Index of Figures

Chapter: 1 2 3 4 5 6 7 8 9

Chapter 1 (Go to beginning of figure index)

Figure 1 - 1: Sherrington's experiments on the electrophysiology of the synapse: Schematic summary of Sherrington's experiments on the electrophysiology of the synapse.
Figure 1 - 2: Loewi's demonstration of chemical neurotransmission: Otto Loewi's experiment demonstrating the chemical transmission of nerve impulses.
Figure 1 - 3: Bernard's experiments on the nerve-muscle junction: Claude Bernard's experiments demonstrating that curare acts at the junction between the nerve and the muscle.
Figure 1 - 4: The source of energy for electrical activity of the nervous system: The separation of charged particles produces a resting potential across the membrane of the neuron.
Figure 1 - 5: Propagation of the action potential: The action potential sets up the stimulus for the continued propagation of the potential, which appears as a wave of electrical activity that travels down the axon.
Figure 1 - 6: Release of neurotransmitter: The arrival of the action potential causes the release of chemical messengers from the terminal endings of the axon.
Figure 1 - 7: Steps in the process of chemical transmission at the synapse: Major steps in the process of chemical transmission.
Figure 1 - 8: Chemical bases of dual control by the autonomic nervous system: Pupillary responses to two different chemical inputs cause contrasting responses to autonomic smooth muscles.
Figure 1 - 9: Dual control by the autonomic nervous system: The autonomic nervous system uses a combination of different anatomical organizations and different chemical mediators to cause different (usually opposing) effects in the same target organs.
Figure 1 - 10: Receptor sites determine response to neurotransmitters: The autonomic control of the urinary bladder exemplifies both the opposing interactions of the sympathetic and parasympathetic system and the differing effects that the same compound can have on different sets of smooth muscles.
Figure 1 - 11: Multiple receptor sites for a neurotransmitter: Schematic summary of some transmitter-receptor possibilities.
Figure 1 - 12: Chemical organization of the autonomic nervous system: Outline of different receptor types and chemical transmitters in the autonomic nervous system.
Figure 1 - 13: Chemical specificity of the hypothalamus: More specific changes in behavior are produced by chemical stimulation than by lesions of brain structures.
Figure 1 - 14: The interactions of brain, behavior and environment: The brain, behavior, and the environment have interpenetrating effects.

Chapter 2 (Go to beginning of figure index)

Figure 2 - 1: Subtractive logic as it applies to lesion and pharmacological experiments: Subtractive logic as it applies to lesion and pharmacological experiments.
Figure 2 - 2: Subtractive logic as it applies to the famous case of Phinnaeus P. Gage: Subtractive logic as it applies to the famous case of Phinnaeus P. Gage.
Figure 2 - 3: Subtractive logic as it applies to the metabolic disorder of phenylketonuria (PKU): Subtractive logic as it applies to the metabolic disorder of phenylketonuria (PKU).
Figure 2 - 4: Encephalization of the developing brain: Schematic representation of the structural development of the brain.
Figure 2 - 5: Life span of a cholinergic neuron: Schematic representation of the life span development of a cholinergic neuron.

Chapter 3 (Go to beginning of figure index)

