Psych 2 chapter 3. comphrensive outline example 2011

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Psych 2 chapter 3. comphrensive outline example 2011

  1. 1. CHAPTER 3 SYNAPSESChapter OutlineI. The Concept of the Synapse A. The properties of synapses (specialized gaps between neurons) 1. Sherrington deduced the properties of the synapse from his experiments on reflexes (an automatic muscular response to stimuli). 2. Reflex arc: the circuit from sensory neuron to muscle response. 3. Sherrington discovered that: a. Reflexes are slower than conduction along an axon. b. Several weak stimuli presented at slightly different times or locations produce a stronger reflex than a single stimulus does. c. Excitation of one set of muscles leads to a relaxation of others. B. Temporal summation: Repeated stimuli within a brief time having a cumulative effect. 1. Presynaptic neuron: The neuron that delivers the synaptic transmission. 2. Postsynaptic neuron: The neuron that receives the message. 3. Graded potentials: Either depolarization (excitatory) or hyperpolarization (inhibitory) of the postsynaptic neuron. 4. A graded depolarization is known as an excitatory postsynaptic potential (EPSP) and occurs when Na+ ions enter the postsynaptic neuron. EPSPs are not action potentials: The EPSP’s magnitude decreases as it moves along the membrane. C. Spatial summation: Several synaptic inputs originating from separate locations exerting a cumulative effect on a postsynaptic neuron. D. Inhibitory postsynaptic potential (IPSP): A temporary hyperpolarization of a postsynaptic cell (this occurs when K+ leaves the cell or Cl- enters the cell after it is stimulated). E. Relationship among EPSP, IPSP, and action potentials 1. The probability of an action potential on a given neuron depends on the ratio of EPSPs to IPSPS at a given moment. 2. Spontaneous firing rate: The ability to produce action potentials without synaptic input (EPSPs and IPSPs increase or decrease the likelihood of firing action potentials).II. Chemical Events at the Synapse A. In most cases, synaptic transmission depends on chemical rather than electrical stimulation. This was demonstrated by Otto Loewi’s experiments where fluid from a stimulated frog heart was transferred to another heart. The fluid caused the new heart to react as if stimulated. B. The major events at a synapse are: 1. Neurons synthesize chemicals called neurotransmitters. Chapter 3 28
  2. 2. 2. Neurons transport the neurotransmitters to the axon terminal. 3. Action potentials travel down the axon. At the axon or presynaptic terminal, the action potentials cause calcium to enter the cell, which leads to the release of neurotransmitters from the terminal into the synaptic cleft (space between the presynaptic and postsynaptic neuron). 4. Neurotransmitters, once released into the synaptic cleft, attach to receptors and alter activity of the postsynaptic neuron. 5. The neurotransmitters will separate from their receptors and (in some cases) are converted into inactive chemicals. 6. In some cells, much of the released neurotransmitter is taken back into the presynaptic neuron for recycling. In some cells, empty vesicles are returned to the cell body. 7. Some postsynaptic cells send negative feedback messages to slow further release of the transmitter by the presynaptic cells C. Chemicals that are released by one neuron at the synapse and affect another neuron are neurotransmitters. D. Types of neurotransmitters include: 1. Amino acids: Acids containing an amine group (NH2). 2. Neuropeptides: Chains of amino acids. A long chain is called a polypeptide; a still longer chain is a protein. 3. Acetylcholine: A chemical similar to an amino acid, with the NH2 group replaced by an N(CH3)3 group. 4. Monoamines: Neurotransmitters containing an amine group (NH2) formed by a metabolic change of an amino acid. 5. Purines: Adenosine and several of its derivatives. 6. Gases: Includes nitric oxide (NO) and possibly others. E. Synthesis of neurotransmitters: Neurons synthesize neurotransmitters from precursors derived originally from food. 1. Catecholamines (dopamine, epinephrine, and norepinephrine): Three closely related compounds containing a catechol and an amine group. 2. Choline is the precusor for acetylcholine. Choline is obtained from certain foods. 3. The amino acids phenylalanine and tyrosine are precursors for the catecholamines. 4. The amino acid tryptophan is the precursor for serotonin. The amount of tryptophan in the diet controls the levels of serotonin. F. Transport and Storage of Neurotransmitters 1. Certain neurotransmitters, such as acetylcholine, are synthesized in the presynaptic terminal. However, larger neurotransmitters, the neuropeptides, are synthesized in the cell body and transported down the axon to the terminal. 2. Transporting neurotransmitters from the cell body to the axon terminal can take hours or days in long axons. 3. Neurotransmitters are stored in vesicles (tiny nearly spherical packets) in the presynaptic terminal. (Nitric oxide is an exception to this rule, as neurons do not store nitric oxide for future use.) There are also substantial amounts of neurotransmitter outside the vesicles. G. Release and Diffusion of Transmitters29 Chapter 3
