions.
    • Result is EPSP (excitatory postsynaptic potential)
    • 2. Concentration gradient of K + (more in than out) means that K + ions flow OUT of the cell (and an efflux of positive charge is hyperpolarization ) .
    • Result is IPSP (inhibitory postsynaptic potential)
    • Concentration gradient of Cl - (more out than in) means that Cl - ions flow INTO the cell (and an influx of negative charge is hyperpolarization ) .
    • Result is IPSP (inhibitory postsynaptic potential)
    Why do certain ions/gradients produce EPSPs as opposed to IPSPs?
  • 184. Movement of Major Ions (EPSPs vs IPSPs)
  • 185. Postsynaptic and Presynaptic Inhibition Simple Rule of Thumb (each causes hyperpolarization of the membrane): Postsynaptic inhibition decreases a neuron’s responsiveness to inputs (acts at inputs) Presynaptic inhibition decreases a neuron’s ability to release transmitter (acts at output)
  • 186. Balance between Excitation and Inhibition
  • 187. 2 Types of Ligand-Gated Receptors
    • Ionotropic Receptors – direct link to ion channel
    • Metabotropic Receptors – indirectly linked to ion channel
  • 188. IONOTROPIC RECEPTORS (e.g., nicotinic AChRs)
  • 189.
    • Neurotransmitter binds
    • G-protein activated
    • Adenylate cyclase activated
        • – converts ATP into cAMP
    • cAMP is a second messenger
    • cAMP has numerous effects
      • – e.g., activates kinases which can alter the excitability of different ion channels
    METABOTROPIC RECEPTORS (e.g., muscarinic AChRs)
  • 190. METABOTROPIC RECEPTORS Effects of Second Messenger Cascades, such as those through metabotropic G-protein-linked receptors, last longer than those through ionotropic ligand-gated receptors.
  • 191. Agonists and Antagonists • Agonist activates the receptor • Antagonist blocks the receptor
  • 192. Two Common Types of Agonists and Antagonists DIRECT INDIRECT Competes for same site as neurotransmitter ( competitive ) Does NOT compete for same site as neurotransmitter ( noncompetitive )
  • 193. FIVE WAYS IN WHICH DRUGS CAN AFFECT SYNAPTIC TRANSMISSION
    • Synthesis of the transmitter ( 1 & 2 )
    • Packaging of the transmitter (loading vesicles; 3 )
    • Shipping of the transmitter (vesicular release; 4 & 5; 8 & 9 )
    • Receiving the transmitter (postsynaptic receptors; 6 & 7 )
    • Recycling or destroying the transmitter (reuptake all of part; 10 & 11 )
    Think in terms of a manufacturing plant that needs raw materials to make the product, needs to wrap it for shipping, needs to ship it, needs someone to receive it, and needs to deal with excess product by destroying or recycling the parts.
  • 194. SUMMARY OF WAYS IN WHICH DRUGS CAN AFFECT SYNAPTIC TRANSMISSION Note: AGO = agonist ( blue Box ); ANT = antagonist ( red Box )
  • 195. END – Lecture 07
  • 196. PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 08 (October 04, 2010)
    • NEUROTRANSMITTER SYSTEMS I
    • Neurotransmitters
    • Acetylcholine
    • The Monoamines
        • • Dopamine
        • • Norepinephrine
        • • Serotonin
  • 197. Neurotransmitters and Neurohormones • Neurotransmitters – substances released by one neuron that bind to receptors on the target neuron e.g., acetylcholine note: some are referred to as Neuromodulators • Neurohormones – released by brain or other organs, travel via bloodstream to target neurons e.g., epinephrine (adrenal gland)
  • 198. Neurohormone Release of epinephrine from the adrenal gland produces sympathetic arousal
  • 199. Examples of Neurotransmitters in the Brain
    • Acetylcholine
    • Dopamine
    • Norepinephrine
    • Serotonin
    • Glutamate
    • GABA
    • Anandamide
  • 200. Neurotransmitter Associated Neurons Acetylcholine cholinergic Dopamine dopaminergic Norepinephrine noradrenergic Serotonin serotonergic Epinephrine adrenergic Glutamate glutaminergic GABA GABAergic Anandamide cannabinergic Names of Neurons Associated with Specific Neurotransmitters
  • 201. Acetylcholine • First neurotransmitter discovered (in PNS) • Most extensively studied neurotransmitter
  • 202. Cholinergic Neurons 1. Dorsolateral Pons ––––––– REM sleep (including atonia) 2. Basolateral Forebrain –––– Activates cerebral cortex (nucleus basalis) facilitates learning & memory 3. Medial Septum ––––––––– Controls rhythms in hippocampus modulates memory formation
  • 203. Synthesis of Acetylcholine Produced by combining the lipid breakdown product choline with acetyl-CoA (made in the mitochondria)
  • 204. Synthesis of Acetylcholine
  • 205. Enzymes Enzymes are proteins that catalyze a reaction that might normally take a long time to occur. If you see a word ending in “ –ase ” it’s an enzyme. The first word or part of the word (if it’s a one-word name) refers to what the enzyme is acting on. For example : • Choline acetyltransferase acts on choline to transfer an acetyl group and thus convert it to acetylcholine • Acetylcholinesterase acts on acetylcholine to break it up.
  • 206. Two Types of ACh Receptors
    • Ionotropic ––– Nicotinic AChRs (fast)
    • Metabotropic – Muscarinic AChRs (slow)
  • 207. Cholinergic Receptors • Muscles contain nicotinic AChRs ( essential for rapid transmitter action at neuromuscular junction! ) • CNS contains both types, though mostly muscarinic AChRs ( nicotinic AChRs tend to be found at axoaxonic synapses )
  • 208. Breakdown & Local Synthesis of ACh Acetylcholinesterase – Inactivates ACh after it is released (AChE) (breaks it into acetate and choline) Choline Re-uptake ––– Choline is transported back into the presynaptic terminal for local synthesis of ACh. Re-uptake is vital because axonal transport of choline from cell body is slow! Re-uptake has an efficiency of ~50% (i.e., about half of released is recovered)
  • 209. Breakdown & Local Synthesis of ACh
  • 210. Acetylcholinesterase ( located in the synaptic cleft ) breaks down acetylcholine into acetate and choline (which is recycled). Hemicholinium is a drug that inhibits the reuptake of choline. Reuptake has an efficiency of 50% (i.e., 50% is reused)
  • 211. Drugs that Affect Cholinergic Receptors Examples 1. Curare • Blocks nicotinic AChRs (or nAChRs) • Had been and still is used by native South American populations • Used to paralyze muscles during surgery 2. Atropine • Blocks muscarinic AChRs (or mAChRs) • Used to treat AChE inhibitors (thus reducing the excess ACh action) • Also used to dilate the pupils for eye exams
  • 212. Toxins that Affect Cholinergic Transmission Examples 1. Botulinum toxin ––––––––––––– Clostridium botulinum Prevents release of ACh thus it blocks muscle excitation VERY POTENT! (e.g., 1 oz can kill 200 million people!) 2. Tetanus toxin ––––––––––––––– Clostridium tetani Prevents release of Glycine & GABA thus it blocks inhibitory transmission indirectly causing excess ACh release Botulinum and Tetanus toxins cleave Synaptobrevin (thus preventing vesicle fusion & transmitter release) 3. Black Widow Spider Venom ––– Stimulates ACh release less toxic, but can be fatal in infants and elderly
  • 213. Drugs that Affect ACh Breakdown Acetylcholinesterase inhibitors (AChE inhibitors) • Prolong the effects of ACh release by preventing its breakdown • Used as insecticides (insects can’t destroy it) • Used medically to relieve symptoms of myasthenia gravis (auto-immune) e.g., neostigmine - AChE inhibitor that can’t cross blood-brain barrier • Used as biological weapons e.g., Sarin, Tabun (treated with atropine sulfate , discussed earlier, and pralidoxime , which rejuvenates the AChE)
  • 214. Summary of Cholinergic Drugs Drug Name Drug Effect Effect on Transmission Nicotine Stim nicotinic AChRs AGONIST Curare Block nicotinic AChRs ANTAGONIST Muscarine Stim. muscarinic AChRs AGONIST Atropine Block muscarinic AChRs ANTAGONIST Black widow spider venom Stim. ACh release AGONIST Botulinum toxin Block ACh release ANTAGONIST Neostigmine (can’t cross blood-brain barrier) Blocks acetylcholinesterase AGONIST Hemicholinium Blocks choline reuptake ANTAGONIST
  • 215. Classification of the Monoamine Transmitters Catecholamines Indolamines Dopamine Serotonin Norepinephrine Epinephrine
  • 216. Synthesis of dopamine (note DA serves as a precursor for norepinephrine)
    • Tyrosine hydroxylase
    • DOPA decarboxylase
    Add –CH 3 to the NH 2 group to get epinephrine
  • 217. Dopaminergic Neurons & Projections 1. Substantia Nigra ––––––––– to neostriatum , part of basal ganglia (involved in the control of movement ) 2. VTA ––––––––––––––––– to nucleus accumbens (involved in reinforcing effects of drugs of abuse ) to amygdala (involved in emotions ) to hippocampus (involved in the formation of memories ) 3. VTA ––––––––––––––––– to prefrontal cortex (involved in short-term memories , planning, problem-solving strategies) Nigrostriatal Mesolimbic projection Mesocortical projection
  • 218.  