Figure 3 - 1: Drug molecules pass through the cell membrane: Basic elements of the cell membrane determine access of drugs to body tissues.
Figure 3 - 2: The dose-response curve: Dose-response curve shows that behavior changes as drug levels in the plasma change.
Figure 3 - 3: Time course of drug effects: Following a single dose of a drug, the concentration of drug in the plasma increases to a peak, and then declines. Behavioral changes coincide with this changing drug concentration.
Figure 3 - 4: Behavioral effects of repeated doses of drug: Repeated doses of a drug maintain the drug in the system, but the plasma concentrations cycle above and below the average level. Behavioral changes follow these fluctuations in plasma concentration of the drug.
Figure 3 - 5: Effects of a drug depend upon initial rates of behavior: The law of initial values refers to the different drug effects that are seen when the initial rates of behavior are different.
Figure 3 - 6: Effects and side effects of drugs: A variety of different effects can be seen with increases in the plasma concentration of a drug. In some cases, these differences in effect might be desirable (e.g., effect A and effect B). Along with these, some combination of undesirable effects (side effects C, D and E) might also occur.
Figure 3 - 7: Effects of epinephrine and acetylcholine on blood pressure: Epinephrine and acetylcholine each produces dose-related changes in blood pressure, but by different mechanisms: Low doses of epinephrine act on beta receptors and decrease blood pressure by vasodilation. High doses of epinephrine act on alpha receptors and increase blood pressure by vasoconstriction. Low doses of acetylcholine act on muscarinic receptors and decrease blood pressure by vasodilation. High doses of acetylcholine act on the nicotinic receptors of the autonomic ganglia and increase blood pressure indirectly through activation of the sympathetic nervous system.
Figure 3 - 8: The blood-brain barrier: The blood-brain barrier protects the brains from certain classes of compounds while allowing other classes of compounds to have free access.
Figure 3 - 9: Summary of the effects of drugs on synapses: Summary of the major biochemical effects that drugs may have at the synapse: 1. Precursor compounds 2. Synthesis blockade 3. Transmitter depletion 4. Prevention of release 5. Receptor inhibition 6. Mimicking 7. Inactivation blockade 8. Reuptake blockade 9. False transmitters (+) 10. False transmitters (-) 11. Conduction blockade
Figure 3 - 10: The interrelationships of molecular structure, biochemical activity and behavioral effect: The interrelationships of the drug classifications that are based on drug effects, drug actions, and drug structures: A. Consistent relationships suggest biochemical substrates for particular behaviors. B. Consistent structure-activity relationships suggest chemical structures for synthesis of related drugs. C. Consistent relationship suggests that the drugs within a particular class may share a common biochemical action.

Chapter 4 (Go to beginning of figure index)

Figure 4 - 1: Pavlovian fear conditioning: Three types of Pavlovian conditioning procedures for modeling of fear: Delay conditioning. Conditioned responses, including fear, begin to occur during the CS presentation before the US is presented. Long-delay conditioning. Conditioned fear responses move forward in time during long CS presentations and, with continued training, reach maximal levels during the interval just preceding the presentation of the aversive US. Trace conditioning. Conditioned fear can be observed during the interval when only the trace, or memory, of the CS is present.
Figure 4 - 2: Shuttle box instrumental fear conditioning: The shuttle box is one of the standard pieces of apparatus for studying learned responses to aversive stimuli: One-way escape conditioning is very simple, requiring only that the subject move to the other end of the chamber to escape the ongoing electric shock. One-way avoidance conditioning adds an explicit warning signal (CS) that shock will begin shortly, providing an opportunity to move to the safety zone and avoid the electric shock altogether. Two-way avoidance provides a CS at either end to allow the avoidance of electric shock, but the conflict of returning to a place that is not always safe sets up conflict and makes the task difficult to learn.
Figure 4 - 3: Sympathetic nervous system response to stress: The sympathetic and adrenal responses facilitate coping with acute episodes of stress.
Figure 4 - 4: Parasympathetic nervous system response to stress: The parasympathetic system predominates when acute episodes of stress provide no obvious coping response. Under non-stressful conditions, each of the effector organs responds individually as necessary.
Figure 4 - 5: Richter's experiments on the emotional causes of stress syndrome: Richter's experiments demonstrated the importance of both the behavioral interpretation of "hopeless" stressors and the activity of the parasympathetic division of the autonomic nervous system.
Figure 4 - 6: The triad design for studying the importance of prediction and control: The triad design has been useful in determining the importance of prediction and control of aversive events and the susceptibility to ulcer formation.
Figure 4 - 7: Stomach ulcers under conditions of prediction, control and conflict: The relative incidence of ulcer formation under various conditions of prediction, control, and conflict.
Figure 4 - 8: Curare as an autonomic nervous system blocker: Curare was used to block the autonomic ganglia of both divisions of the autonomic nervous system.
Figure 4 - 9: Impact of the discovery of chlorpromazine: The discovery of chlorpromazine produced a dramatic decrease in the number of schizophrenia patients who required chronic hospitalization. The curves in the upper panel are based on a one-percent incidence of schizophrenia in the general population, with one-third of these requiring chronic hospitalization before the advent of phenothiazines. Current costs of schizophrenia to society have been estimated at two percent of the gross national product (GNP). Projected values and values prior to 1955 in the lower panel of the figure are based on costs that are four times that value.
Figure 4 - 10: Effects of antianxiety drugs on punished responding: Antianxiety drugs block the suppressant effects of punishment in the Geller-Seifter procedure without changing the rate of food-rewarded responding. (Slash marks on graph indicate reinforcement.)
Figure 4 - 11: Clinical effectiveness of antipsychotic drugs related to effects on dopamine receptors: Antipsychotic drugs that are most effective in the clinic are also most effective in displacing haloperidol from dopamine receptors.
Figure 4 - 12: Clinical effectiveness of antianxiety drugs related to effects on punished responding: Antianxiety drugs that are most effective in the clinic are also most effective in blocking the suppressant effects of punishment in the Geller-Seifter procedure.
Figure 4 - 13: The GABA receptor complex: The benzodiazepines appear to act on receptors that modulate the activity of GABA in the GABA receptor complex.
Figure 4 - 14: Clinical effectiveness of antianxiety drugs related to effects on GABA receptor: Antianxiety drugs that are most effective in the clinic are also most effective in displacing labeled diazepam from GABA receptors.
Figure 4 - 15: Evidence for an endogenous antianxiety substance: Antianxiety drugs bind to receptors that may be specific for some (as yet unidentified) endogenous antianxiety substance.
Figure 4 - 16: Evidence that anticholinergic antianxiety drugs act on the brain: The quaternary forms of atropine and scopolamine block the cholinergic synapses of the periphery but do not cross the blood-brain barrier. The anti-punishment effects of these drugs require action on brain neurons.
Figure 4 - 17: Histamine (H2) blockers decrease stomach acid secretion: Cimetidine (Tagamet) specifically blocks H2 receptors while the other histamine receptors continue to function normally.