  3. 3. 1. When an action potential reaches the axon terminal, the depolarization causes voltage-dependent calcium gates to open. As calcium flows into the terminal, the neuron releases neurotransmitter into the synaptic cleft within 1-2 milliseconds. This process of neurotransmitter release is called exocytosis. 2. After being released by the presynaptic neuron, the neurotransmitter diffuses across the synaptic cleft to the postsynaptic membrane, where it will attach to receptors. 3. The brain uses dozens of neurotransmitters, but no single neuron releases them all. 4. Most neurons release a combination of neurotransmitters and neuropeptides. 5. A neuron may receive and respond to many neurotransmitters at different synapses.H. Activation of Receptors of the Postsynaptic Cell 1. A neurotransmitter can have two types of effects when it attaches to the active site of the receptor: ionotropic or metabotropic effects. 2. Ionotropic effects: The neurotransmitter attaches to the receptor, causing the immediate opening of an ion gate (e.g., glutamate opens Na+ gates). 3. Metabotropic effects: The neurotransmitter attaches to a receptor and initiates a cascade of metabolic reactions. This process is slower and longer lasting than ionotropic effects. Specifically, when the neurotransmitter attaches to the receptor it alters the configuration of the rest of the receptor protein; enabling a portion of the protein inside the neuron to react with other molecules. Activation of the receptor by the neurotransmitter leads to activation of G-proteins which are attached to the receptor. a. G-proteins: A protein coupled to the energy-storing molecule guanosine triphosphate (GTP). b. Second messenger: Chemicals that carry a message to different areas within a postsynaptic cell; the activation of a G-protein inside a cell increases the amount of the second messenger. 4. Neuromodulators: Neurotransmitters, mainly the neuropeptides, that do not by themselves strongly excite or inhibit a neuron; instead, they alter (modulate) the effects of a neurotransmitter. They are released from the neuron, often from the cell body or dendrites, following repeated stimulation.I. Hormones 1. A hormone is a chemical that is secreted primarily by glands but also by other cells and is conveyed by blood to other organs whose activity it influences. 2. Unlike neurotransmitters, which are released directly to another neuron, hormones convey messages to any organ that can receive them. 3. Endocrine glands produce hormones. 4. Protein hormones and peptide hormones are composed of chains of amino acids. Protein and peptide hormones bind to membrane receptors and activate a second messenger within the cell—exactly the same process as at a metabotropic synapse. Some chemicals can act as both neurotransmitters and hormones, such as epinephrine, norepinephrine, insulin, and oxytocin. 5. Hormones secreted by the brain control the secretion of other hormones. 6. The pituitary gland is attached to the hypothalamus and consists of two distinct glands, the anterior pituitary and the posterior pituitary. 7. The posterior pituitary is composed of neural tissue like the hypothalamus. Two hormones, oxytocin and vasopressin (also known as antidiuretic hormone), are Synapses 30
  4. 4. released from the posterior pituitary. However both of these hormones are synthesized in the hypothalamus. 8. The anterior pituitary is composed of glandular tissue and synthesizes and releases six hormones. The hypothalamus controls the release of these six hormones by secreting releasing hormones that stimulate or inhibit the release of the following hormones: adrenocorticotropic hormone, thyroid-stimulating hormone, prolactin, somatotropin (also known as growth hormone), follicle-stimulating hormone, luteinizing hormone. J. Inactivation and Reuptake of Neurotransmitters 1. Neurotransmitters become inactive shortly after binding to postsynaptic receptors. Neurotransmitters are inactivated in different ways. 2. Acetylcholinesterase (AChE): Found in acetylcholine (ACh) synapses; AChE quickly breaks down Ach after it releases from the postsynaptic receptor. 3. Myasthenia gravis: Motor disorder caused by a deficit of acetylcholine transmission. This disease is treated with drugs which block AChE activity. 4. After separation from postsynaptic receptor, serotonin and the catecholamines are taken up by the presynaptic neuron. This process is called reuptake; it occurs through specialized proteins called transporters. 5. Some serotonin and catecholamine molecules are converted into inactive chemicals by enzymes such as COMT (converts catecholamines) and MAO (converts both catecholamines and serotonin). 6. Neuropeptides diffuse away from the synapse. K. Negative Feedback From the Postsynaptic Cell 1. Autoreceptors: presynaptic receptors sensitive to the same neurotransmitter they release. Autoreceptors detect the amount of transmitter released and inhibit further synthesis and release after it reaches a certain level. 2. Postsynaptic neurons can respond to stimulation by releasing special chemicals that travel back to the presynaptic terminal, where they inhibit further release of transmitter. Nitric oxide, anandamide, and 2-AG (sn-2 arachidoylglycerol) are three such chemicals.III.Synapses, Drugs, and Addictions A. Types of Mechanisms 1. Drugs can affect synapses by either blocking the effects (an antagonist) or mimicking (increasing) the effects (an agonist) of a neurotransmitter. A drug that is a mixed agonist-antagonist is an agonist for some behavioral effects or doses and an antagonist for others. 2. Drugs can influence synaptic activity in many ways, including altering synthesis of the neurotransmitter, disrupting the vesicles, increasing release, decreasing reuptake, blocking its breakdown into inactive chemicals, or directly simulating or blocking postsynaptic receptors. 3. Affinity: How strongly the drug attaches to the receptor. 4. Efficacy: The tendency of the drug to activate a receptor. B. What Abused Drugs Have in Common31 Chapter 3