  • 219. MAO (Monoamine Oxidase) – destroys excess monoamines – MAO-B is specific for dopamine – Deprenyl is an MAO-B inhibitor (depression, Parkinson’s) Reuptake – Transporters are used to remove Dopamine from the synaptic cleft and return it to the nerve terminal Regulation of Dopamine
  • 220. Drugs that Affect Dopaminergic Transmission Examples 1. Monoamine oxidase inhibitors (MAO inhibitors) • MAO regulates production of catecholamines (destroys excess) • MAO inhibitors are used to treat depression • MAO-B is specific for dopamine (e.g., deprenyl) 2. Re-uptake inhibitors • Blocks re-uptake of dopamine by nerve terminals • e.g., amphetamine , cocaine , methylphenidate (Ritalin) Also causes release of DA & NE by reversing the direction of transporters Also blocks voltage-dependent sodium channels Used to treat ADHD
  • 221. Examples of Drugs that Affect Dopaminergic Transmission 1. L-DOPA • Used to treat Parkinson’s disease • Crosses blood-brain barrier & enters CNS where it is converted to dopamine 2. AMPT (  -methyl-p-tyrosine) • Binds to tyrosine hydroxylase • Thus it prevents synthesis of L-DOPA and therefore dopamine 3. MPTP (methyl-phenyl-tetrahydropyridene) • Contaminant in synthetic Heroin • It’s metabolized into MPP+, which destroys dopamine neurons and produces Parkinson-like symptoms 4. Reserpine • Prevents storage of monoamines in synaptic vesicles • Acts by blocking transporters that pump monoamines into vesicles • End result is no transmitter is released
  • 222. Effects of Drugs at Dopaminergic Synapses
  • 223. Dopamine Receptors • DA receptors are metabotropic • 5 subtypes of DA receptors (D1 – D5) - D1 & D2 are the most common subtypes • Some are autoreceptors (similar to D2) located pre- and post-synaptic - postsynaptic – act to decrease neuron firing (K current) - presynaptic – act to suppress tyrosine-hydroxylase • Apomorphine has multiple effects on DA receptors - At low doses it binds presynaptic autoreceptors (decrease DA) - At high doses it acts as an agonist at postsynaptic D2 receptors
  • 224. Schizophrenia • Serious mental disorder characterized by hallucinations, delusions, and disruption of normal logical thought processes • May involve hyperactivity of dopaminergic neurons ( excess ) 1. Chlorpromazine ( D2 antagonist ) alleviates hallucinations in schizophrenic patients 2. Clozapine ( D4 antagonist ) also relieves symptoms
  • 225. Summary of Dopaminergic Drugs Drug Name Drug Effect Effect on Transmission L-DOPA Stimulate DA synthesis AGONIST AMPT Inhibit DA synthesis ANTAGONIST Deprenyl MAO-B inhibitor AGONIST Reserpine Block storage of DA in synaptic vesicles ANTAGONIST Amphetamine, Cocaine, Methylphenidate All 3 Block DA reuptake AGONIST MPTP Destroys DA neurons ANTAGONIST Clorpromazine Blocks D2 receptors ANTAGONIST Clozapine Blocks D4 receptors ANTAGONIST
  • 226. Noradrenergic Neurons Locus Coeruleus (located in Reticular Formation) • Contains noradrenergic neurons whose axons extend to most of the brain, including thalamus, hypothalamus, limbic, cerebral cortex • Activation of LC increases vigilance or attentiveness to environment
  • 227. Norepinephrine • Synthesized from dopamine • Synthesis actually occurs inside synaptic vesicles
  • 228. Synthesis of dopamine and norepinephrine Add –CH 3 to the NH 2 group to get epinephrine
    • Tyrosine hydroxylase
    • DOPA decarboxylase
    • Dopamine b-hydroxylase
  • 229. Examples of Drugs that Affect Noradrenergic Transmission 1. Fusaric acid • Blocks DA-  -hydroxylase • Results in blockade of NE production in vesicles 2. Moclobemide • Blocks MAO-A (which normally destroys excess NE) • Results in an increase in NE 3. Desipramine • Blocks re-uptake of NE (and possibly serotonin) • a tricyclic antidepressant
  • 230. Noradrenergic Receptors • NE receptors are called adrenergic because they respond to both norepinephrine (nor adren alin) and epinephrine ( adren alin) • Adrenergic receptors are metabotropic and coupled to G proteins • 2 types of adrenergic receptors are alpha (  ) and beta (  ) -  1 - and  2 -adrenergic (located in CNS & PNS) -  1 - and  2 -adrenergic (located in CNS & PNS) -  3 (located only in PNS) •  1 -adrenergic (slow depolarizing effect; more responsive to excitatory input) •  2 -adrenergic (slow hyperpolarizing effect) •  1 - and  2 -adrenergic are excitatory (they increase neuronal responsiveness to inputs).  1 are mostly on heart muscle whereas  2 are mostly on smooth muscle lining bronchioles & arterioles of skeletal muscle. Example of contraindications: beta-blockers & hypertension in asthmatics!
  • 231.  
  • 232. Summary of Noradrenergic Drugs Drug Name Drug Effect Effect on Transmission Clonidine – has a calming effect (but also interferes with learning) Yohimbine – has an agitating effect; promotes anxiety Clonidine Stimulate  2 receptors AGONIST Yohimbine Block  2 receptors ANTAGONIST Albuterol Stimulate  2 receptors AGONIST Butoxamine Block  2 receptors ANTAGONIST Fusaric acid Inhibits NE synthesis ANTAGONIST Reserpine Inhibits storage of NE in vesicles ANTAGONIST Desipramine Inhibits reuptake of NE AGONIST Moclobemide Inhibits MAO-A AGONIST
  • 233. END – Lecture 08
  • 234. PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 09 (October 06, 2010)
    • NEUROTRANSMITTER SYSTEMS II
    • The Monoamines ( continued …)
        • • Serotonin
    • Amino Acids as Neurotransmitters
      • • glutamate, GABA, glycine
      • • NMDA receptors & GABA receptors
    • Other Neurotransmitters & Neuromodulators
        • • peptides, lipids, nucleosides, soluble gases
  • 235. Serotonin • Synthesized from the amino acid tryptophan • Important in the following: - regulation of mood - control of eating, sleep, arousal - regulation of pain ( hyperalgesia after injury) - control of dreaming
  • 236. Serotonin • PRECURSORS to serotonin Dorsal Raphe –– sends 5-HT projections to cortex & basal ganglia • Medial Raphe –– sends 5-HT projections to cortex & dentate gyrus Note: raphe means “crease” or “seam” (the nuclei are found near the midline of the brain stem) The clusters of nuclei that make up the raphe are found in the medulla, pons, and midbrain.
  • 237. Synthesis of Serotonin (or 5-HT) PCPA ( p -chlorophenylalanine) • blocks tryptophan hydroxylase and thus serotonin production MAO-A (monoamine oxidase A) • inactivates excess serotonin • ultimately converted into 5-HIAA ( measureable metabolite ) (5-hydroxy-indoleacetic acid)
  • 238. Serotonin Receptors • 5-HT receptors are metabotropic ( except 5-HT 3 is an ionotropic Cl - channel ) • At least 9 different subtypes of 5-HT receptors - 5-HT 1A-1B ; 5-HT 1D-1F ; 5-HT 2A-2C ; 5-HT 3 - 5-HT 1B and 1D are presynaptic autoreceptors (axons) - 5-HT 1A are presynaptic autoreceptors (soma & dendrites) • 5-HT 3 are important in nausea & vomiting (antagonists help in chemo patients) Reminder: an autoreceptor is a receptor on its own axon terminal that responds to the neurotransmitter released by the same axon (a negative feedback mechanism)
  • 239. Drugs that Affect Serotonin • 5-HT re-uptake inhibitors ( SRIs or SSRIs ) are useful in treating certain mental disorders (these drugs act by prolonging the action of serotonin at synapses) e.g., Fluoxetine (Prozac) - depression & anxiety disorders • Drugs that stimulate 5-HT release have also been used e.g., Fenfluramine – has been used as an appetite suppressant (in combination with phenteramine which acts on catecholamines to counteract the drowsiness caused by fenfluramine) • 5-HT 2A agonists cause hallucinations e.g., LSD is thought to exert behavioral effects as an agonist of 5-HT 2A receptors in the forebrain • Ecstasy ( MDMA ; 3-4 methylenedioxymethamphetamine ) causes release of serotonin, norepinephrine, and to a lesser extent dopamine (agonistic effect). MDMA damages serotonergic neurons .
  • 240. Summary of Serotonergic Drugs Drug Name Drug Effect Effect on Transmission Fenfluramine Stimulate 5-HT release AGONIST Fluoxetine Inhibits reuptake of 5-HT AGONIST PCPA Inhibits 5-HT synthesis ANTAGONIST Reserpine Inhibits storage of 5-HT in vesicles ANTAGONIST
  • 241. Summary of Neurotransmitter Synthesis Pathways PKU (phenylketonuria) - myelination - brain damage
  • 242. Amino Acid Neurotransmitters Two Major Classes: excitatory and inhibitory 1. The Excitatory Neurotransmitter is Glutamate (in brain & spinal cord) 2. The Inhibitory Neurotransmitter is GABA (in brain) or Glycine (in spinal cord and lower brain)
  • 243. Amino Acid Neurotransmitters
    • GLUTAMATE (PRINCIPLE EXCITATORY TRANSMITTER)
    • • 4 receptor subtypes ( 3 ionotropic & 1 metabotropic )
      • AMPA receptor (ionotropic) is the most common (Na + influx). These ionotropic receptors bind glutamate and open ion channel, even when the cell is at rest.
      • NMDA receptor (ionotropic) is also common but these require depolarization because they are blocked by Mg 2+ when neuron is at rest (see next slide).
