PG 683 Study Guide

Winter, 1999

General Issues

  1. Describe and give examples of the two different forms of reductionism discussed in Marr's paper. Reducing "voluntary" behavior to the three-term contingency would be an example of ________ reduction, while reducing it to the activity of dopamine in the ventral tegmental area would be an example of _______ reduction.
  2. Describe some different approaches to understanding a brain-behavior phenomenon (e.g., developmental, anatomical, behavioral, evolutionary, functional, physiological).
  3. Briefly describe the problem that dualism and monism have attempted to solve, and the different approaches to the solution taken by dualism and two forms of monism. What is distinctive about the radical behaviorist approach to this problem?
  4. List all the phenomena that we have discussed so far whose understanding has not involved the use of nonhuman species.
  5. Describe the split-brain operation and its functional consequences.
  6. Describe the doctrine of specific nerve energies.
  7. Be able to discuss Darwin, natural selection, and, especially, selective advantage in a nonteleological way.
  8. Compare and contrast (define each, identify at least one important similarity and one important difference)
    1. Wernicke's area and Broca's area.
    2. Descartes and Galvani.

Cells of the Nervous System.

  1. Be able to identify the important parts of a neuron on a sketch, spell them, and describe in a sentence their role. Be able to go from the name to the definition or from the definition to the name (as in "fill-in-the-blank").
  2. Be able to draw a representative unipolar, bipolar, and multipolar neuron and show the important parts.
  3. Distinguish between axons and dendrites.
  4. What is an enzyme? Name two that we have discussed in class. What happens if an enzyme is not present? Where do they come from?
  5. Describe glia cells and give examples. Don't forget radial glia.
  6. Be able to spell oligodendrocyte and Schwann. Know how to define them, distinguish between them, and fill-in-the-blank.
  7. What is the blood-brain barrier? How was it discovered? What passes through it and what does not? Describe the characteristics of the class(es) of molecules that pass through the blood-brain barrier. Where is the blood-brain barrier weak?
  8. Define, spell, understand, and give examples of the various combination of hydro/lipo/philic/phobic.
  9. What is the "neural doctrine?" When and how did it arise and who is responsible for it?
  10. Simple electricity.
    1. The measure of electrical potential is:
    2. The measure of the flow of electrical charge is:
    3. The measure of the facility of the flow of charge is:
    4. An _____ is used track changes in ______ across a neural membrane in time.
  11. Compare and contrast:
    1. Voltage and current.
    2. Conductance and resistance.
  12. Positively charged ions are called _____ while negatively charged ions are ______
  13. Describe the separation of charge across the neural membrane. Be specific about which ions are present and the forces acting on them.
  14. Sketch the lipid bilayer. Why does the lipid bilayer organize itself as it does? Show how ion channels are positioned in this layer.
  15. Compare and contrast voltage-gated and chemically gated ion channels. Give examples.
  16. Draw an action potential. Identify the specific portions of it and the membrane events responsible for these different portions. Be able to do this in several directions, i.e., be able to discuss, fill-in-the-blank, identify drawings, and define.
  17. What good is a sodium-potassium transporter (pump)?
  18. What is tetrodotoxin, where is it found and what does it do to manly sushi eaters? Spell it.
  19. Be able to say in a sentence why an action potential does not reverse course and travel backward.
  20. Where does an action potential begin under normal, physiological conditions?
  21. Be able to define saltatory conduction, the role of myelin, the rate law, and the different forms of neural integration, presynaptic and postsynaptic potentials, EPSPs and IPSPs. Be able to state what events on an ionic channel could produce EPSPs and IPSPs.
  22. The following is a form of the Nernst equation for potassium Ek = {(R*T)/(2.3*Z*F) } * log10 ([Ko]/[Ki]). Answer the following questions, where Ek is the Nernst potential for potassium
    1. What would happen to Ek if there is a fever?
    2. What would happen to Ek if the extracellular potassium increases?
    3. What would be the value of Z be for Potassium? Chloride? Calcium?
    4. What is the Nernst potential for Sodium, Chloride, and Potassium?
  23. Distinguish among neurotransmitters, neuromodulators, and odorants. What is the common element across all of them?
  24. Describe and spell the stages of neurotransmission from synthesis through termination. Be able to do this in several ways so you can answer fill-in-the-blank, discussion, draw-picture, and definition type questions.
  25. Note: Page 44, right column, 4th sentence should say ". . . just inside the pre-synaptic . . ."
  26. Compare and contrast an ionotropic and a metabotropic receptor. What is a second messenger?
  27. Be able to describe the:
    1. role of Na+ and K+ channels.
    2. postsynaptic effects of presynaptic action potentials.
    3. role of calcium
    4. quantal nature of neurotransmitter release
  28. Distinguish among post-synaptic, presynaptic, and autoreceptors.
  29. Compare and contrast competitive and noncompetitive binding.
  30. Compare and contrast the non-NMDA and the NMDA, ionotropic glutamate receptor.
  31. Be able to distinguish among the different kinds of signals in table 13-1. Be able to describe how the information in that table was learned
  32. Distinguish among receptor, synaptic, and graded potentials in amplitude, duration, summation, propagation, effect of signal and type of propagation.


