SOCW 6103 Week 1 Discussion – Discussion: The Evolution of Addiction Models
Discussion: The Evolution of Addiction Models
There are differences on how addiction is seen from a moral failing, with people suffering from addiction shunned for their weakness to addiction being considered a disease that can be treated.
Addiction work incorporates several models for understanding addiction and addictive behavior. Addiction models not only attempt to explain the causes and behaviors of addiction, but they are also used as a basis for treatment. To understand the current approach of addiction treatment, it is essential to study the various historical models of addiction, as each has influenced the understanding and treatment of addiction today. It is also imperative to distinguish between different types of addiction because they may be best described by different models. For example, chemical dependence is a type of indigestive addiction of alcohol or drugs, whereas a process or behavioral addiction is considered a behavioral pattern such as gambling addiction (Capuzzi & Stauffer, 2016).
For this Discussion, you consider how the definitions, perceptions, and treatment of addiction have evolved.
To Prepare:
Go to the Walden Library and locate at least two recent articles discussing the current view of addictions.
Provide a Discussion Post which contains the following content, topics, and headings:
– A comparison between two models from the text that explain how addiction treatment has been viewed.
– Briefly explain the articles you located on current conceptualizations of addiction and identify if there are similarities from the models you found in your additional research.
– Explain how these models have influenced perceptions of and treatment for addiction.
Must contain at least 3 references and citations
Week 1: Introduction to Addiction
Jos is a fifty-two year-old Latino male who has worked for a lumber company for the past 20 years. Recently, Jos’s employer asked him to take a random drug test, and it came back positive for drugs. To keep his job, Jos must be evaluated by an outpatient professional, specializing in addictions. For Jos, seeing someone for help seems like a waste of time, not to mention embarrassing for him. He was taught to keep all his problems within his family, so talking about his problems to an outsider is very uncomfortable for him. Jos does not believe he has a drug problem or needs treatment. He is very angry that he is being forced to participate.
How might Jos’s perceptions of treatment impact the helping process? How might a helping professional today approach Jos to address his perceptions? As you begin your journey as a helping professional working in addictions, it is important to understand the perceptions individuals or clients have about treatment.
This week, you consider treatment models and different drug categories.
Learning Objectives
Students will:
Analyze the progression of addiction treatment models
Analyze the influence of historical events on perceptions of addiction
Analyze the influence of historical events on the role of addiction treatment
Compare different drug categories
Learning Resources
Required Readings
Capuzzi, D., & Stauffer, M. D. (2016). Foundations of addictions counseling (3rd ed.). New York, NY: Pearson Education, Inc.
Chapter 1, “History and Etiological Models of Addiction” (pp. 117)
Berridge, V. (2015). History and its contribution to understanding addiction and society. Addiction, 110, 23-26.
Courtwright, D. T. (2012). Addiction and the science of history.Addiction,107(3), 486492.
Frank, L. E., & Nagel, S. K. (2017). Addiction and moralization: the role of the underlying model of addiction. Neuroethics, 10(1), 129-139.
Haldipur, C. V. (2018). Addiction: A brief history of an idea. Psychological Medicine, 48(8), 1395-1396.
Tallaksen, A. (2017). The narcotic clinic in New Orleans, 191921. Addiction, 112(9), 1680-1685.
Required Media
Laureate Education (Producer). (2012e). Timeline of addiction [Multimedia file]. Retrieved from https://class.waldenu.edu
Discussion: The Evolution of Addiction Models
There are differences on how addiction is seen from a moral failing, with people suffering from addiction shunned for their weakness to addiction being considered a disease that can be treated.
Addiction work incorporates several models for understanding addiction and addictive behavior. Addiction models not only attempt to explain the causes and behaviors of addiction, but they are also used as a basis for treatment. To understand the current approach of addiction treatment, it is essential to study the various historical models of addiction, as each has influenced the understanding and treatment of addiction today. It is also imperative to distinguish between different types of addiction because they may be best described by different models. For example, chemical dependence is a type of indigestive addiction of alcohol or drugs, whereas a process or behavioral addiction is considered a behavioral pattern such as gambling addiction (Capuzzi & Stauffer, 2016).