    • • caffeine increases glutamate indirectly by blocking adenosine receptors which normally inhibit glutamate release
    • • MSG (monosodium glutamate) binds glutamate receptors and can produce tingling, burning, ringing in the ears, loss of sensation
  • 244. NMDA Receptor Channel Complex 6 NMDAR Binding Sites 1. Glutamate (natural agonist) 2. Glycine (co-agonist required for glutamate to have any effect on NMDARs) 3. Mg 2+ (binds inside channel and blocks) 4. Zn 2+ (decreases activity) 5. Polyamine (increases activity) 6. PCP (blocks channel) Thus, the NMDA Receptor is a Voltage & Neurotransmitter-Dependent Ion Channel
  • 245. Amino Acid Neurotransmitters GABA (MAJOR INHIBITORY TRANSMITTER IN BRAIN) • 2 main receptor subtypes ( 1 ionotropic & 1 metabotropic ) • [discussed further on next slide] GLYCINE (INHIBITORY TRANSMITTER IN CORD AND LOWER BRAIN) • ionotropic receptors (Cl – influx causes IPSPs) • strychnine is an antagonist (convulsions via excess/uncontrolled excitatatory drive)
  • 246. GABA Receptors • Enzyme GAD (glutamic acid decarboxylase) converts glutamic acid to GABA - GAD is inhibited by allylglycine (thus blocking GABA synthesis) • GABA receptor subtypes: 1. GABA A • ionotropic • opens Cl – channel, causing Cl – influx and hyperpolarization • [see next slide for more details on GABA receptors] 2. GABA B • metabotropic (coupled to G-proteins) • causes K + efflux and thus hyperpolarization • Baclofen is an agonist (relaxes muscles)
  • 247. GABA A Receptors GABA A Receptor has 5 binding sites 1. GABA (natural agonist) • muscimol is a direct agonist • bicuculline is a direct antagonist 2. Benzodiazepine (indirect agonist) • anxiolytic drugs (diazepam or valium) tranquilizers, promote sleep, reduce seizure activity, relax muscles 3. Barbiturate (indirect agonist) • low doses have a calming effect • rarely used as anesthetic due to small therapeutic index (easy to OD) 4. Steroid (indirect agonist) 5. Picrotoxin (indirect antagonist) Note:  -CCM (methyl-  -carboline-3-carboxylate) may be a natural ligand for Benzodiazepine binding site. This is an inverse agonist and thus produces fear, tension, and anxiety. It may be part of our fight or flight danger system.
  • 248. Other Neurotransmitters / Neuromodulators
    • Peptides
      • • 2 or more amino acids linked together
      • • includes various endogenous opioids
      • • Substance P is thought to be the primary neurotransmitter signaling pain
    • Lipids
      • • can transmit between or within cells
      • • e.g., anandamide - endogenous cannabinoid receptor ligand (THC in marijuana binds to the same receptors); altered mood & sensory perception as well as memory and motor impairments
    • Nucleosides
      • • sugar + purine (A&G) or pyrimidine (C&T) base
      • • e.g., adenosine (ribose + adenine) - coupled to G-proteins which open K + channels, thus causing IPSPs (thus it’s inhibitory)
      • • caffeine blocks adenosine receptors and thus is excitatory
    • Soluble Gases
      • • Nitric oxide or NO (NOS converts argenine to NO; blocked by L-NAME)
      • • Carbon monoxide or CO
      • • diffuse out of the cell and activate neighboring cells to produce cGMP
  • 249. END – Lecture 09
  • 250. PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 10 (October 13, 2010)
    • PLASTICITY IN THE NERVOUS SYSTEM
    • Neurogenesis
    • Origin of brain cells & brain development
    • Axon guidance
    • Synaptic pruning
    • Axonal regeneration
    • Denervation supersensitivity
  • 251. Development of the Human Brain Relative Brain Size: At birth: ~ 350 g At 1 yr: ~1000 g Adult: ~1200 g • Forebrain • Midbrain • Hindbrain
  • 252. Timeline of Major Stages in Cerebral Cortex Development Neurogenesis declines significantly by week 20 and is nearly complete by 5 mo., but it does continue throughout life in some regions ( i.e., adult neurogenesis ).
  • 253. Origin of Brain Cells Neurotrophic factors • EGF (epidermal growth factor) – stem to progenitor • bFGF (basic fibroblast growth factor) – progenitor to neuroblast • PDGF (platelet derived growth factor) – progenitor to glioblast (specifically oligodendrocyte)
  • 254. Brain Development
    • Processes involved in neuron production :
    • Proliferation
        • – production of new cells ( primitive glia & neurons )
        • – stem cells continue to divide
    • Migration
        • – occurs inside out
    • Differentiation & Maturation
        • – formation of axons then dendrites (transplantation depends upon age)
    • Myelination
        • – continues gradually over many years
    • Synaptogenesis
        • – formation of synaptic connections ( requires extra cholesterol-from glia )
        • – continues throughout life
  • 255. Axon Pathfinding (how does an axon know where to go?) Roger Sperry (1943)
  • 256. Axon Growth and Neuron Survival Growth Cones extend out as axons seek targets Tropic molecules guide axons; produced by targets (e.g., netrins) Trophic molecules support survival of cells and axons once target is reached neurotrophins (e.g., NGF, BDNF) Neuronal and synaptic pruning (via apoptosis) Important concepts : • Chemoattractant • Chemorepellent
  • 257. Synapse Pruning (Elimination) Synaptic connections are plastic!
  • 258. Effect of Experience on Plasticity
    • Environmental Enrichment
      • • Increases dendrite complexity
      • • Increases number of synapses
  • 259. Regrowth of Axons • Can occur as long as the soma or cell body is intact • Rate is usually ~1 mm/day (PNS) • in CNS, axons usually regenerate only 1-2 mm total (CNS) , thus paralysis due to spinal cord injury is usually permanent • In PNS, axon regrowth follows myelin sheath back to target • Regrowth in PNS may not be perfect • e.g., if a motor neuron’s axon is cut (not crushed), segments may not align and axon may synapse on wrong target muscle
  • 260. Collateral Sprouting
  • 261. Denervation Supersensitivity Remember: Amphetamine causes DA release from existing axon terminals Apomorphine stimulates DA receptors (an appropriately high dose was used)
  • 262. END – Lecture 10
  • 263.
    • MUSCLES & SPINAL REFLEXES
    • Muscle Cell Types and Muscle Fibers
    • Skeletal Muscles and Movement
    • Spinal Reflexes
      • • Spinal cord
      • • Withdrawal reflex
    • Extrafusual vs. Intrafusal Muscle Fibers
        • • Stretch reflex
        • • Reciprocal innervation
        • • Tendon reflex
    • Crossed Extensor Reflex
    PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 11 (October 18, 2010)
  • 264. Muscles and Muscle Fibers
  • 265. 3 Types Muscle
  • 266. Muscles and Muscle Fibers Skeletal Muscle : • Attach to bone or cartilage via tendons • Made up of cells (muscle fibers) • Each muscle fiber contains contractile proteins Actin – thin filaments Myosin – thick filaments • The filaments overlap
  • 267. Major Components of Skeletal Muscle
  • 268. Skeletal Muscle : • Striated appearance due to arrangement of actin & myosin • Actin filaments (thin) are attached to proteins that form the Z-line • Myosin filaments (thick) are found between rows of actin Sliding Filament Theory of Muscle Contraction • During contraction , the following events occur: 1. Actin filaments slide along each myosin filament (from both ends) 2. Z-lines get closer together (because actin is attached to Z-line) 3. Result is that the muscle shortens
  • 269. Sliding Filament Theory
  • 270. Neuromuscular Junction & Muscle Contraction : • Motor neurons innervate skeletal muscle fibers at a special region called the motor endplate • The motor endplate contains ACh receptors (mostly nicotinic) • One motor neuron can innervate multiple muscle fibers Motor Unit = motor neuron plus the muscle fibers it innervates • Muscles used for very fine (discrete) movements have smaller motor units • Muscles used for posture have larger motor units
  • 271. Classification of Skeletal Muscles by Color : Red Muscle – High concentration of myoglobin (carries oxygen) – Relies heavily on oxidation to produce ATP – Engages in heavy activity without fatiguing – Used for slow, sustained movements – e.g., chicken or turkey legs White Muscle – Low concentration of myoglobin – Quickly goes into oxygen debt during contraction – Fatigues quickly – Used for rapid contractions in short bursts – e.g., chicken or turkey breasts Note: In humans and other mammals, red and white muscle fibers are found in the same muscles, unlike birds. For example, sprinting uses white, hiking/walking uses red.
  • 272. Antagonistic Muscles (flexion and extension) Isotonic Contraction (muscle shortens) e.g., legs, produces the movement when carrying heavy box Isometric Contraction (muscle length stays same) e.g., back & arm muscles contract when holding or carrying heavy box Think of the different muscles that are used when carrying a heavy box up a flight of stairs – some contractions are isotonic and some are isometric. Muscular Movements and Contractions
  • 273. Opposing or Antagonistic Muscle Movements Antagonistic Muscles (flexion vs extension)
  • 274. Spinal Control of Movement REFLEXES are rapid movements mediated by either brain stem nuclei or the spinal cord (we’ll only cover spinal cord today). They are very Important (e.g., protect the body, basic life support) They vary in complexity and number of synapses: • Simple (e.g., withdrawal or flexion reflex) • Complex (e.g., postural, involving many different muscles) Note: Simple and Complex are relative terms. Even simple reflexes can involve MANY neurons (even thousands).
  • 275. Three Reflexes Seen in Infants • Grasping • Babinski • Rooting
  • 276. The Babinski Reflex – in children & adults it’s diagnostic of CNS damage • Positive Babinski – fanning of toes with stroking bottom of foot – always seen in infants < ~6 mo. (due to lack of descending inhibition) • Negative Babinski – curling of toes with stroking bottom of foot – seen in older infants and all healthy people – results from descending inhibitio n from brain
  • 277. Withdrawal Reflex is a simple reflex involving only a few synapses between the sensory (afferent) neuron and the motor (efferent) neuron
  • 278. Withdrawal Reflex (involves one or more interneurons between the sensory and motor neuron) Note: the more interneurons (and thus synapses) there are in the reflex arc, the longer the reflex takes
  • 279. Withdrawal Reflex Note: descending projections from the brain can inhibit reflexes
  • 280. 2 Types of Motor Neurons
    • Alpha motor neurons
        • • larger diameter
        • • faster conduction time
        • • innervate extrafusal muscle fibers
    • Gamma motor neurons
        • • smaller diameter
        • • slower conduction time
        • • innervate intrafusal muscle fibers
        • • important for enabling muscle spindle to provide a readout of muscle length ( see gamma motor neuron slide )
  • 281. Extrafusal fibers run the length of the muscle Intrafusal fibers do not run the length of the muscle and are located within the muscle spindle Note that the downward movement of the arm activates stretch reflex, which increases the strength of the muscle contraction and pulls the arm back up Monosynaptic Stretch Reflex
  • 282. Examples • Patellar tendon reflex • Head bobbing upward when falling asleep while sitting in a chair Monosynaptic Stretch Reflex
  • 283. Intrafusal muscle fibers Muscle Spindle – A few intrafusal fibers joined to a nuclear bag (inside the nuclear bag is a stretch receptor called the Annulospiral Receptor ). Axons from annulospiral receptor terminate onto motor neurons in spinal cord . Thus, stretching a muscle activates the annulospiral receptor which then stimulates extrafusal fibers to contract that same muscle. The Muscle Spindle (or annulospiral receptor) is vital for maintaining muscle tone Think of it like a “spring” located inside the muscle.
