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Pinel basics ch03


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Pinel basics ch03

  1. 1. Chapter 3 Neural Activity and How to Study It How Neurons Work <ul><li>This multimedia product and its contents are protected under copyright law. The following are prohibited by law: </li></ul><ul><li>any public performance or display, including transmission of any image over a network; </li></ul><ul><li>preparation of any derivative work, including the extraction, in whole or in part, of any images; </li></ul><ul><li>any rental, lease, or lending of the program. </li></ul>
  2. 2. Parkinson’s Disease <ul><li>The case of Mr. d’Orta demonstrates the importance of understanding how neurons work </li></ul><ul><li>A lack of dopamine underlies this movement disorder, but it can’t be treated with dopamine </li></ul><ul><li>Why not? </li></ul>
  3. 3. The Neuron’s Resting Membrane Potential <ul><li>Inside of the neuron is negative with respect to the outside </li></ul><ul><li>Resting membrane potential is about -70mV </li></ul><ul><li>Membrane is polarized, it carries a charge </li></ul><ul><li>Why? </li></ul>
  4. 4. Ionic Basis of the Resting Potential <ul><li>Ions, charged particles, are unevenly distributed </li></ul><ul><li>Sodium, potassium, and chloride ions are the main ones to be concerned with </li></ul><ul><li>There are more negative charges inside the neuron than there are outside </li></ul>
  5. 5. Why is there greater negative charge inside? <ul><li>Two properties of the neural membrane contribute to the difference </li></ul><ul><ul><li>Differential permeability – some substances pass through the membrane more easily than others, moving through ion channels that can open and close </li></ul></ul><ul><ul><li>Sodium potassium pumps – move positively charged sodium ions out, while moving fewer positively charged potassium ions in </li></ul></ul>
  6. 6. Sodium <ul><li>There is great pressure on sodium to move into the resting neuron </li></ul><ul><li>Positively charged sodium is attracted to the internal negative charge </li></ul><ul><li>Random motion – as there is more sodium out than in, sodium tends to leak in </li></ul>
  7. 7. <ul><li>Figure 3.1 (NEW) </li></ul>
  8. 8. Postsynaptic Potentials and Action Potentials <ul><li>Neurotransmitters bind at postsynaptic receptors </li></ul><ul><li>These chemical messengers bind and cause electrical changes </li></ul><ul><ul><li>Depolarizations (making the membrane potential less negative) </li></ul></ul><ul><ul><li>Hyperpolarizations (making the membrane potential more negative) </li></ul></ul>
  9. 9. Postsynaptic Potentials (PSPs) <ul><li>Postsynaptic depolarizations = Excitatory PSPs (EPSPs) </li></ul><ul><li>Postsynaptic hyperpolarizations = Inhibitory PSPs (IPSPs) </li></ul><ul><li>EPSPs make it more likely a neuron will fire, IPSPs make it less likely </li></ul><ul><li>PSPs are graded potentials – their size varies </li></ul>
  10. 10. EPSPs and IPSPs <ul><li>Travel passively from their site of origination </li></ul><ul><li>Decremental – they get smaller as they travel </li></ul><ul><li>1 EPSP typically will not suffice to cause a neuron to “fire” and release neurotransmitter – summation is needed </li></ul>
  11. 11. Integration of PSPs and Generation of Action Potentials (APs) <ul><li>In order to generate an AP (or “fire”), the threshold of activation must be reached </li></ul><ul><li>Integration of IPSPs and EPSPs must result in a potential of about -65mV in order to generate an AP </li></ul>
  12. 12. Integration <ul><li>Adding or combining a number of individual signals into one overall signal </li></ul><ul><li>Temporal summation – integration of events happening at different times </li></ul><ul><li>Spatial - integration of events happening at different places </li></ul>