  1. Be able to identify on a figure the items in figure 3.9, 3.11, 3.12, 3.18. Be able to state what general functions are associated with those regions.
  2. Know Table 3.2 and Fig. 3.8.
  3. Be able to identify rostral, caudal, dorsal, ventral, anterior, posterior, sagittal, horizontal, and coronal.
  4. Locate the middle cerebral artery, the basilar artery, the four ventricles.
  5. Be able to distinguish between the sympathetic and parasympathetic nervous systems in several contexts. For example, be able to fill in a table, predict drug actions, and distinguish them functionally, chemically (i.e., neurotransmitters) and structurally.
  6. Distinguish the dorsal and ventral roots.
  7. You need not memorize the cranial nerves (but feel free to if you wish!).
  8. What is a dermatome?
  9. What is meant by "migration?"
  10. How do neurons find each other?

  1. Psychopharmacology Part A.
  2. Describe the different routes by which drugs are administered. Give the advantages and disadvantages of each.
  3. Describe the distribution of drugs after administration. Include a discussion of the role of lipophilicity.
  4. Define affinity.
  5. Be able to draw dose-effect curves, with appropriately labeled axes, showing a) two drugs with the same maximal response but different potencies, b) competitive antagonism, and c) a drug with less intrinsic activity.
  6. Be able to draw dose response curves showing ED50's, LD50's, ED01. Define margin of safety.
  7. Know the different stages of new drug development including discovery, preclinical pharmacology and evaluation, the different phases of clinical trials and post-market surveillance.
  8. Spell the amines. The monoamines.
  9. Spell indolamine and give a representative example.
  10. Name the monoamines and the two amino acids that are precursors.
  11. Spell acetylcholine and acetylcholinesterase. Name the two subclasses of ACh receptors that we have discussed and the actions of agonists and antagonists on them. Name one agonist and one antagonist for each class of receptor.
  12. Name the four compounds described in the biosynthesis of norepinephrine.
  13. Where are dopamine cell bodies primarily located? Where do they go to? (Fig. 4.14)
  14. Name two inhibitory and two excitatory amino acids.
  15. Name two neuropeptides.
  16. What is adenosine?
  17. Describe the GABA/Chloride ionophore. What happens to the membrane when this opens? What does this do to neural activity? Be able to describe the drugs that act on this and how they act.


  1. Be able to describe, compare, and contrast the following terms:
  2. Magnetic Resonance Imaging
  3. positron emission tomography
  4. computed axial tomography.
  5. Define stereotaxis.
  6. Compare and contrast
  7. anterograde and retrograde labeling techniques.
  8. microelectrode and macroelectrode.
  9. Define:
    1. electroencephalogram.
    2. autoradiogram.
    3. electrical brain stimulation.
    4. microdialysis
    5. microiontophoresis