For this Discussion, you consider how the definitions, perceptions, and treatment of addiction have evolved.
To Prepare:
Go to the Walden Library and locate at least two recent articles discussing the current view of addictions.
Provide a Discussion Post which contains the following content, topics, and headings:
A comparison between two models from the text that explain how addiction treatment has been viewed.
Briefly explain the articles you located on current conceptualizations of addiction and identify if there are similarities from the models you found in your additional research.
Explain how these models have influenced perceptions of and treatment for addiction. Addiction (2000) 95 (Supplement 2), S91 S117
ANIMAL MODELS IN CRAVING RESEARCH
The psychology and neurobiology of addiction:
an incentivesensitization view
TERRY E. ROBINSON & KENT C. BERRIDGE
Department of Psychology (Biopsychology Program), The University of Michigan,
Ann Arbor, MI, USA
Abstract
The question of addiction speci cally concerns (1), the process by which drug-taking behavior, in certain
individuals, evolves into compulsive patterns of drug-seeking and drug-taking behavior that take place at the
expense of most other activities and (2), the inability to cease drug-taking; the problem of relapse. In this
paper current biopsychological views of addiction are critically evaluated in light of the incentive-
sensitization theory of addiction, which we rst proposed in 1993, and new developments in research are
incorporated. We argue that traditional negative reinforcement, positive reinforcement, and hedonic accounts
of addiction are neither necessary nor suf cient to account for compulsive patterns of drug-seeking and
drug-taking behavior. Four major tenets of the incentive-sensitization view are discussed. These are:
(1) Potentially addictive drugs share the ability to produce long-lasting adaptations in neural systems.
(2) The brain systems that are changed include those normally involved in the process of incentive motivation
and reward. (3) The critical neuroadaptations for addiction render these brain reward systems hypersensitive
(sensitized) to drugs and drug-associated stimuli. (4) The brain systems that are sensitized do not mediate
the pleasurable or euphoric effects of drugs (drug liking), but instead they mediate a subcomponent of
reward we have termed incentive salience (drug wanting). We also discuss the role that mesolimbic
dopamine systems play in reward, evidence that neural sensitization happens in humans, and the implications
of incentive-sensitization for the development of therapies in the treatment of addiction.
Introduction
In thinking about the problem of addiction, and
the development of animal models of addiction,
it is important to remember that at some time
many people experiment with a variety of poten-
tially addictive drugs, but most do not become
addicted.1 In other words, mere self-
administration of a drug, by a human or by a
non-human animal, is not tantamount to addic-
tion.2 Indeed, the factors responsible for exper-
imental or casual drug use may or may not be
directly relevant to the problem of addiction.
Drug-seeking and drug-taking in the addict may
involve factors that are qualitatively different
from those that motivate drug-taking in the non-
addict. The question of addiction speci cally
concerns (a) the process by which drug-taking
behavior, in certain individuals, evolves into
Correspondence to: Dr Terry E. Robinson, Department of Psychology (Biopsychology Program), The University
of Michigan, 525 E. University (East Hall), Ann Arbor, MI 48109, USA. Tel: (734) 763 4361; fax: (734) 763 7480;
e-mail: [emailprotected]
Submitted 1st September 1999; initial review completed 16th November 1999; nal version accepted 10th March
2000.