  13. 13. What type of summation occurs when: <ul><li>One neuron fires rapidly? </li></ul><ul><li>Multiple neurons fire at the same time? </li></ul><ul><li>Several neurons fire repeatedly? </li></ul><ul><li>Both temporal and spatial summation occur simultaneously </li></ul>
  14. 16. The Action Potential <ul><li>All-or-none, when threshold is reached the neuron “fires” and the action potential either occurs or it does not </li></ul><ul><li>Like a gun, it either fires or it does not </li></ul>
  15. 17. Sodium Ions and Action Potentials <ul><li>When summation results in the threshold of excitation (-65mV) being reached, voltage-activated sodium channels open and sodium rushes in </li></ul><ul><li>Remember, at rest, all forces act to move sodium into the cell </li></ul><ul><li>Membrane potential moves from -70 to about +50mV, a considerable depolarization </li></ul>
  16. 18. <ul><li>Figure 3.5 (4.6) </li></ul>
  17. 19. Refractory Periods <ul><li>Absolute – impossible to initiate another action potential </li></ul><ul><li>Relative – harder to initiate another action potential </li></ul><ul><li>Prevent the backwards movement of APs and limit the rate of firing </li></ul>
  18. 20. Axonal Conduction of Action Potentials (APs) <ul><li>The AP travels passively along the axonal membrane until it reaches an area with voltage-gated sodium channels </li></ul><ul><li>Opening sodium channels is an active process that then leads to a new action potential </li></ul><ul><li>This new action potential then travels passively to the next area of voltage-gated sodium channels </li></ul><ul><li>This process is repeated again and again </li></ul>
  19. 21. PSPs Vs Action Potentials (APs) <ul><li>EPSPs/IPSPs </li></ul><ul><li>Decremental </li></ul><ul><li>Fast </li></ul><ul><li>Passive (energy is not used) </li></ul><ul><li>Action Potentials </li></ul><ul><li>Nondecremental </li></ul><ul><li>Conducted more slowly than PSPs </li></ul><ul><li>Passive and active </li></ul>
  20. 22. Conduction in Myelinated Axons <ul><li>Passive movement of AP within myelinated portions occurs instantly </li></ul><ul><li>Nodes of Ranvier (unmyelinated) </li></ul><ul><ul><li>Where ion channels are found </li></ul></ul><ul><ul><li>Where full AP is seen </li></ul></ul><ul><ul><li>AP appears to jump from node to node </li></ul></ul><ul><ul><ul><li>Saltatory conduction </li></ul></ul></ul>
  21. 23. Conduction in Neurons without Axons <ul><li>Many neurons in mammalian brains do not have axons </li></ul><ul><li>Neural conduction is typically by graded, decrementally conducted potentials </li></ul>
  22. 24. Structure of Synapses <ul><li>Most common </li></ul><ul><ul><li>Axodendritic – axons on dendrites </li></ul></ul><ul><ul><li>Axosomatic – axons on cell bodies </li></ul></ul><ul><li>Directed – release and binding sites are close </li></ul><ul><li>Nondirected – release and binding sites are at some distance </li></ul>
  23. 25. Synthesis and Transport of Neurotransmitter (NT) Molecules <ul><li>Small - synthesized in the terminal button and packaged in synaptic vesicles </li></ul><ul><li>Large - assembled in the cell body, packaged in vesicles, and then transported to the axon terminal </li></ul><ul><ul><li>Peptides – chains of amino acids </li></ul></ul><ul><li>Coexistence – many neurons contain both small-molecule and large-molecule NT </li></ul>
  24. 26. Release of NT Molecules <ul><li>Exocytosis – the process of NT release </li></ul><ul><li>The arrival of an AP at the terminal opens voltage-activated calcium channels </li></ul><ul><li>The entry of calcium causes vesicles to fuse with the terminal membrane and release their contents </li></ul>
  25. 27. Activation of Receptors by NT <ul><li>Released NT produces signals in postsynaptic neurons by binding to receptors </li></ul><ul><li>Receptors are specific for a given NT </li></ul><ul><li>Ligand – a molecule that binds to another. </li></ul><ul><li>A NT is a ligand of its receptor </li></ul>