  5. 5. Olds and Milner (1954) conducted the first brain-reinforcement experiments by implanting electrodes in the brains of rats and allowing them to press a lever to produce self-stimulation of the brain. b. Later experiments showed that the reinforcing brain stimulation almost exclusively activated tracts of axons that release dopamine, especially in an area called the nucleus accumbens. Many other reinforcing experiences will lead to increased DA activity including sexual excitement, gambling, and video games. c. Because of its role in reinforcement, the nucleus accumbens is regarded by many as the pleasure area and dopamine as the pleasure chemical. However, several lines of evidence conflict with this interpretation and more recent studies suggest that dopamine and the nucleus accumbens play an important role in attention- getting or craving.C. A Survey of Abused Drugs 1. Stimulant drugs (e.g., amphetamines, cocaine) produce excitement, alertness, elevated mood, decreased fatigue, and sometimes motor activity. Each of these drugs increases activity at dopamine receptors. Stimulant drugs are often highly addictive. a. Amphetamine increases dopamine release from presynaptic terminals by reversing the direction of the dopamine transporter. b. Cocaine blocks the reuptake of catecholamines and serotonin at the synapse. The behavioral effects of cocaine are believed to be mediated primarily by dopamine and secondarily by serotonin. c. The effects of amphetamine and cocaine are both short-lived, because of the depletion of dopamine stores and tolerance. d. Prolonged use of cocaine can cause long-term changes in brain metabolism and blood flow, increasing the risk of stroke, epilepsy, and memory impairments. e. Methylphenidate (Ritalin): Stimulant currently prescribed for attention-deficit disorder (ADD); works like cocaine by blocking reuptake of dopamine at presynaptic terminals. The effects of methylphenidate are much longer lasting and less intense as compared to cocaine. f. Methylenedioxymethamphetamine (MDMA, or “ecstasy”) is a stimulant that at low doses primarily increases the levels of dopamine; however, at higher doses it also releases serotonin and produces hallucinogenic effects. g. MDMA damages serotonin axons in laboratory animals by increasing body temperature and the production of hydrogen peroxide. 2. Nicotine: Compound found in tobacco. Stimulates the nicotinic receptor (a type of acetylcholine receptor) in both the central nervous system and neuromuscular junction of skeletal muscles; can also increase dopamine release by attaching to neurons that release dopamine in the nucleus accumbens. Repeated use of nicotine leads to decreased sensitivity in nucleus accumbens cells responsible for reinforcement. 3. Opiate Drugs: Derived from (or similar to those derived from) the opium poppy. Common opiates include morphine, heroin, and methadone. Opiates have a net effect of increasing the release of dopamine by stimulating endorphin receptors. 4. Marijuana: Contains the chemical Δ9-tetrahydrocannabionol (Δ9-THC) and other cannabinoids (chemicals related to Δ9-THC); Δ9-THC works by attaching to Synapses 32
  6. 6. cannabinoid receptors. Anandamide and sn-2 arachidonylglycerol (2-AG) are brain chemicals that bind to cannabinoid receptors. Marijuana can be used medically to relieve pain or nausea, combat glaucoma (eye disorder), and increase appetite. Common psychological effects of marijuana include intensification of sensory experience and the illusion that time is passing very slowly. Prolonged marijuana use is associated with impaired memory performance. 5. Hallucinogenic drugs: Drugs that distort perception. Many hallucinogenic drugs like lysergic acid diethylamide (LSD) resemble serotonin and bind to serotonin type 2A (5-HT2A) receptors. D. Alcohol and Alcoholism 1. Alcoholism or alcohol dependence: The continued use of alcohol despite medical or social harm, even after people have decided to quit or decrease their drinking. 2. Alcohol: Facilitates transmission at the GABAA receptor, blocks glutamate receptors, and increases dopamine and opiate activity. 3. Genetics a. Researchers distinguish two major types of alcoholism: b. Type I (or Type A) Alcoholism: This type of alcoholism is less dependent on genetic factors, develops gradually over years, affects men and women equally, and is generally less severe. c. Type II (or Type B) Alcoholism: This type of alcoholism has a strong genetic basis, a rapid and early onset, affects men primarily, is more severe, and is more associated with criminality. 4. Risk Factors a. Less than average intoxication after drinking a small to moderate amount of alcohol. b. Experiencing more than average relief from stress after drinking alcohol. c. Having a smaller than normal amygdala in the right hemisphere. E. Addiction 1. Continued use of a substance despite harm to health, wealth, or relationships 2. Seeking pleasure and avoiding displeasure a. Tolerance: Decreased effect of a drug following repeated use. b. Pleasure associated with the drug decreases with time. c. Withdrawal from the drug has unpleasant side effects. d. Receiving the drug during withdrawal increases reinforcement. e. Drug use may continue as individuals seek pleasure or tries to avoid withdrawal symptoms. 3. Cravings in response to cues Stress or visual cues can induce cravings in abstinent former users. 4. Brain reorgnaization a. Addiction causes reorganization of nucleus accumbens b. Nucleus accumbens becomes more sensitive to the drug and less sensitive to natural reinforcers F. Medication to combat substance abuse 1. Medications to combat alcohol abuse33 Chapter 3