Vision and Sensory Function

  1. Describe the physical measurement of light.
  2. Be able to define a receptive field, its properties, how it is detected and characterized.
  3. Relate receptive fields to
    1. two-point thresholds
    2. cortical maps, and the amount of cortical space devoted to a map.
  4. Describe lateral inhibition
  5. Describe how a center-surround receptive field might arise. Be sure to state what a center-surround receptive field is.
  6. Describe a tuning curve.
  7. If a tree falls in the forest and it hits a mime, does anybody care?
  8. Describe the three parallel visual pathways. I will not ask you to reproduce figure 6-37, but you may used it as a guide in remembering the visual pathways.
  9. Define the agnosias.
  10. Compare and contrast rods and cones.
  11. Describe the phototransduction process as illustrated in Fig 6.8.
  12. Be able to name and locate the neurons of the retina (Fig 6.6).
  13. Know and be able to interpret center-surround receptive fields, and state where these can be found. (figure 6.14.)
  14. Trace the visual pathway from retina to the primary visual cortex (Fig 6.12).
  15. Distinguish between monocular and binocular zones. Why do predators have two eyes in the front of their head (or why do creatures with two eyes in front of their head become predators? )
  16. Describe simple and complex cells. Where are they? Describe the experiments (and experimenters) that identified these.
  17. Describe blobs. What are they and what do they do?
  18. Describe the experiments that resulted in the identification of cells that respond to faces.
  19. Describe the columnar and layer structure of the primary visual cortex.
  20. Describe the trichromatic and opponent processing forms of vision.
  21. Know and interpret figure 6.18, 6.19, 6.20.
  22. What are "spatial frequencies" and what do they reveal?

    Regulation of Internal States
  1. Be able to define the important terms in the chapter.
  2. Be able to describe the "negative feedback" system.
  3. Describe the various ways in which endotherms can release heat. Conserve heat. Be sure to include some behavioral forms of thermoregulation.
  4. Pretend that a new regions of the brain has been discovered and it is suspected that it plays a role in thermoregulation. Be able to design experiments that would determine the role it plays in thermoregulation. Name independent variables, dependent variables (be specific) and describe interventions.
  5. Discuss the functional roles that changes in core temperature. Be sure to include roles played control of fever and ultradian rhythms.
  6. Why do peas get cold faster than potatoes?
  7. Describe three "thermostats" in the nervous system. (I don't mean heat-detectors, but three homeostatic mechanisms)
  8. If we think of fluid balance as a homeostatic system, then we need to be able to identify the "detector" and what it detects. With fluid balance, describe what is detected, how, and the results of deviations from the "set point."
  9. Describe the causes and remedies of osmotic and hypovolemic thirst.
  10. What stops drinking?
  11. Discuss the roles of insulin and glucogon, glycogen.
  12. Describe diabetes mellitus. Why do untreated diabetics eat and loose weight?
  13. Describe Type II, or adult-onset diabetes.
  14. What stops a meal?
  15. Lay out why flavor aversion might be considered a form of respondent conditioning. Discuss why it might be an example of negative reinforcement. Are these incompatible?
  16. It is sometimes said that conditioning entails the use of arbitrary stimulus-response relationships. Discuss the viability of this notion.
  17. Compare and contrast lesions to the ventromedial hypothalamus and the lateral hypothalamus. Be sure to include discussion of the syndromes associated with lesions in these areas.
  18. Discuss the conditions under which one begins to eat. The conditions under which one stops eating. Think about how you might design treatments for overeating based upon the material in this chapter. Think about how you might evaluate treatments based upon:
    1. Surgical removal of fat.
    2. Chronic use of psychomotor stimulant.
    3. A diet composed exclusive of "low-fat, low-calorie" meals.
    4. Discuss the concept of a "set point" for body weight. Critique this in view of what is required for there to be transduction (i.e., where is the detector and what does it detect?). What other variables could be used as set-points?
  19. What is cholecystokinin? What is the evidence that it is related to a "satiety" cue? Include the Corwin et al. study in your discussion.
  20. Discuss flavor aversion and its role in dietary selection.
  21. What is fenfluramine? What does it do and how?