ISSN 09652140 print/ISSN 1360 0443 online/00/08S09127 Society for the Study of Addiction to Alcohol and Other Drugs
Carfax Publishing, Taylor & Francis Ltd
S92 Terry E. Robinson & Kent C. Berridge
compulsive patterns of drug-seeking and drug-
taking behavior that take place at the expense of
most other activities, and (b) the inability to
cease drug-taking, that is, the problem of re-
lapse.2 The purpose of this paper is to explore
one view of the psychological and neurobiologi-
cal mechanisms responsible speci cally for the
development of compulsive patterns of drug use
that de ne addiction, and to update our earlier
treatise on this subject.3
Negative and positive reinforcement models
Most contemporary explanations of addiction
suggest that addicts are motivated to take drugs
(crave drugs) for one of two reasons. As put by
Markou et al.,4 Drug craving is characterized by
both the desire to experience the positive hedo-
nic effects of the drug and the desire to avoid
aversive withdrawal symptoms (p. 176).
That is, it is generally thought that addicts are
motivated to take drugs either for the pleasure
drugs produce (basically to achieve remembered
pleasure), or to avoid the unpleasant conse-
quences of withdrawal. Some authors place the
weight of explanatory burden on the aversive
consequences of discontinuing drug use (the
withdrawal syndrome), and thus on the action of
drugs as negative reinforcers.2,5 7 For example,
Koob and colleagues8 10 have argued that: the
motivation for maintenance of compulsive drug
use requires negative reinforcement processes
(Koob et al.,9 p. 519, italics added) and that,
From a motivational perspective, addiction can
be equated with the development of a negative
affect (Koob,11 p. 13).
Limitations of negative reinforcement models
Despite the intuitive appeal of withdrawal avoid-
ance models many authors have pointed out the
short-comings of negative reinforcement models
in general as explanations for addiction.3,12 15
For example, drugs that do not produce strong
withdrawal syndromes, such as psychostimu-
lants, can be highly addictive. Conversely, there
are drugs that produce tolerance and withdrawal
syndromes but do not support compulsive pat-
terns of use. The latter compounds include some
tricyclic antidepressants, anticholinergics and
kappa opioid agonists.14 Thus, as put by Jaffe,14
there is little correlation between the visibility
or physiological seriousness of withdrawal signs
and their motivational force (p. 9). Another
problem for withdrawal-based explanations is
that drug craving is often elicited by drug admin-
istration itself, in association with euphorigenic
effects, at the moments when withdrawal symp-
toms should be at their weakest. Similarly, in
animals trained to self-administer heroin, re-
instatement of drug-taking behavior following
extinction is more potently elicited by a priming
injection of heroin, which elicits a drug-like ef-
fect, than by the injection of an opioid antago-
nist, which induces withdrawal signs.16,17 For
human addicts, the prolonged cessation of drug
use, during which time withdrawal symptoms
decay, is by no means a guarantee of a cure, as
relapse to compulsive use even long after with-
drawal is over remains a major problem in
addiction.18 In conclusion, although there is no
doubt that under some circumstances the desire
to avoid withdrawal can be a potent motive for
drug use, for these and other reasons many
authors have suggested that models of addic-
tion based on the alleviation of withdrawal symp-
toms (whether physical or psychological) are
neither necessary nor suf cient to explain com-
pulsive drug-seeking and drug-taking behav-
ior.3,14,15
Limitations of behaviorist positive reinforcement
models
In part because of the shortcomings of negative
reinforcement models alternative models have
placed considerable emphasis on the action of
drugs as positive reinforcers.14 Positive reinforcers
are stimuli that have the property of increasing
the probability of behaviors that immediately
precede their presentation. Like many natural
rewards, such as food and water, potentially
addictive drugs have this property. In the drug
abuse literature, however, the Skinnerian con-
cept of positive reinforcement is often invoked,
either implicitly or explicitly, as though it were
an explanation of drug-taking behavior, and even
as an explanation of why drug-taking behavior
becomes more and more compulsive in the