  7. 7. a. Acetaldehyde: A poisonous substance created when ethyl alcohol (drinking alcohol) is metabolized in the liver. Acetaldehyde is then further metabolized into acetic acid, a chemical the body can use as a source of energy. b. Acetaldehyde dehydrogenase is the enzyme used to convert acetaldehyde into acetic acid. c. Some people have an abnormal gene for acetaldehyde dehydrogenase so they metabolize alcohol slowly. Approximately 50% of people in China and Japan have the gene that slows acetaldehyde metabolism. d. Anatabuse (disulfiram): A drug that blocks the effects of the enzyme acetaldehyde dehydrogenase by binding to its copper ion. Anatabuse is used to treat alcoholism, because Antabuse causes the ingestion of alcohol to lead to sickness.2. Medications to Combat Opiate Abuse a. Heroin a synthetic compound designed as a “safer” alternative to morphine. b. Methadone is similar to heroin and morphine but can be taken in pill form. Methadone and two similar drugs (buprenorphine and levomethadyl acetate) are used to treat heroin addiction. While people taking these drugs are still addicted to an opiate, they live longer and healthier than people injecting heroin, and are far more likely to hold a job. Synapses 34
  8. 8. Learning Objectives Module 3.1: The Concept of the Synapse 1. Be able to describe Sherrington’s inferences concerning the speed of a reflex and temporal and spatial summation. 2. Understand the mechanisms underlying the excitatory and inhibitory postsynaptic potentials. 3. Understand how synaptic potentials contribute to the firing rates of neurons and the integration of information.Module 3.2: Chemical Events at the Synapse 1. Be able to describe the contributions of T.R. Elliott and O. Loewi to the question of whether most synaptic transmission is electrically or chemically mediated. 2. Be able to list the six major types of neurotransmitters. 3. Understand the role of diet in the synthesis of neurotransmitters. 4. Understand the processes of transport, release, and diffusion of neurotransmitters. 5. Understand the differences between ionotropic and metabotropic effects of neurotransmitters. 6. Be able to describe the similarities and differences between neurotransmitters and hormones. 7. Understand the difference in control mechanisms of the anterior and posterior pituitary and be able to list some of the hormones released from each. 8. Understand why inactivation of neurotransmitters is important and the two major ways this is achieved. Module 3.3: Synapses, Drugs and Addictions 1. Understand why our brains have receptors for plant chemicals. 2. Understand the difference between agonists, antagonists, and mixed agonist- antagonists. 3. Be able to explain the common mechanism of action of nearly all abused drugs. 4. Be able to explain the differences between the effects of amphetamine, cocaine, and methylphenidate. 5. Understand the different ways of increasing dopamine release in the nucleus accumbens used by nicotine, opiates, and marijuana. 6. Understand the relationship between dopamine in the nucleus accumbens and motivation (“wanting”) and why dopamine does not seem to be related directly to pleasure (“liking”). 7. Know the physiological effects of alcohol and the effects of Antabuse on alcohol metabolism. 8. Be able to describe the evidence for a genetic contribution to alcoholism. 9. Know why methadone can be used to treat addiction to heroin or morphine and why it does not end the addiction.35 Chapter 3
  9. 9. Key Termsacetaldehyde excitatory postsynaptic posterior pituitaryacetic acid potential (EPSP) postsynaptic neuronacetylcholine exocytosis presynaptic neuronacetylcholinesterase G-protein protein hormoneaffinity hallucinogenic drugs purines2-AG hormone reflexagonist inhibitory postsynaptic reflex arcalcoholism potential (IPSP) releasing hormoneamino acids ionotropic effect reuptakeamphetamine MAO second messengeranandamide metabotropic effect self-stimulation of the brainAntabuse methylphenidate spatial summationantagonist monoamines spontaneous firing rateanterior pituitary neuropeptide stimulant drugsautoreceptors neurotransmitter substance abusecannabinoids nicotine synapsecatecholamine nitric oxide temporal summationcocaine nucleus accumbens transporterCOMT opiate drugs Type I alcoholismΔ9-tetrahydrocannabinol oxytocin Type II alcoholism (Δ9-THC) peptide vasopressinefficacy peptide hormone vesicleendocrine glands pituitary gland Class Activities and Demonstrations from Selected Web Sites 1. What’s the Connection? This exercise was developed by Sharon Winter for the Neuroscience Laboratory and Classroom Activities Manual. In this exercise, students elicit and observe reflex responses (patellar and pupillary light reflex) and then conduct experiments to understand neural control of reflex responses. The full instruction for this exercise can be found at http://www.nabt.org/sites/S1/index.php?p=85. 2. Reaction Time and Neural Circuitry: This exercise is designed to demonstrate the concept of reaction time, the amount of time required for the nervous system to receive and integrate incoming sensory information and then cause the body to respond. This exercise was developed by Rebecca Sacra for the Neuroscience Laboratory and Classroom Activities Manual. The full instruction for this exercise can be found at http://www.nabt.org/ sites/S1/File/nlca/13NLCAchp11.pdf. 3. Neural Processing Activity: In this exercise students construct simple series and parallel electrical circuits to develop an understanding of how impulses in the nervous system are transmitted. Students will be able to compare series versus parallel circuitry and different ways in which nervous system functioning can be disrupted. This exercise was developed by Synapses 36