  • 284. Gamma Motor Neurons Notice that if the muscle length changes due to muscle contraction (b) , the muscle spindle is “off line” and unable to respond to changes in muscle length. Activation of gamma motor neuron contracts the intrafusal fibers and thus “resets” the spindle so it can once again respond to stretch (c) .
  • 285. Problem inherent in the stretch reflex • Contraction of one muscle would produce contraction of antagonist muscle • For example, the simple bending of the arm by biceps contraction (agonist) would cause the arm to straighten due to activation of the stretch reflex of triceps (antagonist) muscle Solution: Reciprocal Innervation (discovered by Sherrington). With reciprocal innervation, the axons of motor neurons that synapse on a muscle also branch and activate interneurons that inhibit motor neurons that synapse on the antagonist muscles.
  • 286. Reciprocal Innervation Prevents the simple bending of an arm (biceps contraction) from causing the arm to straighten due to stretch reflex of the antagonistic triceps muscle
  • 287. What if the muscle is contracting too vigorously? Golgi Tendon Organ Reflex is activated Golgi Tendon Organ (GTO) – stretch receptor found in the tendon – provides feedback to nervous system about muscle contraction – GTO fires when stretched – GTO axons synapse onto inhibitory spinal cord neurons – result of GTO activation is inhibition of the motor neuron – prevents damage to muscle as a result of excess contraction
  • 288. Golgi Tendon Organ Reflex Think of the GTO like a “spring” located at each end of the muscle (in the tendon)
  • 289. Proprioceptors (stretch receptors)
  • 290. Sir Charles Scott Sherrington (1884-1935) • Studied many kinds of reflexes • Discovered reciprocal innervation • Introduced the term synapse • Principle of the Common Path – motor neuron is final common path for all movement • Principle of the Integrative Action of Neurons – all neurons in the body work together to produce smooth, precise movement – the crossed extensor reflex is an excellent example
  • 291. Crossed Extensor Reflex • Withdrawal Reflex activated by sensory neuron synapsing onto interneuron, which excites motor neurons of the ipsilateral flexor • Interneuron also crosses over and synapses onto and excites the motor neurons of the contralateral extensor Example - if you step on a tack while walking, you’ll fall down without this reflex
  • 292. END – Lecture 11
  • 293.
    • CONTROL OF MOVEMENT BY THE BRAIN
    • Anatomical Considerations
        • • upper & lower motor neurons
        • • motor cortex
    • Two Major Motor Systems
        • • Pyramidal Motor System (lateral system)
        • corticospinal tract
        • • Extrapyramidal Motor System (medial system)
        • basal ganglia & cerebellum
    • Effects of Damage to the Descending Motor System
        • • corticospinal tract damage
        • • basal ganglia and cerebellar damage
    PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 12 (October 20, 2010)
  • 294. Classification of Neurons Associated with the Motor System
    • Upper Motor Neurons
        • • above level of spinal cord motor neurons
        • • e.g., cortical neurons
    • Lower Motor Neurons
        • • spinal cord motor neurons
        • • e.g., those in ventral horn of spinal cord
  • 295. Motor Cortex & Motor Homunculus 1 2 3 4
  • 296. Classification of Descending Motor Systems
    • The Lateral Group or System ( fine or directed movements )
        • • lateral corticospinal tract ( dorsolateral tract )
    • The Medial Group or System ( automatic or postural movements )
      • • anterior corticospinal tract ( ventromedial tract )
      • • basal ganglia & cerebellum
    Contemporary Classification Scheme
  • 297. The Lateral (Pyramidal) Motor System Originates in the Primary Motor Cortex (precentral gyrus) Axons of these Upper Motor Neurons project downward • through internal capsule • through medullary pyramids (hence name) • main branch crosses over at pyramidal decussation in medulla and descends through the contralateral spinal cord forming the lateral corticospinal tract
  • 298. Lateral Corticospinal Tract • fine, directed motor control • hands, fingers, feet, toes • synapse directly onto motor neurons or indirectly via interneurons
  • 299. Effects of Damage to Corticospinal Tract Damage to the Corticospinal Tract at any Level produces: 1. Initial loss of muscle tone ( atonia ) • transient flaccid paralysis immediately upon damage 2. Hyperactive deep tendon reflexes (myotactic) • hyperreflexia 3. Appearance of the Babinski sign ( positive Babinski ) • note: a positive Babinski may be seen during sleep or intoxication, and in infants <~6mo. Thus, appearance of a positive Babinski sign is diagnostic of pyramidal tract damage.
  • 300. Effects of Cortical Damage to Lateral System Damage to the Premotor or Supplementary Motor Cortex or to parts of the Parietal or Temporal cortex produces Apraxia Apraxia “without action” – Difficulty carrying out purposeful movements, in the absence of paralysis or muscle weakness Apraxias are classified according to the systems affected: limb apraxia – movement (parietal lobe damage) (e.g., difficulty if asked to demonstrate a movement) oral apraxia – speech (Broca’s area damage) apraxic agraphia – writing (left parietal lobe damage if right-handed) constructional apraxia - drawing or construction (parietal lobe damage) (e.g., difficulty with spatial perception and execution) NOTE: Apraxias DO NOT involve damage to primary motor cortex or any other lower portions of the lateral motor system
  • 301. Cortical Control of Movement Posterior association cortex is involved with perceptions Frontal association cortex is involved with plans for movement
  • 302. Motor Neuron Disorders Muscular Dystrophy – muscle wasting • 30 different types, Duchenne’s MD is the most common - about 1 in 3-4000, typically between ages of 2 and 6 - due to defect in gene that encodes dystrophan - more common in boys (due to gene on X-chromosome) Myasthenia Gravis – degeneration of acetylcholine receptors at NMJ • results from an autoimmune response against AChRs • treated with immunosuppressants or thymectomy • treated with anticholinesterases (acetylcholinesterase inhibitors) • may also try plasmapheresis (filter the AChR-attacking antibodies from the patient’s blood) Amyotrophic lateral Sclerosis or ALS (Lou Gehrig’s disease) – motor neuron degeneration • degeneration of motor neurons in brain and spinal cord • progresses from muscle weakness to muscle wasting • no treatment • ~5,600 new cases each year, typically between ages of 40 & 70
  • 303. The Medial (Extrapyramidal) Motor System Coordinates gross movements & postural adjustments • Develops before the pyramidal (lateral) system e.g., babies can play patty-cake before learning to hold a crayon • Develops at different times e.g., babies can hold head up before sitting upright
  • 304. The Medial (Extrapyramidal) Motor System
    • Brain Regions
    • Cerebellum
        • • Receives sensory information from all sensory systems and cortex
        • • It must know what every muscle in the body is doing at every moment
        • • Ballistic movements, learned movements
    • Basal Ganglia
        • • Relays info to and from cerebral cortex
        • • Numerous structures work together to coordinate gross movements
    Some drugs (e.g., classical antipsychotics) act to decrease dopamine activity in the brain. Thus, these drugs may have “ extrapyramidal side effects ” , which include tremors, rigidity, and a shuffling gait
  • 305. The Cerebellum and Movement Note: The cerebellum may contain ~50 billion neurons, compared with ~22 billion neurons in the cerebral cortex!
    • • important for rapid coordination of movements
    • • important for ballistic movements
    • • receives information from all senses and cerebral cortex
    • • must know what every muscle is doing at any given time in order to properly coordinate rapid movements
    • • damage results in a variety of impairments:
    • ataxia – inability to walk in a coordinated manner
      • disequilibrium – loss of balance
  • 306. Basal Ganglia – a cluster of neuronal structures concerned with the production of movement.
    • Striatum ( Caudate , Putamen )
        • • receives information from cerebral cortex
        • • sends that information to Globus Pallidus
        • • caudate – process of cognitive information
        • • putamen – relays motor signals
    • Globus Pallidus
        • • sends information back to cortex via thalamus
    • Substantia Nigra
        • • produces DA and projects to caudate and putamen
    • Subthalamic Nucleus (STN)
      • • sends projections to and receives projections from the globus pallidus
  • 307. Location of the Basal Ganglia within the Forebrain
  • 308. Damage to the Basal Ganglia Basal ganglia damage results in movement disorders Tics – brief, involuntary contractions of specific muscles Choreas – involuntary movements of head, arms, legs Huntington’s disease – uncontrolled tics and choreas early, dementia later – disruption of gene on chromosome 4 (excess CAG repeat) resulting in an abnormal Huntingtin ( Htt ) protein (with an elongated string of glutamine residues on it). The Htt mutation ultimately leads to death of GABAergic inhibitory neurons in the putamen (part of striatum) Parkinson’s disease – tremor, loss of balance, rigidity (hard to initiate movement) – caused by loss of dopaminergic neurons in substantia nigra
  • 309. Relationship Between CAG Repeats and Age of Onset • CAG codes for glutamine • 11-24 CAG repeats is normal • >36 is linked to Huntington disease
  • 310. Brain of Patient with Huntington’s Disease
  • 311. Treatments for Parkinson’s Disease 1. Pharmacological Treatments L-DOPA – crosses blood-brain barrier and is converted to dopamine glutamate antagonists – reduce hyperactivity of glutamate in subthalamic nucleus 2. Destructive Surgical Treatments thalamotomy – surgical cut in ventral thalamus pallidotomy – surgical cut through the globus pallidus • both are thought to interfere with excitatory messages that produce symptoms • both reduce the rigidity and tremors (improving posture, gait, locomotion) • cognition and mood may also be improved with pallidotomy 3. Nondestructive Surgical Treatments subthalamic nucleus (STN) stimulation reduces symptoms • also called deep brain stimulation 4. Restorative Surgical Treatments fetal stem cell implantations – insertion of DA-producing cells from dead fetuses • raises serious ethical issues ( adult stem cells may be better, especially from same patient ) gene therapy – introduction of a gene that would rescue function • e.g., use virus to deliver GAD gene to STN, thus restoring lost inhibition
  • 312. END – Lecture 12
  • 313.