development of addiction. (Why do people take
drugs? Because drugs are positive reinforcers.) But
this is a confusion. It is equivalent to saying
that the reason people take drugs is because
drugs promote drug-taking behavior; the cir-
cularity is obvious.15 It is important to remem-
An incentive sensitization view of addiction S93
ber that positive reinforcement, taken as a
behaviorist concept, is only a description of a
behavioral effect, not an explanation of the effect
(Berridge & Robinson,19 see footnote 3 for de-
tailed discussion). In de ning reinforcement
Skinner himself20 said, The only de ning
characteristic of a reinforcing stimulus is that it
reinforces, and argued that, there is nothing
circular about classifying events in terms of their
effects . But he also said, It would be circu-
lar, however, if we then went on to assert that a
given event strengthens an operant because it is
reinforcing (his italics, pp. 72 3). Or, as put so
well by Dews,21 many things can reinforce
and many things can be maintained by reinforce-
ment; which is ne, of course, provided that we
do not come to suppose that in demonstrating
that an event is a reinforcer we have demon-
strated something more than that the event is a
reinforcer. Any worker studying behavioral
phenomena knows that a reinforcer is de ned
and recognized through its effects on behavior;
the sole criteria are behavioral. But any impartial
observer of the same workers will see that teleol-
ogy, like hope, springs eternal in even a scienti c
workers breast (p. 77). In other words, behav-
iorist reinforcement should not be mistaken to
be an explanation of either drug-taking or addic-
tion in either a physiological or psychological
sense. The critical question relevant for addic-
tion is, what explains it. That is, what effect of a
drug is responsible for its positively reinforcing
behavioral property, and how does it cause the
development of compulsive drug-seeking and
drug-taking habits?
Wise & Bozarth15 suggested that, the only
existing positive reinforcement view of addiction
that can qualify as an explanatory theory
identi es positive reinforcement with drug eu-
phoria (p. 474). In this view (hedonia view)
drugs are addicting because they produce positive
affective states that people label with words such
as pleasure or euphoria, and these states are what
addicts seek. This pleasure-seeking view of ad-
diction is the simple common-sense view of ad-
diction. People want drugs (are motivated to
seek and take drugs) because they like drugs
(because drugs give pleasure). In this view the
motivation to take drugs (drug wanting) is di-
rectly attributable to the ability of drugs to pro-
duce pleasure, i.e. there is a necessary causal
relationship between wanting drugs and liking
drugs.
Limitations of drug pleasure (hedonic reinforcement)
models
It is probably true that often people are initially
motivated to take drugs because of the ability of
drugs to produce positive affective states (and
because their peers are doing it, and for many
other complicated psychosocial reasons), but in
the addict the association between the hedonic
consequences of drug consumption and the abil-
ity of drugs and drug-related stimuli to motivate
behavior often become dissociated, revealing that
the relationship between the motivational force
of drugs and their hedonic consequences may
not be a necessary causal relationship. As Dews21
cautioned many years ago, it was supposed
that the prediction of addiction liability was es-
sentially equivalent to prediction of euphorigenic
power. As with most self-evident ideas, the mere
matter of there being essentially no evidence in
favor of it, and much against it, had little effect
on its acceptance (p. 75).
Perhaps the most compelling evidence against
the idea that the ability of drugs to promote
drug-taking is directly attributable to their sub-
jective pleasurable effects comes from studies
showing that subjective states are often poorly
correlated with drug-taking. First, drug-taking
may increase dramatically over time as an addic-
tion develops, but the pleasure induced by a
given dose of a drug is not reported to increase
(see note 5 in Robinson & Berridge3 for a dis-
cussion of this point). If addicts craved drugs in
proportion to their ability to produce pleasure,
then craving late in addiction ought not to be
stronger then craving after the initial drug ex-
periencebut of course that is not the case.