  26. 28. Receptors <ul><li>There are multiple receptor types for a given NT </li></ul><ul><li>Ionotropic receptors – associated with ligand-activated ion channels </li></ul><ul><li>Metabotropic receptors – associated with signal proteins and G proteins </li></ul>
  27. 29. Ionotropic Receptors <ul><li>NT binds and an associated ion channel opens or closes, causing a PSP </li></ul><ul><li>If sodium channels are opened, for example, an EPSP occurs due to the entry of sodium </li></ul>
  28. 30. Metabotropic Receptors <ul><li>Effects are slower, longer-lasting, more diffuse, and more varied </li></ul><ul><li>NT (1 st messenger) binds > G protein subunit breaks away > ion channel opened/closed OR a 2 nd messenger is synthesized > 2 nd messengers may have a wide variety of effects </li></ul>
  29. 32. Autoreceptors <ul><li>Metabotropic receptors </li></ul><ul><ul><li>Bind to their neuron’s own NT molecules </li></ul></ul><ul><ul><li>Located on the presynaptic membrane </li></ul></ul><ul><li>Usually monitor the number of neurotransmitter molecules on the synapse </li></ul>
  30. 33. Termination of NT Effects <ul><li>As long as NT is in the synapse, it is active – activity must somehow be turned off </li></ul><ul><li>Reuptake – scoop up and recycle NT </li></ul><ul><li>Enzymatic degradation – a NT is broken down by enzymes </li></ul><ul><ul><li>Example - acetylcholinesterase </li></ul></ul>
  31. 34. The Neurotransmitters <ul><li>Four classes of small-molecule NT </li></ul><ul><li>One large-molecule variety – peptides or neuropeptides </li></ul><ul><li>Most NT produce either excitation or inhibition, but some may do both by having different effects at different receptor subtypes </li></ul>
  32. 35. Small-molecule Neurotransmitters <ul><li>Amino acids – the building blocks of proteins </li></ul><ul><li>Monoamines – all synthesized from a single amino acid </li></ul><ul><li>Soluble gases </li></ul><ul><li>Acetylcholine (ACh) – activity terminated by enzymatic degradation </li></ul>
  33. 36. Amino Acid Neurotransmitters <ul><li>Usually found at fast-acting directed synapses in the CNS </li></ul><ul><li>Glutamate – Most prevalent excitatory neurotransmitter in the CNS </li></ul><ul><li>GABA – </li></ul><ul><ul><li>synthesized from glutamate </li></ul></ul><ul><ul><li>Most prevalent inhibitory NT in the CNS </li></ul></ul><ul><li>Aspartate and glycine </li></ul>
  34. 37. Monoamines <ul><li>Effects tend to be diffuse </li></ul><ul><li>Catecholamines – synthesized from tyrosine </li></ul><ul><ul><li>Dopamine </li></ul></ul><ul><ul><li>Norepinephrine </li></ul></ul><ul><ul><li>Epinephrine </li></ul></ul><ul><li>Indolamines – synthesized from tryptophan </li></ul><ul><ul><li>Serotonin </li></ul></ul>
  35. 38. Soluble-Gases and ACh <ul><li>Soluble gases – exist only briefly </li></ul><ul><ul><li>Nitric oxide and carbon monoxide </li></ul></ul><ul><ul><li>Retrograde transmission – backwards communication </li></ul></ul><ul><li>Acetylcholine (Ach) </li></ul><ul><ul><li>Acetyl group + choline </li></ul></ul><ul><ul><li>Neuromuscular junction </li></ul></ul>
  36. 39. Neuropeptides <ul><li>Large molecules, close to 100 identified </li></ul><ul><li>Example – endorphins </li></ul><ul><ul><li>“ Endogenous opiates” </li></ul></ul><ul><ul><li>Produce analgesia (pain suppression) </li></ul></ul><ul><ul><li>Receptors were identified before the natural ligand was </li></ul></ul>
  37. 40. How Biopsychologists Study the Brain <ul><li>Stereotaxic surgery </li></ul><ul><li>Conventional, lesion, stimulation, and recording methods </li></ul><ul><li>Pharmacological methods </li></ul><ul><li>Brain imaging </li></ul><ul><li>Genetic engineering </li></ul>
  38. 41. Stereotaxic Surgery <ul><li>Used to position experimental devices within the brain </li></ul><ul><li>Stereotaxic atlas – provides coordinates for locating structures within the brain </li></ul><ul><li>Bregma – a point on the top of the skull often used as a reference point </li></ul><ul><li>Sterotaxic instrument – used to hold head steady and guide the device to be inserted </li></ul>