  10. 10. Peggy Walker for the Neuroscience Laboratory and Classroom Activities Manual. The full instruction for this exercise can be found at: http://www.nabt.org/sites/S1/index.php?p=85.4. Identification of an Unknown Drug Through Behavioral Testing: If you have access to small laboratory animals (i.e., rats or mice), this exercise will improve students’ understanding of the effects of abused drugs. In this exercise, students observe rodents after administration of an unknown drug and record behaviors such as activity level, grooming, exploratory behavior (nose poke, maze exploration), and pain sensitivity. After observing the subjects and researching the behavioral effect of certain drugs, students then try to identify the type of drug the animal was given (stimulant, depressant, or narcotic analgesic). The full instructions and a discussion of this exercise are available at the following source. Schumacher, S. J. (1982). An alternative to the traditional physiological psychology laboratory: identification of an unknown drug through behavioral testing. Teaching of Psychology, 9, 239-241.5. Effects of Various Illicit Drugs: An entertaining overview of the effects of various drugs on the brain is given at http://learn.genetics.utah.edu/units/addiction/drugs/mouse.cfm. Students can learn more about the mechanism of action of the drugs and where in the nervous system they work.6. Survey on Drug Use/Abuse Patterns: Many students believe that drug use and abuse have declined dramatically over the years, regardless of the drug type or classification (e.g., licit vs. illicit, hallucinogens vs. stimulants, etc.). There are several standard questionnaires that are used clinically to determine alcohol abuse or substance abuse. Two of these are reproduced at the end of Chapter 3 of this Instructor Resource Manual. The Substance Abuse Questionnaire was developed by Dr. George F. Koob of the University of California, San Diego, Department of Psychology. One way to foster discussion on this topic is to ask students to complete the surveys before discussing Chapter 3. Dr. Koob has compiled the survey results from his Drugs, Addiction, and Mental Disorder classes for more than a decade and shares indications of certain trends in drug use with his students each year. A good follow-up assignment would allow students to research articles addressing the prevalence of drug use among certain populations (e.g. 18-24 year old male vs. female smoking rates, etc.). Have students determine if the survey results match what the scientific literature concludes regarding drug use in the U.S.?Suggested Other Multimedia ResourcesVIDEOS1. “Bubble, Bubble, Toil, and Trouble” (Film for the Humanities and Sciences, 58 min): This video discusses how neurons are connected into precise circuits that enable us to sense the outside world. The video covers both simple and complex neuronal circuitry and discusses how communication between neurons can be modified by drugs.2. “The Brain” (Film for the Humanities and Sciences, 23 min): The role of chemical neurotransmitters in neuronal communication is highlighted in this video. The film also37 Chapter 3
  11. 11. covers what dreams tell us about brain functioning and how new technologies are being used to study the brain.3. The Hijacked Brain (Films for the Humanities and Sciences, 57 min): An examination of research into the chemistry of addiction and its possible genetic components. This film is not specific for alcoholism, but most of the genetic studies deal specifically with alcoholism.4. Under the Influence: The Science of Drug Abuse (Insight Media, 25 min): Overview of the effects of drugs on the brain. It has some neat pictures of brain scans from people on different types of drugs.5. There are many excellent video clips and animations available from the Psychology Resource Center, available at the Cengage website. In particular, consider the “Drugs and Alcohol” section under the heading “Consciousness and Synaptic Transmission” in the “Biology and the Brain” section, under “Neurons and the Nervous System.”CD-ROM1. “Explorations in Human Anatomy and Physiology” (George B. Johnson; Denoyer Geppert International): This CD-ROM contains interactive segments on action potentials, synaptic transmission, and the neurophysiology of drug addiction.Related Web Siteshttp://faculty.washington.edu/chudler/introb.html#bb This is one of the best resources for teaching basic biological psychology on the web. The site was designed by Dr. Eric Chudler at the University of Washington. He does a good job of making synaptic transmission seem easy.http://www.williams.edu/imput/ Multimedia Neuroscience Education Project, Dr. Betty Zimmerberg (project organizer). Great overview with very nice animation of synaptic transmission.http://themedicalbiochemistrypage.org/nerves.html This is very detailed overview of the process of synaptic transmission and of the neurotransmitters. The site was designed by Dr. Michael W. King at the University of Indiana Medical School.http://www.flyfishingdevon.co.uk/salmon/index.htm#Neurotransmitters_and_Neurotransmission Synapses 38