Chapter 5 (Go to beginning of figure index)

Figure 5 - 1: Distinguishing between the reflexive and emotional components of pain: The flinch-jump procedure can distinguish between the reflexive and emotional components of the response to pain.
Figure 5 - 2: Measuring pain thresholds: The paw-lick and tail-flick tests measure the threshold of pain produced by mild heat stimuli.
Figure 5 - 3: Receptor binding technique: Radioactive substances that have a specific affinity to brain receptors (receptor binding) can be isolated along with the receptor membrane.
Figure 5 - 4: Clinical effectiveness of opiate agonists and antagonists related to effects on opiate receptors: The clinical potency of opiate drugs is related to their affinity for binding to brain opiate receptors. This relationship holds for both opiate agonists and opiate antagonists.
Figure 5 - 5: Beta-lipotropin as source of stress-response chemicals: The beta-lipotropin molecule contains several of the same sequences of amino acids that comprise peptides that are known to be important in the stress response.
Figure 5 - 6: Neurochemical systems in pain perception: Schematic summary of the neural and hormonal systems that mediate pain and pain inhibition.
Figure 5 - 7: Pain produces analgesia: The type of analgesia that is produced is related to the impact of the aversive stimulus.
Figure 5 - 8: Interpretation of painful event determines analgesia: The triad design shows that the interpretation of the painful stimulus determines whether or not analgesia will ensue.
Figure 5 - 9: Effects of naloxone on analgesia induced by social defeat: Analgesia can be produced by the experience of social defeat in mice.
Figure 5 - 10: Cross-tolerance between social defeat and morphine: Cross-tolerance exists between the effects of morphine and social defeat.
Figure 5 - 11: The effects of either morphine, placebo drugs, or acupuncture on dental pain can be blocked by an opiate blocker: The effects of either morphine, placebo drugs, or acupuncture on dental pain can be blocked by an opiate blocker.
Figure 5 - 12: Cellular and humoral immunological responses: Schematic diagram of the two major types of immunological responses.
Figure 5 - 13: Humoral response of the immune system: The B-lymphocytes mediate the humoral response of the immune system.
Figure 5 - 14: Cellular response of the immune system: The cellular response of the immune system involves the proliferation of T-cells.
Figure 5 - 15: Influence of genetics and early environment on milk allergies: The incidence of allergic reactions to milk is related to both the genetic history and infant feeding styles of the individual.
Figure 5 - 16: Effects of inescapable shock on immune system: Inescapable shock suppresses the proliferation of T-cells.
Figure 5 - 17: Experimental allergic myasthenia gravis: Experimental allergic myasthenia gravis can be produced by antibodies to foreign nicotinic receptors.
Figure 5 - 18: Experimental "allergic" diabetes: A model for an immunological response that interferes with receptors.
Figure 5 - 19: Limbic system mediation of the hypothalamic stress response: A summary model of the general features of the hypothalamic and pituitary contributions to different forms of stress reactions.