Secondly, after pharmacological manipula-
tions there is often a dissociation between the
reported subjective effects of cocaine and co-
caine-taking behavior.22 27 For example, Haney
et al.26 reported recently that pergolide decreased
cocaines cardiovascular effects, decreased rat-
ings of its subjective effects (high,
stimulated), increased ratings of I want co-
caine, while having no effect whatsoever on
cocaine self-administration behavior. Similarly,
Haney et al.27 reported: that even a 50% de-
crease in certain of cocaines subjective effects by
ABT-431 did not shift cocaine self-adminis-
tration (p. 108). Along the same lines, Comer et
al.28 reported that doses of intranasal and intra-
venous heroin that maintained the same
breakpoint on a progressive ratio schedule re-
S94 Terry E. Robinson & Kent C. Berridge
sulted in very different subjective ratings of
high.
Thirdly, it has been reported that people will
work for low doses of morphine or cocaine that
produce no subjective pleasure at all; doses that
indeed produce no reported subjective effects of
any kind.22,24,29 In summarizing their ndings
Lamb et al.29 concluded: The reinforcing effects
of morphine can occur in the absence of self-re-
ported subjective effects and thus, do not appear
to be causally related to drug-liking or euphoria
(p. 1172). These kinds of data are very import-
ant because they establish that the motivation to
take drugs (drug wanting) is not always directly
attributable to the subjective pleasurable effects
of drugs (drug liking), and it is possible this is
especially true in addicts. That is, one must
consider the possibility that in addicts the sub-
jective pleasurable effects and the motivational
effects of drugs are merely correlated effects. They
occur together most of the time, but they can be
dissociated and there is no necessary causal
relationship between them.
Incentivesensitization
If compulsive drug-seeking and drug-taking be-
havior are often not motivated by either the
desire to obtain pleasure or by the desire to
relieve withdrawal, then what motivates addic-
tive behavior in these instances? Why do addicts
compulsively seek drugs? We have attempted to
address these questions by proposing the con-
cept of incentive sensitization.3,30 The basic
thesis of the incentive sensitization view of ad-
diction can be summarized in four points.
(1) Potentially addictive drugs share the ability
to produce long-lasting adaptations in neural
systems (i.e. addictive drugs change the
brain).
(2) The brain systems that are changed include
those normally involved in the process of
incentive motivation and reward.
(3) The critical neuroadaptations for addiction
render these brain reward systems hypersen-
sitive (sensitized) to drugs and drug-
associated stimuli.
(4) The brain systems that are sensitized do
not mediate the pleasurable or euphoric ef-
fects of drugs (drug liking), but instead
they mediate a subcomponent of reward we
have termed incentive salience or
wanting.3,19,30 33 It is the psychological
process of incentive salience speci cally that
is responsible for instrumental drug-seeking
and drug-taking behavior (drug wanting).
We have hypothesized that when sensitized,
this incentive salience process produces compul-
sive patterns of drug-seeking behavior.3,30
Through associative learning the enhanced in-
centive value becomes focused speci cally on
drug-related stimuli, leading to more and more
compulsive patterns of drug-seeking and drug-
taking behavior. Furthermore, the persistence of
neural sensitization is hypothesized to leave ad-
dicts susceptible to relapse even long after the
discontinuation of drug use. In the following we
will review some of the evidence for incentive
sensitization, and elaborate some of the major
features of this view of addiction.
Psychomotor sensitization
Most studies showing that the repeated adminis-
tration of drugs of abuse can produce sensitiza-
tion (i.e. an increase in drug effect) involve
measures of the psychomotor activating effects of
drugs, such as their ability to enhance locomotor
activity, rotational behavior or stereotyped motor
patterns.3,34 36 The majority of these studies in-
volve psychomotor stimulant drugs. Studies on
the psychomotor activating effects of drugs are
thought to be relevant to addiction because of
the assumption that the neural substrate that
mediates these effects is either the same as, or at
least overlaps with, the neural substrate respon-
sible for the rewarding effects of drugs.15 This
neural substrate is, of course, the mesotelen-
cephalic dopamine system, and especially do-
pamine projections to the nucleus accumbens
and accumbens-related circuitry (often called the
mesolimbic or mesocorticolimbic dopamine
system).
