Poling Objectives
Chapter 1
1. Poling launches into an explanation of respondent conditioning. He describes the all-tofamiliar experiments by Pavlov. Check out the first 2 paragraphs on page 11. What was
Pavlov’s important contribution to a science of behavior?
2. What was Watson’s contribution? Why is S-R psychology an inappropriate description of
behavior analysis?
3. What was Thorndike’s law of effect? What was its major contribution?
4. What is the difference between behaviorism and EAB?
5. What is the difference between radical and methodological behaviorism?
6. Look at Table 1-2. Given a dimension, be able to talk about how EAB deals with it vs
how traditional psych does.
7. What was the first report of a behavioral pharmacology study that clearly used EAB
methods? (see Table 1-3) Look at Figure 1-1. Given this figure, or a figure like it, be
able to interpret it.
a. In this study, they tried to see if the effect was due to “hunger.” How did they do
this, and what was found?
b. Take the conclusions in “a”, and then identify the effect of caffeine.
8. When did behavioral pharmacology really develop? What were some of the factors that
contributed to this rise in popularity?
9. Check out the discussion of chlorpromazine. This drug produced calming without gross
sedation in pre-surgical routines, and was therefore interesting. Poling talks about
“animal models” used by the drug companies. One such model was pole-climbing.
Explain this procedure, and why it was used to screen for antipsychotics.
a. Also, explain what drug self administration is used to screen for.
10. On page 21, Poling talks about 3 concepts. See these below, and explain what each
means.
a. Behavioral loci of drug action
b. Mechanism of action
c. Behavioral mechanisms of drug action
Chapter 3
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What is a drug?
What is psychoactive vs. psychotropic?
What are the 3 kinds of drug names? (there are also “slang” terms for drugs)
How can drugs be classified?
Which are most common?
Describe the 4 stages of pharmacokinetics?
7. Examine the route of administration graph on page 47. Be able to draw it with the
appropriate labels.
8. Which route has the quickest effect? Which has the longest lasting effect?
9. What are some of the limitations of oral administration?
10. Advantages/disadvantages of IV?
11. How long does it take for distribution, after a drug is in the blood? Where does it go first?
12. To reach the brain, what is the path?
13. What is protein binding?
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What is depot binding?
What is the blood brain barrier?
Which drugs pass through the best?
Is the placenta a good barrier? Relate this to teratogenic effects.
18. What are metabolites?
19. Explain how enzyme induction can lead to tolerance.
20. What is cross tolerance?
21. NOTE: drugs are usually transformed in liver. So liver damage will increase the
magnitude and duration of drug effects.
22. Where does excretion typically occur?
23. Explain linear kinetics (sometimes called 1st order) and nonlinear kinetics (sometimes
called 0 order)
24. How often should drugs be given to maintain a stable blood level?
25. What is accumulation?
26. What is the difference between chronic and acute?
27. How are drug doses measured in the applied and laboratory situations?
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Be able to draw a dose response curve with a continuous or binary dependent variable.
What is the median effective dose (ED50)? Given a graph, be able to identify it.
What is peak efficacy? Given a graph, be able to identify it.
What is potency? Given 2 drugs, identify which is more potent.
Explain the median lethal dose (LD50)
How is the TI computed? How is it interpreted?
Look at figure 3-6. The TI suggests Drug D is more reasonable. However, why could
you make a case for Drug C?
35. Look at the 4 basic facts of pharmacology. Make sure you know them.
36. What is tolerance? What are the 3 kinds?
37. What is sensitization?
38. What is physical dependence and withdrawal syndrome?
39. Explain why the w/d syndrome occurs.
NOTE: tolerance and physical dependence do not always occur together.
40. Do drugs produce qualitative or quantitative changes in the body?
41. Give an example of a drug interaction. How might it occur?
Chapter 4
1. Know the following facts about the nervous system
a. Motor vs. sensory systems of neurons
b. Central (CNS) vs. peripheral nervous system (PNS)
c. Under central: brain and spinal cord
d. Under PNS: Somatic vs autonomic
e. Under autonomic: sympathetic vs parasympathetic
2. Be able to draw a neuron with the following elements: soma, dendrites, axon, terminal
buttons, and synapse (with a 2nd neuron). On your diagram, label and describe each
element.