  1. Be able to define all the bolded terms in the chapter.
  2. Describe the various stages of sleep and how they are measured and defined.
  3. Compare and contrast REM and NREM sleep according to 1) the way that they are measured using EEGs and EMGs, 2) their physical manifestations, 3) the neurochemistry underlying them, and 4) the determinants (as far as they are understood) of how much occurs.
  4. Describe two sources of "jet-lag." Describe how one might approach its treatment pharmacologically. Environmentally.
  5. Define a hertz (no, this has nothing to do with rental cars).
  6. Describe the effects of sleep deprivation. Describe the methods used to provide selective sleep deprivation with humans. With nonhuman species.
  7. Define Narcolepsy, Sleep attack, cataplexy, sleep-paralysis, and REM Without Atonia.
  8. Describe drug-dependency insomnia, its causes, and its treatments.
  9. Describe the encéphale isolé and cerveau isolé experiments and what they revealed about sleep and arousal.
  10. Discuss the role of "sleeping pills" and insomnia. Describe the role of, and approach to diagnosis, the class of pills often used and their effects on sleep quality. Be sure to consider the importance of kinetics (how long a drug remains active) in this.
  11. Describe two ways of measuring the basic rest-activity cycle.
  12. Define zeitgeber, circadian rhythm, and entrainment.
  13. Describe the experiments used to determine circadian rhythms.
  14. Describe some of the roles of the suprachiasmatic nucleus in circadian rhythms. Be able to describe the experiments underlying this understanding.
  15. Discuss evidence for a genetic basis for circadian rhythms. Discuss the interaction between genetic and environmental influences over circadian rhythms.
  16. Describe the roles of serotonin, norepinephrine, dopamine, and acetylcholine on sleep.
  17. Discuss some of the biological functions attributed to sleep. Include the role of REM-NREM cycling in thermoregulation.
  18. What is the suprachiasmatic nucleus? Melatonin? The Pineal gland?.
  19. Describe the chemical control of sleep, and the roles of Ach, NE, 5-HT.
  20. Describe jet lag, its treatment, prevention, and the occasions on which it can appear.
  21. Describe the biological functions that have been attributed to sleep.

Learning and Memory

  1. Compare and contrast:
    1. Respondent and operant conditioning.
    2. Explicit and implicit memory
    3. Short-term and long-term memory
    4. Associative and nonassociative learning.
  2. Define learning.
  3. Describe the elements of respondent conditioning and their temporal requirements.
  4. Define match-to-sample and the experiment that pointed to a role of the inferior temporal cortex. Be able to spell "inferior ..."
  5. Define long-term potentiation. Distinguish between associative LTP and that produced by repeated (tetanic) stimulation.
  6. Interpret figure 14.6.
  7. Describe the Kelso and Brown (1986) experiment.
  8. Describe the experiment by Magee and Johnston (1997) as described in figure 14.14. Go back and review the role of TTX in the formation of the action potential.
  9. Describe and give an example of a Hebbian synapse. Why did Hebb offer this as speculation and not as Truth?
  10. Be able to draw the various model of synaptic strengthening (or weakening) that could account for long-term potentiation (Fig 14.16, 17)
  11. Describe the role of serotonin (5-HT) in sensitization.
  12. Draw the NMDA receptor. Describe the roles of calcium, magnesium, glutamate and action potentials. Does the sequence of events in the NMDA receptor correspond to those required for a "relative enduring change in behavior" (which forms part of some definitions of learning) or the temporal characteristics seen in respondent conditioning?
  13. Describe habituation and its neural mechanism in the aplysia. Similarly with sensitization.
  14. Describe the potential roles of: glutamate, NMDA, Nitric Oxide, Protein Kinase C, Calcium-calmodulin Kinase, and tyrosine kinase in LTP.
  15. Name and spell the inputs and outputs to the hippocampus.
  16. Describe the experiment used to demonstrate electrical brain stimulation.
  17. Describe the ascending dopamine pathways originating in the brainstem. Describe the various roles of the VTA, MFB, and NA. Be able to spell everything.
  18. Relate intracranial administration of drugs to EBS. Define a reinforcer.
  19. . Discuss the roles of dopamine in reinforcement and evidence for these roles.
  20. Describe the drug-discrimination procedure. Are the animals conscious of the drug?