There is now considerable evidence that the
repeated intermittent administration of psycho-
motor stimulant drugs results in a progressive
increase in their psychomotor activating effects,
and an example of this effect is illustrated in Fig.
1. Although most studies of psychomotor sensi-
tization involve the administration of psychomo-
tor stimulants, such as amphetamine or cocaine,
psychomotor sensitization has been reported
with many other drugs of abuse as well, includ-
ing methylphenidate, fencamfamine, morphine,
An incentive sensitization view of addiction S95
Figure 1. An illustration of three ways of quantifying sensitization of rotational behavior in rats with a unilateral 6-OHDA
lesion given repeated i.p. injections of 3.0 mg/kg of d-amphetamine sulfate (data from Anagnostaras & Robinson73). Left
panel: mean ( 6 SEM) number of rotations per 5-minute interval over 10 consecutive 90-minute test sessions in animals given
amphetamine (open circles) or saline (closed circles). Test sessions were every 3 4 days. Sensitization is indicated by the
progressive increase in drug effect seen with repeated amphetamine treatment. Middle panel: the time course of the behavioral
response when both saline and amphetamine pretreated animals were given a challenge injection of 1.5 mg/kg of
d-amphetamine. The challenge session was 3 4 days after the last (10th) pretreatment session. Sensitization is indicated by
a signi cantly greater behavioral response in amphetamine than in saline pretreated animals. Right panel: sensitization can
also be quanti ed by measuring the magnitude of the shift to the left in the amphetamine doseeffect function in drug versus
saline pretreated animals (see Anagnostaras & Robinson73).
phencyclidine, MDMA, nicotine and ethanol
(for references, see Robinson & Berridge3).
Most directly relevant to the topic of this
volume on alcohol abuse is evidence for sensi-
tization to ethanol. There is relatively little re-
search on this topic, and it is especially dif cult
to study the psychomotor activating effects of
drugs that also have motor depressant effects,
such as morphine or ethanol. With morphine this
problem has been obviated to some extent by
using direct injections of the drug into the ven-
tral tegmental area. Nevertheless, there is a
growing literature that suggests the repeated ad-
ministration of ethanol does indeed induce psy-
chomotor sensitization.37 44 There is also
evidence for cross-sensitization between ethanol
and other drugs of abuse, including reports that
pretreatment with ethanol enhances the sub-
sequent psychomotor effects of cocaine,40 am-
phetamine45 and morphine,46 and that cocaine
pretreatment potentiates ethanols effects.40
Cross-sensitization between stress and ethanol
has also been reported.44 Especially relevant to
the present discussion is evidence that repeated
treatment with amphetamine increases ethanol
intake when rats are tested 3 months after the
cessation of amphetamine treatment,47 suggest-
ing there may be long-lasting sensitization to
ethanols rewarding effects.48,49
Research on the neurobiology of ethanol sensi-
tization is in its infancy, but there are reports
that ethanol sensitization is associated with neu-
roadaptations in dopamine and accumbens-
related circuitry40,46 that are reminiscent of
changes seen with other drugs of abuse. For
example, Nestby et al.46 have reported that re-
peated treatment with cocaine, amphetamine,
morphine or ethanol all increase the electrically
evoked release of dopamine and acetylcholine
from striatal slices in vitro. The extent to which
different drugs of abuse induce similar neuroad-
aptations in brain reward circuitry remains an
open question. It is highly likely, however, that
different drugs will induce different adaptations,
especially at the cellular and molecular level (e.g.
White et al.50). It is possible that the overall
outcome will be similar for the operation of
neural systems that mediate the incentive moti-
S96 Terry E. Robinson & Kent C. Berridge
vational effects of drugs, including ethanol. This
remains an important topic for future investiga-
tion.
Psychomotor sensitization is a very complex
and rich phenomenon with many interesting fea-
tures, most of which are not well understood.