3. NOTE: communication between neurons occurs chemically (with neurotransmitters) and
within neurons electrically
4. Read over the material on pages 70-71. There is a lot of details herein, but just know a
couple of facts:
5. Note that some drugs directly affect the flow of ions from inside to outside (and vice
versa), while the majority affect neurotransmitters.
6. Be able to draw an illustration of synapse, presynaptic neuron, and postsynaptic neuron.
7. From what substances are neurotransmitters synthesized?
8. Briefly describe the process through which neurotransmitters are released and affect the
next neuron. (don’t include many details, just the basic steps)
9. What is the “lock and key” analogy?
10. Note that neurotransmitters bind to receptors. These receptors may be directly linked to
ion channels, so the neurotransmitter directly opens the channel. Or, the
neurotransmitters indirectly affect the channels through more complex metabolic
processes.
11. Read over the bottom paragraph on page 74. Explain depolarization and
hyperpolarization. Make sure you relate these to excitatory and inhibitory effects.
12. Briefly describe the 2 ways of deactivating the neurotransmitter.
13. What are agonists and antagonists?
14. There are 5 neuropharmacological mechanisms of drugs. List each and describe one
example of how the mechanism might work.
15. Note that ACH is the neurotransmitter at the nerve-muscle junction. Any drug that affects
ACH will affect motor responses.
16. How do the neuroleptics work? Why do some of these drugs cause Parkinsonian
symptoms?
17. What is tardive dyskinesia?
18. What are endorphins and enkephalins? How are they used in the body?
19. What is down-regulation? Up-regulation?
20. What neurotransmitter is involved in schizophrenia? Why might d-amphetamine produce
similar symptoms?
21. In the last section, Poling describes some studies that report direct measurement of
neurochemical processes. However, our knowledge of drug effects on learned behavior
is woefully lacking.
22. Keep in mind that most drugs that function as positive reinforcers ultimately increase DA
activity in the forebrain.
Chapter 5
1. Review the Subjects and Equipment sections. Be able to diagram an operant chamber.
2. What is steady state behavior? Check out Fig 5-2, and comment on why less variability
allows for seeing smaller effects of the Tx.
3. Give an example of a probe design.
4. What is vehicle. Why is it needed?
5. Note the dose-response curves in 5-4. Note also the dependent variable in this graph:
“% of control”. What is this?
6. Explain what “pre-chronic” and “post-chronic” are. What effects of chronic
administrations are shown herein?
7. Suffice it to say that interpreting drug effects is complex (e.g., decreases in response
rate may make the animal more efficient), and no single experiment can identify and
make sense out of behavioral drug effects.
8. How are doses identified?
9. Poling makes a point in the last paragraph on page 95. It has to do with relating doses
that are behaviorally disruptive to doses that are therapeutic. For example say that the
therapeutic dose of a drug is 5 mg/kg, but behavioral disruption occurs only from 10
mg/kg and higher doses. That behavioral disruption occurs from 10 mg interesting, but it
is little clinical significance for the therapeutic effects. Be able to explain this point.
10. How does repeated acquisition work? What is it said to measure?
11. Explain the respondent conditioning procedure.
12. What is the point about show “learning” is defined?
13. What is DMTS and how does it work?
14. What is the Morris water maze?
15. Explain how FCN and FCN-SD work. Which is more sensitive to drugs?
16. Explain the drug self administration experiment with food vs cocaine.
17. Discuss the drug discrimination procedure.
18. Discuss the reaction time procedure.
Chapter 6
1. What are the 3 areas of research?
2. Note that human research must be approved by HSIRB. You need a proposal of the
research that includes risks and a statement of their right to withdraw at any time.
3. What kind of participants are used when studying drugs of abuse?
4. Note that basic research occurs in a laboratory, and involves the use of “arbitrary”
operants such as button pressing.
5. Within-subject designs are typically used. What kind of dose range is used? Stability
criteria?