  12. 12. This is an excellent source of information on synaptic transmission. It is clearly written and has lots of color and animation. I think most students would find it very interesting. The site was designed by Dr. Paul Kenyon at the University of Plymouth.http://www.nida.nih.gov/DrugAbuse.html The web page for the National Institute of Drug Abuse (NIDA). This is the best place to get the latest information on most common drugs of abuse.http://www.niaaa.nih.gov/ The home page of the National Institute for Alcohol Abuse and Alcoholism. You can find anything you want to know about alcoholism on this site.InfoTrac Virtual Reader Exercises1. Nerve Gas: Nerve gases work by interfering with acetylcholine inactivation in the synaptic cleft. Although these gases have been around since WWII, information about their long-term effects is still scarce. Recent incidents of bioterrorism have increased our awareness of the deadliness of these compounds. Article 1 http://infotrac-college.thomsonlearning.com/itw/infomark/402/417/665125w16/purl= rc1_WAD_0_A108646496&dyn=38!xrn_55_0_A108646496?sw_aep=olr_wad Nerve agent attacks on children: diagnosis and management. Authors: Joshua S. Rotenberg, Jonathan Newmark. Journal: Pediatrics Publication Date: Sept 2003 Volume: 112 Page Number: 648 Number of Pages: 11 Article 2 http://infotrac-college.thomsonlearning.com/itw/infomark/402/417/665125w16/purl= rc1_WAD_0_A83476590&dyn=45!xrn_32_0_A83476590?sw_aep=olr_wad Chemical weapons. Authors: D. Evison, D. Hinsley, and P. Rice. Journal: British Medical Journal Publication Date: Feb. 9, 2002 Volume: 324 Page Number: 332 Number of Pages: 4 Article 3 http://infotrac-college.thomsonlearning.com/itw/infomark/673/707/110282897w3/purl= rc1_WAD_0_A141438773&dyn=79!bmk_3_0_A141438773?sw_aep=olr_wad Long-term effects of sarin. Author: David Sharp. Journal: The Lancet Publication Date: Jan 14, 2006 Volume: 367 Page Number: 95 Number of Pages: 3 Essay Questions39 Chapter 3
  13. 13. 1. Describe how exposure to nerve-gas agents can lead to death. Would nerve gases still be deadly if their actions were limited to muscarinic synapses? 2. Why would acetylcholine agonists not be as effective as AChE inhibitors in chemical warfare?2. Pituitary Dysfunction: The pituitary gland releases hormones that direct activity in a number of organs. These hormones affect numerous physiological and behavioral functions such as sexual behavior, physical growth, activity levels, thirst, etc. Unsurprisingly, when the pituitary is damaged a number of physiological disorders can result. Article 1 http://infotrac-college.thomsonlearning.com/itw/infomark/673/707/110282897w3/purl= rc1_WAD_0_A54618839&dyn=98!bmk_1_0_A54618839?sw_aep=olr_wad Growth-hormone and prolactin excess. Authors: Gaetano Lombardi, Annamaria Colao. Journal: The Lancet Publication Date: Oct 31, 1998 Page Number: 1455 Number of Pages:1 Article 2 http://infotrac-college.thomsonlearning.com/itw/infomark/402/417/665125w16/purl= rc2_WAD_1_depression+thyroid&dyn=sig!17?sw_aep=olr_wad Thyroid dysfunction and affective illness; check the hypothalamic-pituitary-thyroid axis in patients resistant to treatment. Author: E. Szabadi. Journal: British Medical Journal Publication Date: April 20, 1991 Volume: 302 Page Number: 923 Number of Pages: 2 Article 3 http://infotrac-college.thomsonlearning.com/itw/infomark/402/417/665125w16/purl= rc1_WAD_0_A160590205&dyn=72!bmk_3_0_A160590205?sw_aep=olr_wad Stress predicts brain changes in children: a pilot longitudinal study on youth stress, posttraumatic stress disorder, and the hippocampus. Authors: V.G. Carrion, C.F. Weems and A.L. Reiss. Journal: Pediatrics Publication Date: March 2007 Volume: 119 Page Number: 509 Number of Pages: 8 Essay Questions 1. What is the difference between gigantism and acromegaly? 2. Discuss the relationship between HPA function and mood and anxiety disorders.Critical Thinking ExercisesElectrical Synaptic Transmission Synapses 40
  14. 14. Reflect on how synaptic communication would differ if electrical rather than chemical transmission was used. In particular, have students decide if phenomena like temporal and spatial summation would be possible, and if we would still have EPSPs and IPSPs.Tryptophan Tryptophan is the amino acid precursor to the neurotransmitter serotonin. It is also an essential amino acid, which means that our bodies are not capable of making this compound. Decide what effects a no-tryptophan diet would have on neurotransmission.Bliss Pretend a new chemical named Bliss has been found in the central nervous system. Moreover, protein receptors have also been located that interact with this chemical. Is this chemical a neurotransmitter? Describe what additional evidence would be necessary before Bliss could be declared a neurotransmitter.Substance Abuse Substance abuse remains a significant challenge to our society, despite our increasing understanding of the brain basis of addiction and the development of pharmaceuticals to combat substance abuse, such as antabuse and methadone. However, these medications have had limited success in reducing addiction. Why might this be?Inactivation of Neurotransmitters All neurotransmitters are inactivated after they are released. What would happen if this inactivation was prevented from occurring? How would the function of the nervous system change?What about Nicotine? Have students research the addictive properties and the health consequences of using nicotine. Then have