Chapter 6 (Go to beginning of figure index)

Figure 6 - 1: Generalized learned helplessness: The learned helplessness that results from exposure to the absence of control generalizes to other situations.
Figure 6 - 2: Catecholamine degradation enzymes: Catecholamines that are not protected within compartments of the terminals are metabolized by MAO. Free-floating catecholamines in the synaptic zone outside the cell are metabolized by COMT.
Figure 6 - 3: Depletion and repletion of catecholamines affect reward: The depletion and repletion of transmitter stores has linked the catecholamines to reward.
Figure 6 - 4: Medial forebrain bundle (MFB): Noradrenergic fibers arising from the locus coeruleus and dopaminergic fibers arising from the ventral tegmental area converge in the MFB reward system.
Figure 6 - 5: The brain-behavior-environment interaction: Manipulations of brain chemistry or anatomy change the response to rewards. The remainder of this chapter will show how behavior and the environment can change the brain systems that are responsible for mediating reward.
Figure 6 - 6: Swim test of learned helplessness: Rats that have been exposed to uncontrollable electric shocks engage in fewer coping responses in the modified swim test.
Figure 6 - 7: Stress affects tyrosine hydroxylase levels: Exposure to uncontrollable shock produces a temporary decrease in the production of norepinephrine. Repeated exposure to mild, controllable stress increases the activity of this system.
Figure 6 - 8: Role of alpha-2 autoreceptors in neuromodulation: Autoreceptors in the locus coeruleus regulate transmitter release in the anterior cortex.
Figure 6 - 9: Effects of amphetamine and cocaine on catecholamine synapses: Amphetamine displaces dopamine from vesicles. Cocaine blocks dopamine reuptake. Both effects increase the activity of the synapse.
Figure 6 - 10: Role of MAO in depression: The effects of MAO inhibitors in the reserpine model of depression.
Figure 6 - 11: Specificity of MAO inhibitors: The ability to specifically block the MAO-B isoenzyme may result in fewer side effects in the treatment of depression. Nonspecific MAO blockers also influence MAO-A in the periphery, leading to increases in norepinephrine. Then, dietary tyramine (from wine, cheese, etc.) can indirectly release the NE, causing dangerous side effects such as increased blood pressure.
Figure 6 - 12: Effects of tricyclic antidepressants on monoaminergic synapses: The tricyclic drugs avoid the "wine and cheese" problem, but still have potentially dangerous interactions with other drugs.
Figure 6 - 13: Metabolites of norepinephrine: Abnormalities in the metabolic pathways of catecholamines may provide information for better diagnosis and treatment of depression. The numerous alternatives for pathways of degradation of NE can alter the amounts of DHPG, MHPG, and VMA that are produced. These biochemical markers may help to predict which drugs will be effective.
Figure 6 - 14: Antidepressant drugs affect neuromodulation: The long delay of the therapeutic effects of antidepressant drugs suggests that the drugs may trigger neuromodulatory changes.
Figure 6 - 15: Lithium controls mania: Lithium appears to control bipolar depression by eliminating the manic phase of the disorder.
Figure 6 - 16: Exposure to stress increases vulnerability to helplessness: A single exposure to the lack of control makes the subjects more vulnerable to the effects of similar stressors that occur shortly thereafter.
Figure 6 - 17: Behavioral reward increases norepinephrine levels: The attainment of rewards produces neurochemical changes in the brain, enhancing the synthesis and release of NE.