6. See the Table 6-1. Note the kinds of behavioral measures and the examples for each.
7. What kind of physiological measures are used with humans?
8. Poling describes a study on 114-115. What is the general result?
9. In Poling’s view, what is the difference between objective and subjective events?
Behavior Pharmacologists usually include objective events if subjective events are a
dependent variable.
10. He mentions some issues regarding radical behaviorism and private events. These kind
of behavior analysts acknowledge the existence of these events, and hold that they
should be part of our science of behavior. The question is, how to we come to identify
these events? There are 3 ways that we may come to tact these private events:
a. Tacts of private events are reinforced if there are collateral responses (e.g., kid is
reinforced for saying “I hurt” when he is also crying and holding his head.)
b. Tacts of private events are reinforced if there are public accompaniments (e.g.,
kid is reinforced for saying “I hurt” when we see him get hit with a ball.)
c. We may tact a private event as a case of stimulus generalization, as the private
stimuli may be similar to other public stimuli for which we have established tacts
(e.g., kid learns to say “those are stars” in the presence of stars; then, when hit
in the head, he may say “I see stars” because the stimuli are similar to those of
real life stars)
11. Know the 3 ways that we come to tact private events in #10.
12. Check out the repeated acquisition section. This is similar to the nonhuman procedure.
But, the control procedure is a little different. Explain this.
13. What were the results of the alcohol and cocaine admins, and the combination thereof?
14. Now check out the DMTS procedure. What kind of design was used, and what were the
results?
15. See the term ecological validity. Don’t learn that one. Just substitute a Sidman term for
it.
16. Now, the PR schedule is an interesting application. How did this work in the study by
McLeod and Griffiths? What is the “breaking point”? (interesting term) Note that this is a
single-access procedure; there is no choice component.
17. Discuss the Kelly et al. single access with THC. What was the overall result?
18. Discuss the single-access + choice procedure used by Kelly et al. The single-access
procedure is sometimes called “forced exposure”, as the participants have to experience
the outcomes that are later used in the choice procedure.
19. From the Kelly study, which procedure is more sensitive in identifying potential
reinforcers? Can you relate this to an applied arrangement?
20. Read over the study of nicotine that showed it can function as a positive or negative
reinforcer. This is odd, but Poling makes an important point: specifically, the functions of
a stimulus can indeed depend on the procedures used to evaluate those functions. This
point has applied implications: can you think of one?
21. In conclusion of this section, nicotine can serve as a powerful positive reinforcer,
particularly for those who have prior exposure to the drug. It may be likely to function as
a negative reinforcer for nicotine-naïve people.
22. The section on conditioned reinforcement is heavy on the details. Don’t worry about
these. Just know that drugs can become conditioned reinforcers. See the example of
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cigar smoke. Discuss this. This phenomenon can also occur with the taste of alcoholic
drinks like Scotch.
Review the section on Eos. Start with explaining the 2 effects of an EO.
How can d-amphetamine function as an EO? Are there other EO effects?
What is the a-motivational syndrome? When used to explain “apathy” or “lethargy”, and
resulting behavior, it can easily become an explanatory fiction; that is, the only evidence
of the a-motivational syndrome is the behavior it is said to explain.
Poling mentions a couple of studies that have examined this alleged syndrome. What
were the results? (see table 6-2)
Read over the drug discrimination section. Suffice it to say that humans can discriminate
drug effects. One study used 3 drugs (saline, hydromorphine, and naloxone: an
antagonist).
Chapter 7
Stimulus Properties of Drugs
1. What is the difference between a physical stimulus and functional stimulus? Note that for
Jack Michael, a stimulus is by definition a “functional stimulus.”
2. Give examples of the drugs that have the following functions:
a. US
b. CS
c. SD
d. MO – both establishing and abolishing
e. Positive reinforcer
f. Negative reinforcer
g. Positive punisher
3. What is state-dependent learning? Give an example.
Chapter 8
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Describe some pharmacological variables that might influence drug effects.
What is the fate of a drug?
What are some physical characteristics of a person that might influence a drug effect?