  39. 43. Lesion Methods <ul><li>Lesion (or destroy) a structure to observe the effect on behavior </li></ul><ul><li>Electrolytic lesion – electrical current used to destroy the target structure </li></ul><ul><li>Aspiration lesions – suction - cortex </li></ul><ul><li>Knife cuts – may damage surrounding area </li></ul>
  40. 45. Stimulation Methods <ul><li>Conventional methods involve using brain stimulation to determine the effects of a given brain structure </li></ul><ul><li>Current is delivered used a permanently implanted electrode </li></ul><ul><li>Rarely used in humans </li></ul>
  41. 46. Recording Methods <ul><li>Unit recording – recording the activity of individual neurons </li></ul><ul><li>Multiple-unit recording – recording the overall firing rate of many neurons in an area </li></ul><ul><li>EEG – electrodes on the scalp record the difference between 2 large electrodes </li></ul>
  42. 48. Pharmacological Methods <ul><li>Many drugs act to alter NT activity </li></ul><ul><li>Agonists – increase or facilitate </li></ul><ul><li>Antagonists – decrease or inhibit </li></ul><ul><li>Drugs may act to alter NT activity at any point, from synthesis to termination </li></ul>
  43. 51. Agonist - Example <ul><li>Cocaine - catecholamine agonist </li></ul><ul><li>Blocks reuptake – preventing the activity of the neurotransmitter from being “turned off” </li></ul><ul><li>Cocaine causes dopamine and norepinephrine to remain active in the synapse for a longer period of time </li></ul>
  44. 52. Acetylcholine Antagonists <ul><li>Curare – Binds and blocks nicotinic receptors, the ionotropic receptors at the neuromuscular junction </li></ul><ul><ul><li>Causes paralysis </li></ul></ul><ul><li>Botox – Blocks release of acetylcholine at the neuromuscular junction </li></ul><ul><ul><li>A deadly poison </li></ul></ul><ul><ul><li>Minute doses at specific places, however, has medical and cosmetic uses </li></ul></ul>
  45. 53. Selective Chemical Lesions <ul><li>Neural poisons (neurotoxins) selectively target specific nervous system components </li></ul><ul><li>Kainic acid – destroys cell bodies </li></ul><ul><li>6-hydroxydopamine (6-OHDA) – destroys noradrenergic and dopaminergic neurons </li></ul>
  46. 54. Brain Imaging <ul><li>Contrast X-Rays – inject something that absorbs X-rays less or more than surrounding tissue </li></ul><ul><ul><li>Cerebral angiography </li></ul></ul><ul><li>X-Ray Computed Tomography (CT) </li></ul><ul><ul><li>2-D images combined to create a 3-D one </li></ul></ul><ul><li>Magnetic Resonance Imaging (MRI) </li></ul><ul><ul><li>Produces 3-D images with high spatial resolution </li></ul></ul>
  47. 55. Brain Imaging <ul><li>Positron Emission Tomography (PET) </li></ul><ul><ul><li>Inject radioactive 2-DG </li></ul></ul><ul><li>Functional MRI (fMRI) </li></ul><ul><ul><li>Visualizing oxygen flow in the brain </li></ul></ul><ul><ul><li>Currently the predominant brain recording technique of cognitive neuroscience </li></ul></ul>
  48. 56. fMRI Vs PET <ul><li>Nothing injected. </li></ul><ul><li>Provides both structural and functional information in one image </li></ul><ul><li>Spatial resolution is better than with PET </li></ul><ul><li>Can create 3-D images of activity over the entire brain </li></ul>
  49. 57. Weaknesses of fMRI <ul><li>To create an fMRI image, brain activity from many subjects is needed and there are differences among people </li></ul><ul><li>Not able to detect small areas of brain activity </li></ul><ul><li>Only infers neural activity from changes in blood flow </li></ul>
  50. 58. Genetic Engineering <ul><li>Gene knockout techniques </li></ul><ul><ul><li>Subjects missing a given gene can provide insight into what the gene controls </li></ul></ul><ul><ul><li>Difficult to interpret results – most behavior is controlled by many genes and removing one gene may alter the expression of others </li></ul></ul><ul><li>Gene replacement techniques </li></ul><ul><li>Both are currently being intensely studied </li></ul>