Chapter 7 (Go to beginning of figure index)

Figure 7 - 1: Genetics of schizophrenia: Close relatives of schizophrenic patients are much more likely to develop the disorder.
Figure 7 - 2: Neurotoxic effects of 6-hydroxy dopamine: The administration of 6-hydroxy dopamine (6-OHDA) to rats blocks the lever-pressing for rewarding brain stimulation and produces the waxy flexibility that characterizes some forms of schizophrenia.
Figure 7 - 3: Catecholamine synthesis: Synthetic pathways of the catecholamines.
Figure 7 - 4: Blockade of tyrosine hydroxylase reduces NE synthesis: Tyrosine hydroxylase is shown to be the rate-limiting enzyme by blocking experiments: Only the blockade of tyrosine hydroxylase produces a direct reduction of NE synthesis.
Figure 7 - 5: The dopamine beta hydroxylase (DBH) model of schizophrenia: The DBH model proposes a shift in the location of the rate-limiting enzyme in catecholamine synthesis (compare to Fig. 7-3).
Figure 7 - 6: The clinical potency of antipsychotic drugs is related to ability to block D2 receptors: Phenothiazines that are most effective in treating schizophrenia are also most effective in blocking the D2 (but not the D1) receptors for dopamine.
Figure 7 - 7: Dual effects of dopamine receptors: The D1 receptors facilitate adenyl cyclase, whereas the D2 receptors inhibit this second messenger. These processes change the protein-synthesizing capabilities of the cell.
Figure 7 - 8: Effects of endorphins on dopamine: Endorphins can influence the release of dopamine or alter the number or sensitivity of dopamine receptors.
Figure 7 - 9: Multiple transmitters and receptors regulate neuron's response to stimulation: The most recent models of the synapse suggest the presence of multiple transmitter substances that may be stored within different vesicles. In the example shown, low levels of stimulation involve only the primary neurotransmitter. Intermediate levels of stimulation also involve the blocking of inhibitory autoreceptors. Strong stimulation releases this inhibition and allows maximal postsynaptic stimulation.
Figure 7 - 10: Neuromodulatory effects of phenothiazines: The dynamic regulation of the synapse has led to a neuromodulatory model of the action of phenothiazines in schizophrenia.
Figure 7 - 11: Dopaminergic pathways in the brain: Dopaminergic pathways that serve the extrapyramidal motor system arise from the substantia nigra; those that serve the limbic system arise from the ventral tegmental area. The latter are presumably those involved with schizophrenia.

Chapter 8 (Go to beginning of figure index)