Give an example of an antecedent stimulus that influences drug effects.
What is the point about disruption of behavior under strong vs weak stimulus control?
Describe an example of behavioral tolerance.
What is the reinforcement loss hypothesis? Interpret Fig 8-2.
Give an example of a response form that is related to drug effects.
Give an example of a drug effect that depend on the consequence.
Interpret Fig 8-4. What are rate-dependent effects? What about rate constancy?
What is the point about separating drug effects on behavior and sensitivity to stimuli?
Describe the procedure and results of the study by Hughes et al. Note the use of rules in
this study.
13. Note the important point on page 185 about instructions and placebo. To wit, rules can
alter the behavioral functions of drugs. Be able to explain this in terms of the functionaltering effects of rules, and give examples thereof.
Chapter 9
1. Read over the section on evaluating behavior-change meds vs other meds. What is the
main point herein?
2. What are the 4 essential features of a drug evaluation? Element “c” should sound
familiar to you. To what concept does this refer?
3. Prescribing drugs to special populations in need of protection should involve 3
safeguards. What are they? #2 has special importance for behavior analysts, as we can
assist in this area.
4. The next section deals with experimental designs. What are the 3 factors that influence
the type of design that is ultimately used?
5. Check out Figure 9-1. Be able to discuss these 3 dimensions and how they are
represented in a particular experiment. Where does the typical ABA experiment fit in?
6. Examine the study depicted in Fig 9-3. This is a withdrawal design where the IV was
Thorazine. Looking at the graphs, what is the overall conclusion?
7. What is Poling’s point about the use of anti-psychotics with mentally retarded individuals?
8. Read over the characteristics of an appropriate measure. These can be distilled into a
couple of points: the measure, which should probably be a rate of response, should
measure something of importance and be sensitive to the Tx.
9. Now examine the study on Ritalin using CBM as a DV. See the material below on CBM.
CBM material from http://www.ahsd25.k12.il.us/Assessment/CBM.html
Curriculum-Based Measurement
Curriculum-based measurement (CBM) is a tool for measuring student competency and progress in the
basic skill areas of reading fluency, spelling, math, and written language.
CBM uses "probes" developed from the district curriculum, so that it measures what the students are taught.
Curriculum-based measurement uses four different measures.
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Reading fluency measures how many words a student correctly reads in one minute. In practice,
three reading probes are given; the middle score is reported.
The spelling measure presents 10 words (first grade) or 17 words (second through fifth grades).
Spelling lists are scored for words spelled correctly and correct letter sequences.
The math probe presents sets of mixed or single skill probes with a three-minute time limit. The
student's responses are scored for correct digits written per minute.
For the written expression task, students are presented with a "story starter" and given three
minutes to write a story. The student work is scored for total words written, words spelled
correctly, and correct writing sequences.
10. What kind of design is used? What were the measures? What might you conclude from
looking at the graphs? Note that side effects were also studied using the Stimulant Drug
Side Effects Rating Scale. After reading the text, you will see that in a 2 nd participant, the
most effective dose was 15 mg.
11. Check Fig 9-5. You will see different data and interpretations of the data, depending on
what recording procedure is used. What is the point here?
12. Poling makes the point about the importance of looking at side effects. See below for
information on side effects.
Side effects of antipsychotics
Antipsychotic medication can produce a wide range of side-effects ranging from mildly unpleasant to severe and
potentially debilitating. It is beyond the scope of this article to list every single possible side-effect, but here are a few of
the more common ones.
Extrapyramidal side-effects, or EPS, are the most common side-effects of typical antipsychotic medication and occur
when these drugs affect transmission of the neurotransmitter, dopamine which has a key role in the brain in controlling
movement. Figures for the incidence of EPS vary widely (from 5-50%) but some people are more at risk of certain sideeffects than others. Schizophrenia itself may be a risk factor for developing EPS because altered dopamine transmission
is an inherent feature of the disease. (Atypical antipsychotics are generally associated with few or no EPS.)