  1. Dscribe the monosynaptic stretch reflex. Be able to define the sensory, neural, and effector elements, sketch the pathway, and describe the function, and the neurotransmitters that we have discussed.
  2. B sure to know what the Golgi Tendon Organ, extrafusal and intrafusal fibers, alpha and gamma efferents, spindles are.
  3. Dscribe a polysynaptic stretch reflex as a 1) inhibitory pathway on the originating muscle or 2) an inhibitory pathway to an antagonist muscle.
  4. State what happens when a load is applied to the limb. Specifically, be able to reproduce the material in figure 8.4
  5. Describe the gamma efferent system and contrast it with the alpha system. Be sure to identify the critical components of each system.
  6. Describe the cortical control over movement.
  7. Characterize the "motor homunculus." Be able to explain why some areas are larger than other and to relate that to the size of the motor unit.
  8. Describe the four major descending motor pathways. Then describe the major cortico-brainstem-spinal tracts. Describe the pyramidal/extrapyramidal systems.
  9. Sketch and identify the major components of a "closed-loop" system. Do the same with an "open-loop" system. Give an example of a motor system that uses each approach.
  10. Describe the inputs to the cerebellum and the nature of the cerebellum's contribution to motor function.
  11. Describe the sources of afferents to the cerebellum. Where to efferents go?
  12. Name the components of the basal ganglia. Where do the inputs derive from and what portion of the basal ganglia receive them? What are the output regions of the basal ganglia and where do the efferents synapse?
  13. Compare and contrast the signs and symptoms of Parkinson's and Huntington's disease and relate them to the pathology observed.
  14. What is MPTP and what does it do? Describe two approaches to treating Parkinson's disease, one surgical one nonsurgical, that have arisen since the MPTP episode.
  15. Describe the Nigral-Striatal pathway, its neurochemistry, and how this provides some understanding of the motor effects of neuroleptics. Be able to name and describe those motor effects.
  16. Describe the various movement disorders.
    1. Include the appearance, the underlying pathology, where known, and the cause.
    2. For Parkinson's disease, Myasthenia Gravis, and Tardive Dyskinesia discuss the pharmacological treatment of them, and its rationale.
  17. Discuss the changes in motor function associated with aging.
  18. Describe a motor disorder and its associated symptoms for the following elements of the motor system: neuromuscular junction, spinal cord, brain stem, cerebral cortex, basal ganglia, and cerebellum.
  19. What are the functions of the cerebellum?

Affective Disorders

  1. Compare and contrast tricyclic antidepressants, MAO inhibitors, and SSRIs.
  2. When fluoxetine was first introduced in the U.S. it was noted that there were many suicides associated with its use. Is this a problem? Why or why not?
  3. Discuss the relationship between depressants and sleep. Relate this to the neurochemistry of sleep and the effects of antidepressants.
  4. Discuss the strengths and weaknesses of theories of a genetic basis for schizophrenia.
  5. Describe the impact of the introduction of chlorpromazine on the treatment/management of schizophrenia.
  6. Contrast the positive and negative signs of schizophrenia.
  7. Discuss the heritability of schizophrenia.
  8. Define epidemiology.
  9. In a sentence describe three putative causes of schizophrenia.
  10. Compare the structure of chlorpromazine and imipramine.
  11. Why are atypical antipsychotic drugs called that? Give an example of one.
  12. Discuss the use of antiparkinsonian drugs in the pharmacological management of schizophrenia. Why do they work?
  13. Define Tardive Dyskinesia and discuss current ideas of its development.
  14. Discuss the dopamine theory of schizophrenia. Give evidence in support of it and describe the limitations of the theory.
  15. Why are anticholinergic drugs sometimes prescribed concurrently with neuroleptics?

Psychopharmacology and Drug Abuse.