Figure 8 - 1: The ascending reticular activating system (ARAS): The ascending reticular activating system (ARAS) controls the level of arousal.
Figure 8 - 2: Active sleep and arousal centers in the brain: The location of active centers for sleep and arousal have been shown by the effects of three different transections.
Figure 8 - 3: EEG changes in sleep: Stylized examples of the relationship between the EEG and levels of arousal.
Figure 8 - 4: Neurotransmitters of sleep and arousal: The major neurotransmitters of sleep (5-HT) and of arousal (NE, DA, and ACh).
Figure 8 - 5: Brain circuitry of circadian rhythms: Brain circuitry involved with the maintenance of circadian rhythms.
Figure 8 - 6: Barbiturate effects depend on circadian rhythms: The dosage of barbiturate required to reach the anesthetic level varies as a function of circadian rhythms.
Figure 8 - 7: Interaction of Yerkes-Dodson Law with task difficulty: The inverted U-shapes relationship between arousal and performance, known as the Yerkes-Dodson law, interacts with the complexity of the task.
Figure 8 - 8: Interactions among arousal, behavior, and environment: The interactive effects of arousal, behavior, and the environment. Drugs that influence these interactions have powerful effects on behavior.
Figure 8 - 9: Effects of strychnine and tetanus toxin on spinal reflexes: Strychnine blocks the receptors of inhibitory circuits within the spinal reflex systems. Tetanus toxin blocks the release of the inhibitory transmitter.
Figure 8 - 10: Effects of picrotoxin on GABA receptors: Picrotoxin acts on the GABA receptor complex to reduce the effects of GABA.
Figure 8 - 11: Effects of pentylenetetrazol on action potential recovery time: Pentylenetetrazol reduces the recovery time between consecutive action potential.
Figure 8 - 12: Effects of xanthine derivatives on Ca++ channels: Xanthine derivative (caffeine, theophylline, and theobromine) increase Ca++ permeability. Ca++ plays an essential role in many aspects of cell membrane excitation. Xanthine derivatives facilitate Ca++ entry and increase levels of excitation.
Figure 8 - 13: Effects of nicotine on acetylcholine receptors: Nicotine mimics acetylcholine at the autonomic ganglia but can block function by producing sustained depolarization.
Figure 8 - 14: Effects of amphetamine on catecholamine release: Amphetamines cause indirect stimulation by releasing newly synthesized catecholamines (especially dopamine).
Figure 8 - 15: Effects of cocaine on catecholamine reuptake: Cocaine cause indirect stimulation by blocking the reuptake of catecholamines (especially dopamine). The local anesthetic effects are caused by blocking Na+ permeability.
Figure 8 - 16: Effects of barbiturates and benzodiazepines on GABA receptors: Barbiturates and benzodiazepines enhance the effects of inhibitory GABA neurons via two different receptors on the GABA receptor complex.
Figure 8 - 17: Behavioral symptoms of alcohol ingestion: Increases in the amount of alcohol consumption cause a progressive loss of sensory and motor capabilities. Large amounts can cause coma and death.
Figure 8 - 18: Anticholinergic effects on the septohippocampal system: Atropine and scopolamine block ACh receptors and interfere with septohippocampal theta activity.

Chapter 9 (Go to beginning of figure index)

Figure 9 - 1: Physiological mechanisms of tolerance: Physiological mechanisms of tolerance that reduce the contact of the drug with the receptors.
Figure 9 - 2: Compensatory responses to drug effects: Some compensatory responses to drug effects. Both excitatory and inhibitory systems may change (in response to the presence of a drug) to return function to normal.
Figure 9 - 3: Mechanism of tachyphylaxis: Ephedrine effects as a model of tachyphylaxis. (b.p. = blood pressure; D1 to D6 refer to doses.)
Figure 9 - 4: Tolerance due to reduction of receptors: Reduction of receptors through neuromodulation results in tolerance to the high levels of acetylcholine that are maintained during inhibition of acetylcholinesterase (AChE).
Figure 9 - 5: Enzyme induction speeds drug metabolism: Enzymes induction provides a way to increase the speed of drug metabolism.
Figure 9 - 6: Development of barbiturate tolerance: Barbiturate effects before and after the development of tolerance.
Figure 9 - 7: Drug withdrawal produces rebound effects: Continued exposure to a drug can sometimes trigger compensatory responses that effectively counteract the drug effects. Under these conditions, the response to the absence of the drug can be greater than the response to the drug itself.
Figure 9 - 8: Behavioral tolerance: The pre-post design has been useful in demonstrating behavior tolerance. The shaded areas indicate the amount of some behavior that is being tested.
Figure 9 - 9: Affective withdrawal produces rebound effects: Opponent-process theory of emotion suggests naturally occurring rebound effects.
Figure 9 - 10: Opponent-Process model of addiction: The opponent-process model of the development and maintenance of heroin addiction.
Figure 9 - 11: Drugs as reinforcers: Rats and other laboratory animals can demonstrate abuse potential of drugs through the self-administration procedure.
Figure 9 - 12: Drug effects depend on expectations: Real or false information about alcohol can change the behavioral effect. This is the so-called think-drink effect described by Carpenter.