Some EPS (such as parkinson-like symptoms) appear within days of beginning treatment and decrease as the brain
adjusts to the drug. Others, e.g. tardive dyskinesia may not appear at first but can develop during the course of treatment.
The types of EPS are listed below.
Parkinson-like symptoms
Characterised by muscle rigidity, tremor, people with symptoms of drug-induced Parkinsonism may appear to
have fixed facial expressions and speak slow manner with a monotonous tone.
Parkinsonism affects up to 4 out of 10 people on typical neuroleptic medication and older people are more
susceptible to the symptoms at lower does of medication. Symptoms appear within days of starting medication
but usually improves spontaneously within 3 months of treatment.
Dystonia
Sustained muscle contraction, contorting and twisting movements are all signs of dystonia. Spasms are often
painful and distressing and can be frightening. In extreme cases, dystonic movements can cause injuries such as
dislocated jaw.
The prevalence of dystonia is rare but is more common in younger people and children. Acute dystonia can
appear within one or two days of beginning treatment and is usually transient. 1.5-2% of people are affected by
persistent or tardive dystonia.
Akathisia
Characterised by jittery and restless movements, akathisia literally means 'can't sit down'. It is one of the more
common EPS side-effects (it affects about a quarter of people on neuroleptic treatment) and can be extremely
distressing.
Tardive dyskinesia
Abnormal facial movements; smacking lips, chewing, sucking, twisting the tongue can all be signs of tardive
dyskinesia (TD). Jerky, often purposeless limb movements are also characteristic signs.
Approximately 1 person in 5 on antipsychotic medication will experience TD, although the incidence increases
with prolonged exposure to neuroleptic medication.
Neuroleptic malignant syndrome
Neuromalignant syndrome (NMS) is a very rare, yet potentially fatal side-effect of neuroleptic medication.
Symptoms include movement disorders typical of EPS and an extremely high temperature and it is important to
detect the symptoms early in order to treat this condition.
Sedation is a common side-effect of neuroleptic treatment. Patients may feel tired, lethargic or weak when they are taking
antipsychotics such as chlorpromazine.
Anticholinergic effects - a dry mouth, feelings of dizziness or light headedness, constipation and blurred vision while
taking antipsychotics are due to the action of these drugs on cholinergic receptors in the brain and in the rest of the body.
Anticholinergic effects may also get worse if patients are also prescribed anticholinergic medication such as procyclidine.
Convulsions - some antipsychotics can increase the risk of convulsions, a factor that is possibly related to their
anticholinergic action.
Weight gain is a relatively common side-effect of antipsychotics and often causes a great deal of distress. It is also
associated with health risks such as high blood pressure, diabetes and respiratory problems.
The mechanism for antipsychotic-related weight gain unknown - they may stimulate the appetite or lead to an altered food
preference for foods rich in fats and carbohydrates. Alternatively, they may alter the body's metabolic rates. Monitoring
diet and instigating a program of exercise may help to keep weight gain to a minimum.
Information to follow on: increased prolactin levels, sexual dysfunction, cardiac effects, hypotension, agranulocytosis and
skin, eye, kidney, gastrointestinal, respiratory, liver disorders and drug interactions associated with antipsychotic use.
What is Neuroleptic Malignant Syndrome?
Neuroleptic malignant syndrome is a life-threatening, neurological disorder most often caused by
an adverse reaction to neuroleptic or antipsychotic drugs. Symptoms include high fever,
sweating, unstable blood pressure, stupor, muscular rigidity, and autonomic dysfunction. In most
cases, the disorder develops within the first 2 weeks of treatment with the drug; however, the
disorder may develop any time during the therapy period. The syndrome can also occur in people
taking anti-Parkinsonism drugs known as dopaminergics if those drugs are discontinued abruptly.
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Poling also makes a good point about drugs interacting with other Tx.
Read over the discussion on page 205. What are the limitations of the MPH studies?
In general, what is the outcome of the study by Gulley and Northrup?
What is the difference between typical and atypical anti-psychotics? How does Clozaril
work, according to the experts?
Read over the study re: Clozaril. Be able to contrast the research method with that of a
within-subject study.