  1. Name the classes of inhalants and one example from each. What is common about all of them.
  2. Distinguish among the chemical, generic, and proprietary names of drugs.
  3. Be able to name all the classes of drugs. For the classes that we covered in class (including sub-headings) be able to name (generic and proprietary) a representative drug, give its half-life and mechanism of action.
  4. How much blood is there in the average adult human? How much is pumped each minute? How much clears the kidney each minute?
  5. Describe the principle ways by which drug action is terminated.
  6. Compare and contrast first-order and zero-order elimination. Be able to give examples and draw graphs with appropriately labeled axes. Define and spell pharmacokinetics.
  7. Describe the principle types of tolerance.
  8. Describe the experimental protocol used to identify behaviorally augmented tolerance of ethanol.
  9. What is acute tolerance?
  10. Know the difference between signs and symptoms.
  11. Describe the stages of sedation
  12. Define addiction according to the DSM-IV, and the WHO.
  13. Name and define the four common elements of drug addiction according to Carlson.
  14. Describe the respondent conditioning mechanism proposed by Siegel to account for some presentations of drug tolerance. How might you test for the presence of this form of tolerance?
  15. Define "antagonist precipitated withdrawal."
  16. Discuss the antipunishment effects of benzodiazepines. How might they become relevant when the drugs are used for "chemical restraint?"
  17. Describe the following for barbiturates, amphetamine, methylphenidate, nicotine, imiprimine , Parnate, fluoxetine, chlorpromazine
    1. Conditions under which they might be used.
    2. Acute effects
    3. Side effects and toxicity
    4. Physical dependence (if any)
    5. Signs of withdrawal (if any).
    6. Symptoms of withdrawal (if any)
    7. Abuse potential
    8. Tolerance (if any). (i.e., is there any and is it specific to certain effects?).
    9. Mechanism of action.
    10. Antagonists
    11. Effects of overdose.
  18. Describe the metabolism of ethanol. Describe the acute effects of disulfiram and why it does that.
  19. Describe the distribution of ethanol in the body.
  20. Know the model describing the putative substrates of pharmacological reinforcement as described in figure 5.4.
  21. Define teratogen and give two examples.
  22. Compare the kinetics of cocaine after oral, intranasal, and inhalation exposure.
  23. Describe the putative mechanisms by which cocaine affects the fetus.
  24. Discuss the "reinforced abstinence" approach to treating cocaine abuse. Describe the "yoked-control" procedure and its advantages.
  25. Interpret the following equation:
    1. B = kR/(R+r0).
    2. State what k, R, and R0 are. Show a graph of the function and show how k and R0 can be estimated on a graph. Be sure to label the axes.
    3. Describe the "break-point analysis" for identifying the abuse potential of a drug.
    4. Describe the drug self-administration procedure. Identify the discriminative stimulus, the operant, and the reinforcer. Any chance for conditioned reinforcers to act?
  26. Describe the experiments conducted by Pickens and Thompson that identified cocaine as a reinforcer.
  27. Describe the characteristics of addictive substances.
  28. Describe the two types of tolerance, one physiological and the other behavioral, described in your text.
  29. Describe the experiment by Schuster et al. on behavioral tolerance. What mechanism was proposed to explain it?
  30. Understand the conditioned compensatory response.
  31. Describe the role of dopamine in self-administration.
  32. Describe and give an example of a drug-discrimination procedure. What kind of information can be gained from it?
  33. Distinguish between "subjective" and "discriminative" effects of drugs.
  34. Discuss the relative roles of physical dependence and reinforcing properties of drugs in understanding addiction. (Don't even think of using the phrase "psychic dependence.")
  35. Describe and interpret the experiment in which cocaine and nicotine facilitates electrical brain stimulation.
  36. How might a heterogeneous reductionist approach drug abuse? A homogeneous reductionist? Which is right?
  37. A tobacco company executive testified before the Waxman Committee on Health that nicotine is not addictive because there is no physical withdrawal syndrome associated with quitting. Assume that he is correct about the withdrawal syndrome, so what?
  38. For each of the following drugs, state what broad class they belong to (narcotic, stimulant, hallucinogen, tranquilizer/anxiolytic), the neurotransmitter most strongly associated with its effects (be able to do this in both directions, definition and fill-in-the-blank), and its most important effects: morphine, nicotine, cocaine, caffeine, marijuana, alcohol, barbiturate, diazepam (valium).
  39. Discuss evidence for heritability of alcoholism. Suppose a teenage boy's father is alcoholic, would you bet $100 that boy would also be alcoholic?

Behavioral Toxicology

215. Discuss lead poisoning. Describe the epidemiological studies conducted by Needleman and Bellinger. Discuss the public health consequences of a 5-point shift in the score on an IQ test in a population 1,000,000 people. Compare the results of studies conducted with human and nonhuman species.

  1. What is Weiss's view of the hypothesis that some forms of hyperactivity can be traced to food-additives?
  2. Discuss some of the evidence in support of establishing acceptable exposure levels to mercury.

Drug Discrimination.

  1. Describe the drug-discrimination procedure.
  2. In the Holtzman et al. study, how did training dose influence the shape of the generalization curve when viewed as a function of dose of caffeine.
  3. In the Holtzman et al. study, describe how training dose influenced the drugs to which caffeine was generalization.


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Last modified: July 08, 2010