    • THE VISUAL SYSTEM I
    • Electromagnetic Spectrum & Waves
    • Anatomy of the Eye
    • Eye anatomy and blindspot
    • Visual Receptors
        • • rods
        • • cones
    • Cells of the Retina
    • Effects of light stimulation on transmission through retina
    PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 12 (October 20, 2010)
  • 314. Many Stimuli are Transmitted as Waves (e.g., electromagnetic radiation, vibration, and sound) The Electromagnetic Spectrum 1. Wavelength (nm, 1 nm = 10 -9 m) 2. Frequency (Hz, Hertz, cycles per s) 3. Amplitude (dB, decibels, range: 0 to 160) Wavelength ~380-760 nm is visible to humans Q: Why is the sky blue during day but reddish at sunrise or sunset?
  • 315. v = ƒ  Electromagnetic Radiation (e.g., Light Waves) Relationship between velocity ( v ) , frequency (ƒ) , and wavelength (  ) of light can be described by the following equation: • Don’t worry about doing any calculations, this is just an example e.g., blue light with a wavelength of 455 nm (455 x 10 -9 m) would have a frequency of: ƒ = v /  ƒ = (3 x 10 8 m/s) / (455 x 10 -9 m) ƒ = (3/455) x 10 17 / sec ƒ = .00659 x 10 17 Hz ƒ = 659 x 10 12 Hz Notes: speed of light ( v ) is 3 x 10 8 m/s or 186,000 miles/sec m = meters; s = seconds nm = nanometers (10 -9 meters)
  • 316. Stimulus Intensity is encoded by changes in action potential frequency Adaptation is a decrease in the firing rate in response to a continuous stimulus (e.g., odor perception decreases as you get used to it)
  • 317. Distribution of Visual Receptors Why is this baby owl’s head nearly upside down?
  • 318. The Visual System
  • 319. The Visual System
  • 320. Cornea – transparent covering in front of eye, curvature aids in focusing light Aqueous humor – fluid behind cornea Pupil – opening in center of iris Lens – transparent structure that focuses images on retina • controlled by ciliary muscles ( smooth muscle ) • when image is far away , the lens flattens (gets thinner/weaker) • when image is close , the lens shortens (gets fatter/stronger) • process of lens changing shape is accommodation • presbyopia is age-related loss in lens elasticity (need reading glasses) Vitreous humor – clear gelatinous liquid inside main part of eyeball Retina – interior lining of the back of the eye • contains photoreceptors (rods and cones) Optic Nerve – carries visual signal from retina into the brain Anatomy of the Eye
  • 321. Anatomy of the Eye • Optic Axis - imaginary straight line through eye to fovea centralis • Fovea Centralis - cones only (no rods are in fovea!) - the highest density of rods is in the area right next to the fovea (rods decrease in density with distance from fovea) • Optic Disk - where optic nerve exits - blind spot • Sclera - tough outer white covering Right Eye
  • 322. Blindspot on the Retina (due to optic nerve exiting eye)
  • 323. Blindspot is due to the Optic Disk Self Test: (1) Draw 2 objects about 2 inches apart. (2) Close left eye. (3) Hold paper at arms length and focus on the left (medial) object with right eye. (4) Slowly move paper closer. (5) The right (lateral) object will eventually disappear.
  • 324.
    • Rods - respond best to dim light (black & white)
        • • 1 kind of rod
        • • more numerous than cones (~120 million rods)
        • • dispersed throughout the retina
        • • insensitive to detail; peripheral vision
        • • extremely sensitive to light (best in dim light)
        • “ scotopic or dark vision”
    • Cones - respond best to bright light (color)
        • • 3 different kinds of cones
        • • less numerous than rods (~5 million cones)
        • • concentrated in fovea centralis (macula)
        • • fine detail
        • • less sensitive to light (best in bright light)
        • “ photopic or light vision”
    Visual Receptors
  • 325. Visual Receptors
    • Outer Segment - photopigments
      • • e.g., rhodopsin (rods)
      • • photopigments absorb photons (light)
      • • 2 parts: protein opsin & lipid retinal
      • • 11-cis-retinal ( benefits of Vitamin A )
      • • bleached after absorption of photons
      • • unbleached after removal of light
      • (called dark adaptation )
    • Inner segment - nucleus & organelles
    isomerization
  • 326. Visual Receptors
  • 327. Bleaching of Photopigments Rods – very sensitive to light (thus sensitive to bleaching) • photopigments bleach faster and more completely than cones Cones – less sensitive to light • photopigments bleach more slowly • if light is bright enough, even cones will bleach e.g., sun reflecting off snow is blinding Note: when a photoreceptor absorbs light, it is bleached (unresponsive to light). Following removal of light, recovery (unbleaching) occurs and photoreceptor is ready to respond to light once again. This unbleaching is called dark adaptation .
  • 328. 5 Layers of Cells in the Retina (listed from the back or outer layer of the eye) (only worry about the 3 main layers, highlighted blue) 1. Visual receptors – Located near the back outer layer of retina, just in front of the pigment epithelium. They absorb photons (light waves). 2. Horizontal cells – (don’t worry about these!) 3. Bipolar cells – transfer generator potentials from visual receptors to ganglion cells. 4. Amacrine cells – (don’t worry about these!) 5. Ganglion cells – Located just behind the vitreous humor and fire action potentials. Their axons form the optic nerve. Pigment epithelium back layer of cells that contains blood vessels that nourish the retina and also serves to absorb stray photons (thus minimizing distortion). Other mammals (dogs, cats, deer, cattle) lack a pigment epithelium but instead they have a reflecting tapetum that is important for night vision (reflects light to make maximal use in dim light conditions).
  • 329. 3 Main Layers of the Retina
  • 330. Retina
  • 331.
    • Visual receptors – in the dark, rods and cones are depolarized and release inhibitory transmitter onto bipolar cells (hyperpolarizing them). Light closes ion channels that are permeable to Na + , results in hyperpolarization of visual receptors and less transmitter release, thus depolarizing bipolar cells .
    • Horizontal cells – inhibit nearby visual receptors in response to activation by light ( lateral inhibition which enhances contrast between edges .
      • (Don’t worry about these!)
    • Bipolar cells – transmit between visual receptors and ganglion cells (releases excitatory transmitter glutamate onto and activates ganglion cells)
    • Amacrine cells – provide feedback to bipolar and ganglion cells
      • (Don’t worry about these!)
    • Ganglion cells – just behind the vitreous humor and fire action potentials. Their axons form the optic nerve.
    Retina
  • 332.
    • Normally the visual receptor is depolarized and inhibiting the bipolar cell.
    • Light hyperpolarizes the visual receptor (rods or cones) which then depolarizes the bipolar cell.
    • Depolarization of the bipolar cell causes depolarization of the ganglion cells.
    • Depolarization of the ganglion cell causes it to fire more action potentials.
    • Net Result is that light shining on the photoreceptor excites the ganglion cells
    Summary of the Effects of Light Stimulation
  • 333. Effects of Light on Retinal Circuitry (Summary) -30 – -50 – -70 – -90 – Membrane potential (mV)
  • 334. END – Lecture 12
  • 335. THE VISUAL SYSTEM II 1. Transmission of visual information through brain 2. Color vision • Trichromatic color theory • Opponent-process theory 3. Disorders of the visual system PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 13 (October 25, 2010)
  • 336. Transmission of Visual Information Through the Brain Retina Optic Nerve (CN II) Optic Chiasm ( nasal hemiretina crosses over ) 1° Visual Cortex (Occipital lobe) Visual Association Cortices (Occipital, parietal, temporal) Lateral Geniculate (Thalamus) Superior Colliculus (Mesencephalon) Optic Tract (Blindsight) Main Path SC processes the location of objects Minor Path
  • 337. Receptive Field & Visual Acuity Images on retina are upside down and backwards
  • 338. Color Vision Young-Helmholtz or Trichromatic Color Theory (1802) • Proposed independently by Thomas Young and Hermann von Helmholtz • Only 3 different color receptors (cones) are needed to see all shades of color 3 Different cones • S-Cones (Short wavelength or Blue) - excited by Blue light • M-Cones (Medium wavelength or Green) - excited by green light • L-Cones (Long wavelength or Red) - excited by red light
  • 339. Light Mixing and Pigment Mixing
  • 340. Color Vision For Normal Color Vision, all 3 Cones are Needed: Trichromats – have all 3 functional cones: S, M, L – normal color vision Dichromats – only have 2 functional cones: S, M or S, L (e.g., either M or L is nonfunctional) Monochromats – only have 1 functional cone – can only see black, white, and grays Note: Other mammals (and some non-human primates) are Dichromats , and have only two types of cones: S and LM (intermediate cones that respond to yellow light). Certain color-deficiencies occur most commonly in males (XY) because the genes for cones are on the X-chromosome (usually the defective gene is rescued in females by a normal X-chromosome)
  • 341. Color Deficiencies (Red-Green) - Ishihara Test NORMAL Color Vision A B C Top 25 45 6 Bottom 29 56 8 RED-GREEN Color Blind A B C Top 25 spots spots Bottom spots 56 spots A B C
  • 342. 1878 – Ewald Hering Opponent Colors
  • 343. Red–green Blue–yellow White–black 1878 – Ewald Hering Opponent-Process Theory (explains negative afterimage and why we can’t imagine “reddish-green” or “bluish-yellow” colors) How Individual Ganglion Cells Code for Color }
  • 344. Negative Afterimage
  • 345. Opponent-Process Coding
  • 346. Summary of Opponent-Process Color Coding 1. Red light activates Red Cone which activates Red-Green ganglion cells. • Result is Red 2. Green light activates Green Cone which inhibits Red-Green ganglion cells. • Result is Green 3. Yellow light activates Red & Green Cones equally . The Red Cone activates both Red-Green and Yellow-Blue ganglion cells . The Green cone (1) inhibits the Red-Green ganglion cell (thus canceling activation by red) and (2) activates the Yellow-Blue ganglion cell. • Result is Yellow ( red is canceled by activation & inhibition ) 4. Blue light activates Blue Cone which inhibits Yellow-Blue ganglion cells. • Result is Blue
  • 347. Retinex Theory Both the cerebral cortex and retina work together to determine brightness and color perception. Example: afterimage of an illusion
  • 348. Retinex Theory Both the cerebral cortex and retina work together to determine brightness and color perception. Example: afterimage of an illusion
  • 349. Retinex Theory Both the cerebral cortex and retina work together to determine brightness and color perception. Example: afterimage of an illusion
  • 350. Visual Illusion – What colors do you see?