Give an example of taking a psychiatric diagnosis and matching a drug intervention.
Read over the Thompson study with SIB. How was this done, and what were the
results?
Give a couple of examples of behavioral mechanisms of drug action.
In the concluding comments section, and elsewhere, Poling talks about the kinds of
questions that can be answered by between-subject and within-subject designs. What 2
kinds of questions are these?
Chapter 10
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The death data are interesting, and note which drugs cause the most deaths.
What is drug abuse?
What is the point re: licit vs illicit drugs?
Poling makes an interesting point about drug abuse over the millennia. The first example
are the shamans. How did they use drugs?
What is the history of alcohol? Know about the 18th and 21st Amendments. Ask the
elders of your respective families if they recall these events, and if they remember the
WTU (Women’s Temperance Union). They were an important element of the
prohibitionist movement, which is alive and well today in the form of “zero tolerance”.
What does the prohibitionists’ model say about free will? How does this translate into
their recommendations for drug abuse?
What is the disease model of drug abuse? What are the problems with it?
Check Fig 10-1. What are the 3 most used drugs? Note that pot is a distant 4th.
Explain the behavior-analytic model of drug abuse. Relate this to the research results
with nonhumans.
Using this model, talk about why people smoke cigarettes, and why it is so difficult to
abstain. Include in your discussion some mention of concurrent schedules.
Explain the role of imitation in the initial stages of drug taking.
Give an example of how rules might strengthen drug taking. The effect to which Poling is
referred is called a “function-altering” effects. That is, a rule may endow stimuli
associated with drug taking with reinforcing properties.
Talk about how social reinforcers, both positive and negative, can operate to strengthen
drug taking.
How does the drug subculture operate? What sometimes happens to the contingencies
arranged by non-members of the group?
He makes 2 important points about drug takers: 1) drug use may reduce the availability
of other non-drug reinforcers and 2) these people may not have ever learned non-drug
taking behavior that might contact non-drug behavior, such as social skills, work skills,
academic skills, etc.
How can stimuli produced by the drug itself acquire conditioned reinforcing properties?
Explain, using the operant conditioning model, how stress might affect behavior.
Read over the section on the matching law. In its simplest form:
R1
=
R1 + R2
r1
r1+r2
Where R1 is the rate of response for a particular option, R2 is the rate of a second response
option, r1 is the rate of reinforcement for the first option, and r2 is the rate of reinforcement for the
second option. R2 and r2 can refer to the total sum of other responses and reinforcers.
19. What are the implications of a decrease or increase of r2?
20. Read over the section on economic conditions. Suffice it to say that for some people,
increasing the price of a drug will not affect consumption. For others, it will reduce it.
Think of variables that will determine which effect will obtain.
21. Explain how respondent conditioning is involved in the experiences of “needle freaks.”
Here the CRs are in the same direction as the URs.
22. See below for some material on Siegel’s morphine tolerance theory.
The Form Of The Conditioned Response: Drug Tolerance
A. Stimulus Substitution Theory
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Pavlov: conditioning involves formation of a new neurological connection
between the CS and the UR.
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In Pavlov's view, the UR and the CR are exactly the same.
Stimulus substitution theory: CS substitutes for US eliciting the same reflex
response.
B. Difficulties with stimulus substitution theory
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The CR and UR are not always the same.
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CR is weaker than UR
CR appears more slowly than the UR.
Explanation: CS may simply provide weaker stimulation of US area of the
brain.
1. The CS also elicits behavior the US does not.
2. The CR is sometimes the opposite of the UR.
3. Stimulus substitution theory defenders: only responses that involve the
central nervous system should be considered unconditional responses, then
CR and UR are essentially the same.
4. Stimulus substitution theory is generally not accepted as a general
explanation of respondent conditioning.
C. Preparatory Response Theory
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The major challenger to stimulus substitution theory is preparatory
response theory which argues that what is learned during respondent
conditioning is a response that prepares the organism for the appearance of
the US.
D. Classical Conditioning And Drug Tolerance
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Tolerance
is a decrease in the effectiveness of a drug.