them debate whether it is appropriate for nicotine to be legal.Open-Ended Discussion Questions1. Why are spatial and temporal summation important in the nervous system?2. In the nervous system there are both electrical synapses, which pass on electrical signals quickly and directly between cells, and chemical synapses, which use a chemical message. What are the advantages and disadvantages of each?3. How do postsynaptic potentials differ from action potentials?4. What determines if a neuron will generate an action potential?5. How could your diet influence your behavior?6. What effects can a neurotransmitter have on the recipient cell?7. What commonalities exist between all addictive drugs in terms of their effects on the brain?8. Should drugs that improve cognitive functions such as attention be available to everyone or only to people with significantly impaired function, such as attention deficit hyperactivity disorder (ADHD)?41 Chapter 3
  15. 15. Author’s Answers to Thought QuestionsModule 3.11. When Sherrington measured the reaction time of a reflex (i.e., the delay between stimulus andresponse), he found that the response occurred faster after a strong stimulus than after a weakone. Can you explain this finding? Remember that all action potentials—whether produced bystrong or weak stimuli—travel at the same speed along a given axon. Author’s Answer: A strong stimulus induces a greater frequency of action potentials in the sensory axon. Through the process of temporal summation, the next neuron in the sequence can reach its threshold faster if it is stimulated by an increased frequency of synaptic excitation. That is, the reflex is faster with a strong stimulus because of decreased delay of reaching the threshold in the postsynaptic neuron.2. A pinch on an animal’s right hind foot excites a sensory neuron that excites an interneuronthat excites the motor neurons to the flexor muscles of that leg. The interneuron also inhibits themotor neurons connected to the extensor muscles of the leg. In addition, this interneuron sendsimpulses that reach the motor neuron connected to the extensor muscles of the left hind leg.Would you expect the interneuron to excite or inhibit that motor neuron? (Hint: The connectionsare adaptive. When an animal lifts one leg, it must put additional weight on the other legs tomaintain balance.) Author’s Answer: The interneuron excites the extensor muscles of the left hind leg. When the animal flexes one hind leg, it extends the other hind leg.3. Suppose neuron X has a synapse onto neuron Y, which has a synapse onto Z. Presume that noother neurons or synapses are present. An experimenter finds that stimulating neuron X causesan action potential in neuron Z after a short delay. However, she determines that the synapse ofX onto Y is inhibitory. Explain how the stimulation of X might produce excitation of Z. Author’s Answer: If the synapse of Y onto Z is also inhibitory, and if neurons Y and Z have spontaneous firing rates, then the excitation of X would inhibit Y and thereby decrease Y’s inhibition of Z. The net effect is an increased frequency of action potentials in Z. This sort of inhibition of inhibition is common in the nervous system; thus, there is no consistent relationship between the excitation or inhibition of a synapse and the excitation or inhibition of behavior. Norepinephrine and dopamine are generally inhibitory at their synapses, but drugs that stimulate norepinephrine or dopamine (e.g. amphetamine, cocaine) tend to excite behavioral activity.Module 3.21. Suppose that axon A enters a ganglion (a cluster of neurons) and axon B leaves on the otherside. An experimenter who stimulates A can shortly thereafter record an impulse traveling downB. We want to know whether B is just an extension of axon A or whether A formed an excitatorysynapse on some neuron in the ganglion, whose axon is axon B. How could an experimenterdetermine the answer? You should be able to think of more than one good method. Presume thatthe anatomy within the ganglion is so complex that you cannot simply trace the course of anaxon through it. Synapses 42
  16. 16. Author’s Answer: Many possibilities exist. First, the better methods: (a) Time the transmission of an impulse from a point on A to a point on B and then compare that velocity to the velocity of transmission along A alone or B alone. If the velocity from A to B is slower than the velocity along either axon alone, then there is a synapse between A and B; they are axons of different neurons. If the velocity is the same, then B is an extension of A. (b) Compare axons A and B. If they differ in diameter or in velocity of action potentials, they must be different axons. If they are equal in diameter and velocity, we can draw no conclusion. B might be an extension of A, or the two might be different axons that coincidentally have the same diameter and velocity. (c) Use antidromic conduction, a concept introduced in a previous thought question. Stimulate B and record from A. If stimulation of B produces an antidromic impulse in A, then A and B are almost certainly the same axon. This procedure fails if A is constantly firing action potentials, which would block transmission of an antidromic impulse. (d) Cut either axon A or axon B. If the other one degenerates, the two must be parts of the same axon. If cutting one does not harm the other, they must be separate axons. (e) Inject a dye into A or B and see whether it spreads to the other. If it does, they are probably the same axon, although a few dyes do cross synapses. If