  • 351. Visual Illusion – What colors do you see?
  • 352. Cornea (smooth, transparent covering of front of eyeball) • Any scratches or damage will create distortions of light passing through to the retina and can cause astigmatism . • Astigmatism - blurring of objects in certain orientations Aqueous Humor (clear liquid between lens and cornea) • shape of eyeball is maintained by pressure and aqueous humor drains fluid via ducts. If ducts clog, excess pressure builds up. • Glaucoma - damage to optic nerve due to excess pressure leading cause of blindness in the U.S. Disorders of the Visual System: Eye
  • 353. Lens (elastic, transparent structure that focuses light onto the retina) • Presbyopia - age-related inability of lens to fatten (less elasticity), which impairs ability to bring close objects into focus • Cataract - lens becomes opaque with age (UV damage). Light cannot pass and vision is disrupted. Surgical removal of lens and replacement with a monofocal lens (usually a flat lens to allow distant focus only, so glasses would be required for near objects). Multifocal lenses are available too. Prevention? Sunglasses . • Myopia (nearsighted) - lens focuses distant objects in front of retina ( eyeball too long or lens too strong ), but vision for near objects is intact. • Hyperopia (farsighted) - lens focuses near objects behind retina ( eyeball too short or lens too weak ), but vision for distant objects is intact. Disorders of the Visual System: Eye
  • 354. Retina (multi-layered structure containing photoreceptors) • Macular degeneration - degeneration of macula lutea (area that contains the fovea & thus cones). Symptoms: loss of ability to see detail or even read . Eventually spreads to all photoreceptors and blindness results. • Retinitis pigmentosa - genetic disorder (chromosome 8) affecting rhodopsin (rods). Symptoms: night blindness, tunnel vision . Eventually, disease spreads to cones - total blindness. • Diabetes can produce blindness due to weakening of blood vessels lining the retina (resulting in bleeding into vitreous humor, as well as oxygen and nutrient deprivation). Disorders of the Visual System: Eye
  • 355. Emmetropia Myopia Hyperopia
  • 356. Focusing of Distant and Near Sources It takes a stronger lens (accommodation) to focus a near image at the same distance that it takes a weaker lens to focus a distant image ( compare a and c ). Thus, the human lens accommodates (gets fatter or stronger) in order to properly bring a near object into focus on the retina. Note: the rays from a distant source are essentially parallel (a) whereas the rays from a near source are still diverging (b & c). Thus, without changing lens shape - e.g., without getting fatter (as in c) - the near source would fall beyond the focal point (b) of the distant source.
  • 357. END – Lecture 13
  • 358. THE VISUAL SYSTEM III • Visual Pathways from Retina to Cerebrum • The Parvocellular or Ventral Stream the “what” system • The Magnocellular or Dorsal Stream the “where” system • Disorders of Visual Processing • Types of Cells in Visual Cortex PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 14 (October 27, 2010)
  • 359. Note: The Ganglion Cell to LGN pathway is actually 2 pathways (parvocellular & magnocellular)
      • Ganglion Cells LGN V1
  • 360. Two Kinds of Ganglion Cells Project to Separate Layers of LGN (and thus different Targets in V1)
    • 1. Large Ganglion Cells or Magnocellular
        • • from rods
        • • 10% of ganglion cells
        • • project to LGN layers I-II (e.g., bottom 2 layers)
        • • V1 target is interblob region
        • • origin of the “where” or dorsal system
        • • processes form, motion, spatial relations
    • 2. Small Ganglion Cells or Parvocellular • from cones
        • • >80% of ganglion cells
        • • project to LGN layers III-VI (e.g., top 4 layers)
        • • V1 target is blob region ( cytochrome oxidase-rich )
        • • origin of the “what” or ventral system
        • • processes color, form, detail
  • 361. LGN (thalamus) 6 layers: Top 4 layers (L3–6) • parvocellular layer • from cones • 2 layers from left eye • 2 layers from right eye Bottom 2 layers (L1–2) • magnocellular layer • from rods • 1 layer from left eye • 1 layer from right eye Thus, each layer of LGN only receives monocular information (from one eye or the other). Parvo Magno
  • 362. Brodmann’s Area 17 is Primary Visual Cortex Brodmann used microscopic appearance to classify brain regions Primary Visual Cortex (V1) is located in the Occipital lobe and corresponds to Brodmann Area 17
  • 363. Two Streams of Visual Information Flow
  • 364. Two Streams of Visual Information Flow
    • Dorsal “where”
      • • magnocellular
      • • from rods
    • Ventral “what”
      • • parvocellular
      • • from cones
      • • well-developed in primates
  • 365. Mapping the Visual Field onto V1 (Primary Visual Cortex)
  • 366. Disorders of Visual Processing
    • Damage to V1
      • • if tiny, Scotoma (blind spot)
      • • if in one hemisphere, Hemianopia (blind in contralateral visual field)
      • • if complete and bilateral, Blindness results (may exhibit blindsight)
    • Damage to V2 and V3
        • • hard to exclusively damage with damaging V1, usually blindness
    • Damage to V4
        • • unable to see, perceive, or even remember seeing colors ( achromatopsia )
    • Damage to V5
        • • unable to perceive movement or moving objects ( akinetopsia )
  • 367. Disorders of Visual Processing
    • Damage to IT (Inferior temporal cortex)
    • Creates family of disorders called visual agnosia (can’t recognize familiar objects)
        • • Prosopagnosia (cannot recognize familiar faces)
        • - results from damage to right IT alone or from bilateral IT damage
        • - particularly damage to the fusiform gyrus (fusiform face area)
        • • Can have visual agnosia without prosopagnosia
        • - thus object recognition areas are not the same as face recognition areas
        • • Pure alexia (cannot put letters together but can recognize individual letters)
        • - results from damage to left IT cortex
    • Damage to Posterior Parietal cortex
    • Creates disturbances in ability to locate and reach for objects
        • • Balint’s syndrome
        • - difficulty perceiving more than one object at the same time (simultanagnosia)
        • - can’t scan environment and fixate on objects
        • - difficulty with visually-guided hand movements (optic ataxia)
        • - results from bilateral damage to posterior parietal cortex
        • • Visual extinction
        • - ignore object in visual field contralateral to damaged area
        • - usually results from unilateral damage to right posterior parietal cortex
  • 368. Fusiform Face Area (IT cortex)
  • 369. Visual Object Agnosia (w/o prosopagnosia)
  • 370. Activation of Fusiform Face Area by Faces (e) and Blurry Shapes in the appropriate position (a)
  • 371. Damage to Posterior Parietal Cortex (unable to visually localize objects)
  • 372. Damage to Posterior Parietal Cortex (unable to visually localize objects )
  • 373. END – Lecture 14
  • 374. THE SOMATOSENSORY SYSTEM I 1. Somatosensory system and receptors 2. Anatomy of the Somatosensory Pathways • Types of axons carrying somatosensory information • Lemniscal path • Spinothalamic (or extra lemniscal) path 3. Somatosensory Processing “What” & “Where” Systems 4. Somatosensory Plasticity • Phantom limb pain PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lectures 15 (November 1, 2010)
  • 375. The Somatosensory System • What are Somatosensory Receptors ? - various types of receptors in the skin - various types of receptors in muscles, tendons, and joints • What is Kinesthesia ? - ability to sense movement • What is Proprioception ? - ability to know where a body part is in 3D space • What is Interoception ? - sense that arises from the internal organs (e.g., receptors in smooth muscle) Kinesthesia & Proprioception work together to create body image.
  • 376. The Somatosensory System • Most Somatosensory Receptors are mechanoreceptors • e.g., annulospiral receptors (muscle spindles) and GTOs (tendons) • pressure and vibration activate mechanoreceptors in the skin • Temperature changes activate both mechanoreceptors and chemoreceptors • expansion and shrinking of skin with temperature ( mechano ) • cold sensors and warmth sensors exist ( carried by different types of axons ) • Transduction is via Transient Receptor Potential family of proteins (called TRP receptors) - some TRP receptors respond to chemicals (e.g., menthol, in mints, feels cool) Pain information can be carried via both mechanoreceptors and chemoreceptors • e.g., excess pressure on skin ( mechano ) • e.g., bradykinin and prostaglandin release from bee sting ( chemo ) Somatosensory Receptors include both mechanoreceptors and chemoreceptors
  • 377.