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Shepard Siegel due to classical conditioning:
o (a) a compensatory CR that is
o (b) elicited by contextual stimuli.
E. The Morphine Experiments
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Morphine produces analgesia (UR), that is, a decreased response to pain.
Within four trials, the animals had developed tolerance for morphine.
Siegel's explanation of this tolerance is that, in part, it is due to the
compensatory CR associated with the context in which the animal is
injected (sights, sounds, and smells).
According to Siegel, the contextual stimuli acquired the power to produce a
compensatory CR: hyperalgesia an increase in pain sensitivity.
F. The Contextual Experiment
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If Siegel is correct, then it should be possible to test the contextual
explanation by changing the setting on the fourth trial on which tolerance is
observed.
The results showed that these animals behaved as if this was their first shot.
Extinguishing Tolerance (CR)
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If drug tolerance is truly a CR, then we should be able to extinguish it by
withholding the US.
In this case, we would present the CS (the context) in the absence of the US
(the morphine).
The morphine tolerance was partially extinguished.
To completely demonstrate that this was the case, the animals were reinjected with morphine which again produce a modest analgesic response.
G. Human Compensatory CR Experiments The Caffeine Experiments
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One way of demonstrating the effects of a compensatory CR is to present
the CS (smell and taste of coffee--the context) and withhold the US (the
drug, coffee)
Experiment
Regular coffee drinkers served as subjects who drank either a cup of coffee
either with caffeine or without caffeine--the Ss did not know which.
Results
Drank caffeinated coffee: showed a small increase in salivation (as
expected).
Drank coffee without caffeine: showed a substantial decrease in salivation.
Compensatory CR: decrease in salivation.
Experiment
Drink a cup of hot apple juice with caffeine.
Results
Substantial increase in salivation, thus demonstrating that these people had
not developed a general tolerance to caffeine.
Tolerance seen only when the caffeine was associated with its normal
context, the sights, smell, and taste of coffee (the CS).
H. Nonlaboratory Evidence of Compensatory CRs
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Heroin users who overdose or nearly overdose when taking the drug in a
new setting: the compensatory CR that had decreased the effects of the drug
are absent in the new setting.
23. Now explain why a heroin addict is more likely to overdose when the drug is taken in an
unfamiliar environment.
24. How could respondent conditioning be involved in increasing the reinforcing efficacy of a
drug? (2 ways) Check out the experimental evidence for the latter on page 235.
25. The next section deals with several variables that are thought to determine the extent to
which a person will consume large, chronic amounts of alcohol. The first variable is
sensitivity to the reinforcing effects of alcohol. What evidence exists to support this?
26. The next 2 variables are initial sensitivity and how quickly tolerance develops. Give the
general outcome of the study that investigated these variables, and the report involving
the sons of alcoholics.
27. Poling also notes that the contribution of genotype to alcoholism in humans is still
somewhat speculative.
28. Learn the diagram below that describes the metabolic path of alcohol.
Alcohol  Acetaldehyde  Acetyl CoA (this is done by 2 enzymes)
29. So, using the above diagram, how does Antabuse work? What is the behavioral
mechanism of this drug? Note the discussion of the genotype of some people of Asian
decent. They have the same kind of metabolic effect as Antabuse.
30. Poling makes the point that opiate-dependent people are very likely to have a psychiatric
diagnosis. He provides a several reasons why this might be so. What are they?
31. What is the general approach in the community reinforcement procedures?
32. How does the contingency management procedure work? What kind of schedule is this?
33. The voucher system is a variation of the above procedure. How does this work?
34. Be able to interpret Fig 10-2. The studies by Higgins et al. are interesting and provide yet
another useful application of behavioral principles.
35. There are 5 criticisms of behavioral drug treatments. I have listed them below. Be able
to respond to each. By the way, similar objections to behavioral treatments have been
offered for years.
a. $ reinforcers are contrived
b. $ reinforcers might decrease abuse of a particular drug, but “symptom
substitution” will occur.
c. It is immoral!
d. It is costly
e. $ reinforcement procedures don’t help a substantial number of abusers.