the dye spreads through the injected axon but does not invade the other one, then A and B are separate axons. (f) Stimulate A at a high rate and record from both A and B. Synapses fatigue faster than axons, so if A and B are separate, B should stop responding before A does. (g) Inject into the ganglion large amounts of magnesium to prevent calcium from entering the presynaptic terminals. That procedure should block synaptic transmission. If A stops firing B, they are separate axons. Less satisfactory answers: (a) Stimulate other axons entering the ganglion and see whether any of them excites B. If an experimenter finds such an axon, one could conclude that A and B are connected by a synapse. However, failure to find additional axons that stimulate B would not lead to any conclusion. (b) Inject chemicals into the ganglion that facilitate or block various neurotransmitters and see whether they block the effect of A on B. If some chemical does block the transmission to B, then we would not only know that an A-to-B synapse exists, but we would also be able to infer which transmitter it uses. However, if all the chemicals we try have no effect, we could not draw a conclusion. Axon A might release some other transmitter that is not blocked by the chemicals the experimenter tried. (c) “Look for evidence of temporal summation.” This is an inappropriate answer, because the question postulated that a single impulse in A is enough to excite B.2. Transmission of visual and auditory information relies largely on ionotropic synapses. Why isionotropic better than metabotropic for these purposes? For what purposes might metabotropicsynapses be better? Author’s Answer: It is important to detect rapid changes in what we see and hear, and ionotropic synapses produce quick, brief responses. Metabotropic synapses would be better for processes with slow onset and offset, such as hunger, thirst, anger.43 Chapter 3
  17. 17. Module 3.31. People who take methylphenidate (Ritalin) for control of attention-deficit disorder often reportthat, although the drug increases their arousal for a while, they feel a decrease in alertness andarousal a few hours later. Explain. Author’s Answer: A dose of amphetamine or cocaine causes increased alertness and arousal because of increased net release of dopamine. Later the individual has withdrawal symptoms because the neurons have released dopamine faster than they can resynthesize it, so dopamine availability has declined. Methylphenidate operates by the same principle, only slower and less drastically. It too increases net release of dopamine (by blocking reuptake), and produces a later decrease in dopamine availability because the neurons have not yet resynthesized as much dopamine as they have released.2. The research on sensitization of the nucleus accumbens has dealt with addictive drugs, mainlycocaine. Would you expect a gambling addiction to have similar effects? How could someonetest this possibility? Author’s Answer: We could use fMRI or other brain scan devices to detect the amount of arousal in the nucleus accumbens in response to gambling and to other experiences, such as food or listening to music. Compare the responses by gamblers and nongamblers. The prediction would be that gamblers would show a greater nucleus accumbens response to gambling and a weaker response to other events. Synapses 44
  18. 18. Substance Abuse Questionnaire A. Do not write your name on the questionnaire (responses are anonymous). B. Please circle the most correct response. C. State both medical and recreational experiences. ________________________________________________________________________ Age: ________________ Sex: M F 1. Do you smoke cigarettes (tobacco)? No Yes 2. Do you smoke other tobacco products (cigar, pipe, clove)? No Yes 3. Do you chew or snuff tobacco? No Yes 4. Have you ever consumed marijuana or hashish? No Yes 5. Have you consumed marijuana/hashish within the last 30 days? No Yes 6. Have you ever tried amphetamines (speed, crystal)? No Yes 7. Have you consumed amphetamines within the last 30 days? No Yes 8. Have you ever tried cocaine? No Yes 9. Have you ever tried crack cocaine (smoked freebase)? No Yes 10. Have you consumed cocaine within the last 30 days? No Yes 11. Have you ever tried: LSD (acid)? No Yes Heroin? No Yes Morphine? No Yes Barbiturates (e.g., Luminal, Nembutal, etc.) No Yes PCP (angel dust)? No Yes Darvon (propoxyphene)? No Yes Hallucinogenic mushrooms? No Yes Ecstasy (MDMA)? No Yes Inhalants (e.g., nitrous oxide, etc.) No Yes 12. Do you drink: alcoholic beverages? No Yes Some beer each week? No Yes Some wine each week? No Yes Some mixed drinks each week? No Yes 13. Within the last 30 days have you used: Prescription sleeping pills? No Yes Over-the-counter pain relievers? No Yes Minor tranquilizers (e.g., Xanax, etc.)? No Yes Diet pills? No Yes 14. Do you think you have a problem with substance abuse? No Yes If yes, which substance(s)?_______________________________________45 Chapter 3
  19. 19. CAGE QuestionsThe CAGE questions are a quick clinical survey of alcohol use. Each “Yes” answer is onepoint and a score of two or more may indicate alcohol dependence.1. Have you ever felt you should cut down on your drinking? No Yes2. Have people annoyed you by criticizing your drinking? No Yes3. Have you ever felt bad or guilty about your drinking? No Yes4. Have you ever had a drink first thing in the morning to steady No Yes your nerves or get rid of a hangover (eye-opener)? Synapses 46

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