    • Types of Receptors in the Skin (only focus on these 4)
    • Pacinian Corpuscles (PRESSURE & VIBRATION)
        • Sensory fiber surrounded by concentric layers (located deep, below dermis)
    • Meissner’s corpuscles (TOUCH)
        • Composed of axonal loops, separated by nonneuronal support cells
        • Important for detecting movement along skin (e.g., adjusting grip)
    • Basket endings (MOVEMENT OF HAIR)
        • Wrapped around individual hairs and detect movement
    • Free nerve endings (PAIN or TEMPERATURE)
        • Single, bare nerve endings at end of sensory fiber
    The Somatosensory System
    • There are others, such as the following (but don’t worry about these)
    • • Ruffini’s endings (STRETCH) (& WARMTH?)
        • Sensory fibers terminate among collagen fibers in skin
    • • Krause endbulbs (COLD?)
    • • Merkel’s disks (TOUCH, RESPOND TO SUSTAINED PRESSURE)
  • 378. The Somatosensory System
  • 379. The Somatosensory System
    • Two Types of Axons Carry Sensory Information to the CNS
    • A-fibers (large myelinated axons; 3 types)
      • A  ( alpha) are large diameter (15-20 µm)
      • most heavily myelinated & fastest (100 m/s or ~224 mph)
      • axons of muscle spindles & GTOs
      • A  ( beta) are medium diameter (5-15 µm)
      • well-myelinated & fast (50 m/s)
      • axons of Pacinian & Meisner’s corpuscles and Merkel disks
      • A  (delta) are small diameter (1-5 µm)
      • poorly myelinated & slower (10-30 m/s)
      • some pain & pressure
      • cold sensors (temp)
    • C-fibers ( very small diameter axons, <1 µm)
        • unmyelinated axons & slow conduction (0.4-2 m/s)
        • axons of free nerve endings (pain or nociception)
        • most numerous (~80% of axons terminating in the skin)
        • warmth sensors (temp)
  • 380.
    • General Rule of Thumb
    • 1. Info about pressure & touch travels to the brain quickly
      • ( more recent system )
    • 2. Info about pain & temperature travels to the brain more slowly ( older system )
  • 381.
    • Lemniscal Path (A-fibers)
        • • ascends dorsal column
        • • crosses over in medulla
        • • processes precise touch & kinesthesia
    • Spinothalamic Tract (C-fibers)
        • • crosses over in spinal cord
        • • processes pain & temperature
    Somatosensory Paths from the Body to the Cortex All paths go through ventral posterior thalamus
  • 382. Somatosensory Paths from the Body to the Cortex Lemniscal (touch) • crosses over in hindbrain Spinothalamic (pain) • crosses over in cord
  • 383. Somatosensory Paths from the Face & Head to the Cortex The “Trigeminal System or Pathway” via Cranial Nerve V (Trigeminal nerve)
  • 384.  
  • 385. Primary Somatosensory Cortex is topographically organized Remember – Fine touch & pressure go via lemniscal path Pain & temperature travel up the spinothalamic tract
  • 386. The Somatosensory System 1. “What” System – What is the perceived sensation? • Inferior Parietal Cortex Damage to Inferior Parietal Cortex produces Tactile Agnosia an inability to recognize objects through touch 2. “Where” System – Where on my body is the sensation coming from? • Posterior Parietal Cortex ( note this is also part of visual “where” system too ) Damage to Posterior Parietal Cortex produces Inability to process the location of a stimulus and its spatial relationship to other tactile stimuli
  • 387. Plasticity of the Somatosensory System (1) The cortex is continuously being re-organized by experience (2) The 1° somatosensory cortex is also re-organized following amputation of a body part (e.g., lower arm and hand) • In such cases inputs to neighboring cortices invade the hand area • Thus, the brain can “ hallucinate ” the presence of a phantom limb every time an area which invaded the phantom limb’s cortex is activated (e.g., touching face would now activate neurons in amputated hand area) Notice that in the 1° somatosensory cortex, the distal arm/hand area is flanked by the upper arm area above and the face area below (both of which invade following amputation)
  • 388. Recall that in 1° somatosensory cortex, the distal arm/hand area is flanked by the upper arm area above and the face area below (both of which invade following amputation) Plasticity of the Somatosensory System
  • 389. END – Lecture 15
  • 390. PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 16 (November 3, 2010) THE SOMATOSENSORY SYSTEM II • Perception of pain • Neurochemistry of pain • Gate-control theory of pain • Cortical processing of pain
  • 391. Pain Perception Gate-Control Theory (Melzack & Wall, 1965) 1. C-fibers carry information to substantia gelatinosa (dorsal horn of spinal cord) 2. Substantia gelatinosa relays information to the brain stem 3. Brain stem relays information to the cerebral cortex (conscious experience) 4. Certain brain structures and A-fibers can stop pain messages by sending inhibitory signals to the substantia gelatinosa (thus “Closing the Gate” on pain): (a) Periaqueductal gray or PAG (located in midbrain) (b) Periventricular gray or PVG (hypothalamic area, near 3rd ventricle) (c) A-fibers transmitting tactile information
  • 392. Neurochemistry of Pain Neurotransmitter that Transmits Pain Messages: Substance P - neurotransmitter used by pain receptors - released by C-fibers that synapse onto substantia gelatinosa neurons - signals the presence of tissue damage and pain Class of Neurotransmitters that Inhibit Pain Messages: Endorphins - endogenous opiates (also called enkephalins) - neurons in PAG and PVG send axon terminals to substantia gelatinosa • there they form axoaxonic synapses onto the C-fiber terminals • they release endorphins onto C-fiber terminals • block ascending pain by presynaptic inhibition - also released by pituitary gland in response to stressful or painful situations - effects of endorphins can be blocked by opiate antagonists such as naloxone
  • 393. Substantia Gelatinosa is Lamina II of the Dorsal Horn **
  • 394. Gate-Control Theory of Pain Explains how a severely injured individual can ignore pain to, for example, rescue a loved one (higher brain centers activate neurons in PAG and PVG which “close the gate” on ascending pain).
  • 395. Gate-Control Theory of Pain
  • 396. Why A-fiber Stimulation Can Also Reduce Pain Explains why rubbing an area produces relief.
  • 397. Cortical Processing of Pain
    • 3 Dimensions of Pain Perception:
    • Sensory-discriminative
        • • detect pain and identify its source ( can be wrong: e.g., referred pain )
        • • processed initially in 2°(secondary) somatosensory cortex
    • Motivational-affective
        • • emotional and motivational aspects - can it be endured
        • • processed in anterior cingulate cortex
        • (if anterior cingulate is damaged, pain is felt but not viewed as unpleasant)
    • Cognitive-evaluative
        • • severity and how to deal with the pain
        • • processed in prefrontal cortex
    Allodynia may be experienced following tissue & nerve damage (abnormal enhanced pain response).
  • 398. END – Lecture 16
  • 399. PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lectures 17 & 18 (November 08 & 10, 2010) COGNITIVE PROCESSES I & II • The Frontal Lobe & Working Memory • Memory Consolidation & Reconsolidation • Long-Term Declarative Memory - episodic and semantic - patient H.M. - emotions and memory • Long-Term Nondeclarative or Procedural Memory • Amnesia and Alzheimer’s disease (medial temporal lobe) • Effects of Prefrontal Cortex Damage
  • 400. In Humans, the Frontal Lobe is the Largest Lobe
  • 401. The Frontal Lobe and Cognition • Frontal lobe is the largest brain structure occupies ~1/3 of the human brain • Divided into 3 functional zones or areas 1. prefrontal cortex (most anterior region – cognition, planning, etc… ) 2. premotor cortex (anterior to motor cortex - movement ) 3. primary motor cortex (or precentral gyrus - movement )
  • 402. Relative size of the Prefrontal Cortex in different animals
  • 403. Prefrontal Cortex is important for Working Memory Working Memory (Baddeley & Hitch, 1974) • Coordinated, temporary storage of information in various sites in the cerebral cortex. • WM allows you to perform calculations in your head, to read, and solve problems. • Intelligence may be linked to working memory capacity .
  • 404. 1. Working Memory for Object Identification - • can hold an object or series of objects in mind • thus can put a series of objects in order (e.g., also face recognition ) • IT cortex (visual object recognition) and PFC (storage centers) 2. Working Memory for Spatial Location - • holding in memory the spatial location of several objects at the same time (e.g., playing chess ) • right hemispheric regions are involved: posterior parietal , hippocampus , PFC 3. Working Memory for Verbal Information - • holding words in mind (e.g., reading or listening to someone speaking ) • Broca’s and Wernicke’s areas (speech centers in the left hemisphere) • anterior cingulate cortex (in medial PFC) • left premotor cortex (rehearsing verbal material sub-vocally) Brain Regions involved in Working Memory (WM) (depends upon the kind of information being held in WM)
  • 405. Overview of Circuits Involved in Speech Production Speech Paul Broca (1861) and Carl Wernicke (1874)
  • 406. Anterior Cingulate Cortex (in medial PFC) • activated when working memory is used • coordinates working memory? *
  • 407. PET scans illustrating activation of brain regions during working memory for verbal information (e.g., think of uses for nouns or some other verbal task) Note: PET scan measures changes in blood flow (increased blood flow is correlated with increased activity)
  • 408. Memory and Consolidation of Memories Short- and Long-term memory (William James, 1890) • a limited memory system (e.g., can hold ~7 pieces of information) • holds information effortlessly for ~30 seconds before decaying • can hold information longer with rehearsal • postulated by Donald Hebb (1949) to result from reverberating circuits in the frontal lobes - Chunking information will allow compartmentalization and thus more retained Short-term memory (i.e., working memory) • postulated by Hebb to describe the shift of a memory from a relatively labile short- term to a relatively stable long-term form ( which can be made labile again by retrieval of the memory – reconsolidation ) Consolidation (& Reconsolidation) • a memory system capable of storing large amounts of information for long periods of time (e.g., years to decades) • Hebb proposed that long-term memory results from structural changes to memory circuits • there are two main long-term memory systems ( declarative & nondeclarative ) Long-term memory
  • 409. A Simple Model of the Learning Process
  • 410. A Schematic Description of the Experiment by Misanin, Miller, and Lewis (1968)
  • 411. Declarative Memory • Also called explicit memory • Involves conscious retention of facts and events • Requires the hippocampus for initial storage - patients with hippocampal damage exhibit amnesia - retrograde am nesia (backward - old) cannot remember events just prior to injury - anterograde amnesia (forward- new) cannot create new declarative memories e.g., patient H.M. cannot form new memories • Over time, the hippocampus is no longer required for declarative memory retrieval - thus, hippocampus serves a temporary , time-limited role
  • 412. Schematic Definition of Retrograde Amnesia & Anterograde Amnesia
  • 413. • 1953 - bilateral removal of medial temporal lobe structures to ameliorate epilepsy (e.g., hippocampus, entorhinal cortex, perirhinal cortex, amygdala) • H.M. could not form new conscious memories since the surgery (e.g., impaired declarative memory) Note: MRI involves placing a persons head in a strong magnetic field to detect radio waves emitted by hydrogen atoms throughout brain tissue MRI of patient H.M.’s Brain ( left image )
  • 414. 2 Forms of Declarative Memory
    • 1. Episodic Memory
      • • memory for events or episodes in one’s own life
        • (e.g., what one did yesterday or a meeting you had recently)
        • • such memories are organized in time and identified by a particular context
        • • includes not just verbal memory but also the perceptions
        • (e.g., can visualize the surroundings while recalling the information)
        • Organized in time and space.
    • 2. Semantic Memory
        • • general knowledge or learned facts
        • (e.g., knowing the multiplication tables, history, geography, etc…)
        • • does not include information about the context in which facts were learned
  • 415. Effects of Emotional Arousal on Consolidation of Long-Term Memory
    • 1. Memory is greater for emotionally charged events
      • • easier to remember where you were on 9/11/2001 than other 9/11s
      • • easier to remember your first date
    • 2. When aroused, your body releases hormones (e.g., epinephrine)
    • • Epinephrine activates the amygdala which enhances consolidation of memory
        • • drugs that block effects of epinephrine interfere with memory formation
  • 416. Nondeclarative Memory • Also called implicit or procedural memory • Involves nonconscious memory for learned behaviors • Does NOT require the hippocampus - instead, involves cerebellum and corticostriatal system • One example of nondeclarative memory is the Priming Effect - improved ability to recognize particular stimuli after experience with them - e.g., word-stem completion task ( rehearsal not permitted ) garden gar- (person would complete garden faster) window tar- tennis sin- - priming involves posterior parietal and occipital cortex for the visual information and Broca’s area for conceptual information
  • 417.
      • • neurodegenerative disease
      • characterized by severe memory loss
      • • Diagnosed by presence of plaques (  Amyloid protein deposits) and tangles (tau protein filaments) which first form in temporal lobes and spread throughout forebrain
      • • initially, the disease destroys synapses
      • and then eventually kills the neurons in the later stages of AD
      • • most common form of senile dementia in the elderly
      • • anterograde amnesia for episodic and semantic memories
      • • also retrograde amnesia
      • • ACh levels (& other transmitters) are severely depleted in AD brains
      • • current therapies involve acetylcholinesterase inhibitors (don’t work very well)
      • • potential future therapies may involve immunization against  Amyloid
    Alzheimer’s disease
  • 418. AD brain Control brain Senile plaques in hippocampus Senile Plaques and Neurofibrillary Tangles Alzheimer’s disease
  • 419. AD brain Control brain Alzheimer’s disease
  • 420. Alzheimer’s disease AD neurons Control neuron
  • 421. Reconstruction of Phineas Gage’s Brain 1848 - explosion sent iron rod through his cheek and up out the top of his head ( destroyed mPFC ) Phineas Gage was a railroad foreman • before accident - very polite • after accident - disinhibited (displayed many of the symptoms of PFC damage)
  • 422. Disorders Associated with Prefrontal Cortex Damage
    • 1. Dysexecutive Syndrome
        • • inability to coordinate complex behaviors with respect to goals and task specific constraints
        • (e.g., might stir coffee cup first and then add cream to the coffee)
    • 2. Disinhibition
        • • lack of behavioral control
        • • impulsive, quick to anger, prone to rude childish remarks
        • (e.g., demonstrates utilization behavior - when left alone patient will inappropriately pick up a comb from a desk and use it)
        • • can also be tested using the Stroop Test or Wisconsin Card Sorting Test ( PFC patients perseverate - i.e., unable to alter initial response)
    • 3. Emotional Impairments
        • • indifferent and apathetic to their own situation and to the needs of others
        • (e.g., people with PFC damage might laugh if they see someone crying)
        • • irritable and prone to angry outbursts
    • 4. Difficulty Planning
        • • unable to organize behavior to plan several steps in advance
        • • assessed by Tower of Hanoi Test or Multiple Errands Task
  • 423. The Stroop Test for damage to prefrontal cortex Patients with damage to prefrontal cortex do fine reading the words, naming the colors, but have great difficulty naming the color of the word when they are different
  • 424. The Stroop Test for damage to prefrontal cortex Patients with damage to prefrontal cortex do fine reading the words, naming the colors, but have great difficulty naming the color of the word when they are different
  • 425. The Stroop Test for damage to prefrontal cortex Patients with damage to prefrontal cortex do fine reading the words, naming the colors, but have great difficulty naming the color of the word when they are different
  • 426. Tower of Hanoi Test of PFC function Patients with damage to prefrontal cortex have great difficulty planning ahead to solve the Tower of Hanoi test
  • 427. The Wisconsin Card Sorting Task Patients with damage to prefrontal cortex do well initially but they perseverate on the initial rule and are unable to change (e.g., sort by number after initially being asked to sort by shape)
  • 428. END – Lectures 17 & 18
  • 429. COGNITIVE PROCESSES III 1. Associative Learning • Classical Conditioning • Trace vs. Delay Conditioning 2. Synaptic Plasticity PHYSIOLOGICAL PSYCHOLOGY (PSY 254) Lecture 19 (November 29, 2010)
  • 430. Classical or Pavlovian Conditioning
    • Model system for studying associative learning (implicit & explicit)
    • Allows for excellent experimental control over stimuli
    • Studied in many species (e.g. human, monkey, rabbit, rat, mouse)
    • Engages both cortical and subcortical brain regions
  • 431. Ivan Pavlov 1849-1936, physiologist
  • 432. Classical ( Pavlovian ) Eyeblink Conditioning
    • CS = conditional stimulus
        • (e.g., neutral stimulus such as an auditory tone)
    • US = unconditional stimulus
        • (e.g., airpuff delivered to eye)
    • UR = unconditional response
        • (e.g., eyeblink following airpuff)
    • CR = conditional response
    • (e.g., eyeblink in response to the tone CS - prior to delivery of US)
    • ISI = interstimulus interval
        • (e.g., time between onset of CS and onset of US)
    • ITI = intertrial interval
    • (e.g., time between trials; from US offset to next CS onset)
  • 433. Simple Neural Model of Classical Conditioning
  • 434. Delay vs. Trace Eyeblink Conditioning Delay Conditioning • CS and US are temporally contiguous (overlap in time) • requires fewer training trials • depends on brainstem and cerebellar circuitry • implicit learning Trace Conditioning • CS and US are discontiguous (separated by stimulus-free trace interval) • requires many more training trials • still depends on brainstem and cerebellum to elicit a CR • but now also depends on higher brain structures ( e.g., hippocampus ) to learn • explicit learning (i.e., subjects that learn the task also express awareness whereas subjects that fail to learn do not express awareness)
  • 435. Cellular Mechanisms of Learning and Memory
    • Synapses are plastic!
      • • they can be added or removed
      • • they can be strengthened or weakened
      • • Synaptic Plasticity has two basic forms
      • long-term potentiation or LTP (strengthening)
      • long-term depression or LTD (weakening)
      • LTP is a form of cellular memory!
  • 436. Hebb’s Postulate (regarding conditions that cause a synapse to change) “ When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased.” - Donald Hebb, 1949 Modern interpretation? “Cells that fire together wire together! Synaptic Plasticity
  • 437. LTP was first discovered in the Hippocampus
  • 438. Long-Term Potentiation Strong Stimulus can be: • high frequency stimulation (e.g., 100 Hz) Note: stimulation must be sufficient to produce enough postsynaptic depolarization to open NMDA receptors ( see slide on induction of LTP, 3 slides from this one )
  • 439. The Role of Summation in Long-Term Potentiation
  • 440. LTP is input specific
  • 441. Hebbian Plasticity Can Think of the Weak Path as the CS and the Strong Path as the US (Classical Conditioning)
    • When 2 Different Pathways are Stimulated (e.g., One Weak and One Strong)
    • Weak-alone does nothing
    • Strong-alone strengthens strong pathway only
    • Weak + Strong together strengthens both pathways
  • 442. Associative Long-Term Potentiation Action potential primes NMDA receptors so that weak synapses active at the same time will become strengthened
  • 443. Induction of LTP Requires Strong Postsynaptic Depolarization The postsynaptic Ca 2+ influx during depolarization is a critical trigger for induction of LTP
  • 444. • Under normal conditions, synaptic stimulation activates only AMPA receptors ( and thus a small synaptic response or EPSP occurs ) • Strong depolarization leads to activation of NMDA receptors, which let Ca 2+ into the cell • Ca 2+ influx activates 2 nd messengers, which leads to insertion of more AMPA receptors ( and thus a larger synaptic response or larger EPSP ) Long-term potentiation (LTP)
  • 445. Copyright (c) Allyn & Bacon 2004 Copyright © Allyn & Bacon 2004 Postsynaptic Mechanism of LTP (insertion of more AMPA receptors)
  • 446. Expression of LTP and LTD 1. Silent Synapses result from an absence of postsynaptic AMPA receptors 2. Synapses that were previously silent can become active following LTP ( due to LTP causing insertion of AMPA receptors ) Final Note: • insertion of AMPA receptors = LTP (strengthening of synapse strength) • removal of AMPA receptors = LTD (weakening of synapse strength)
  • 447. END – Lecture 19 (End of Material on Final Exam)