For example, for many drugs sensitization is
typically seen only when drugs are administered
intermittently, and the most robust sensitization
occurs when injections are widely spaced in
time.34 Sensitization is dose-dependent; the most
robust sensitization occurs after treatment with
relatively high doses.51,52 Sensitization is also of-
ten time-dependent.53 That is, sensitization is
typically more evident long after the discontinu-
ation of repeated drug treatment than shortly
after the discontinuation of drug treatment. Per-
haps the most remarkable feature of sensitization
is its persistence. Once they have been sensitized,
animals may remain hypersensitive to the psy-
chomotor activating effects of drugs for months
or years.34,54 There is relatively little parametric
research on this aspect of sensitization, but its
persistence is probably dependent on complex
interactions among the dose administered, the
interval between treatments, the number of
treatments, the route of administration, the en-
vironment in which the drug is given, the sex and
strain of the animal and, of course, what drug is
administered.34,55 57 Finally, it important to em-
phasize that the ability of drugs to induce psy-
chomotor sensitization is not a function of the
fact that in most animal studies the drug is
administered by the experimenter. There are
now a number of reports that drug self-
administration experience also promotes psycho-
motor sensitization.58 60
Individual differences in susceptibility to sensitization
There are two other important features of sensi-
tization that deserve mention. One is individual
variation. There is enormous variation across
individuals in susceptibility to sensitization.56
Even in animal studies, some individuals show
rapid and robust sensitization with a given dose
of a drug, whereas others sensitize very little, if at
all. There are many factors that contribute to
individual variation in the susceptibility to sensi-
tization, including genetic, hormonal and experi-
ential factors. For example, genetic factors have
been implicated by studies showing that there
are marked strain differences in the susceptibility
to psychomotor sensitization in both rats61,62 and
mice.44,56,63 Gonadal hormones have been impli-
cated in studies reporting sex differences in sus-
ceptibility to sensitization,64 66 and these sex
differences are attenuated by castration of male
rats.66,67 Experiential factors have been impli-
cated by studies reporting cross-sensitization be-
tween stress and psychostimulant drugs.44,56,68
The mechanisms by which these factors
in uence susceptibility to sensitization are
largely unknown, although the factors that pre-
dispose animals to sensitization appear to be
different than those that confer acute sensitivity
to drugs.56,63,69 71 Nevertheless, the incentive
sensitization theory posits that factors which ren-
der people susceptible to sensitization will also
contribute to individual variation in susceptibil-
ity to addiction.
Modulation of sensitization by the circumstances
surrounding drug administration
Another important feature of sensitization we
want to emphasize is that sensitization is not an
inevitable consequence of repeated exposure to
drugs. Instead, the ability of drugs to induce or
express sensitization is powerfully modulated by
learning and the circumstances surrounding drug
administration. 72 There are at least two ways that
the circumstances surrounding drug administra-
tion modulate sensitization. The rst is modu-
lation of the expression of neural sensitization
that has already been induced. Perhaps the best
example of environmental modulation of ex-
pression is the phenomenon of context-speci c
sensitization. In studies of this type, typically one
group of animals receives drug injections in a
unique test environment and another group re-
ceives injections in a different environment (of-
ten in its home cage). On the test day all animals
receive a challenge injection in the same environ-
ment (the test environment). Only the animals
treated with drug in the test environment usually
express sensitization. The animals treated with
drug in a different environment often fail to
express sensitization in the test environment,
where drug has never before been experienced.
Thus, the expression of sensitization is said to be
context-speci c.73 76 An implication for hu-
mans is that the expression of neural sensitiza-
tion in addicts can be expected to be strongest in
those contexts in which drugs have often been
taken before.
An incentive sensitization view of addiction S97
Despite this powerful associative (conditioned
stimulus) control over the expression of sensi-
tization there are at least two reasons to believe
that neural sensitization occurs even in the ani-
mals that do not express behavioral sensitization.
The rst is that animals receiving drug treat-
ments in an environment other than the test
environment (e.g. in a third world) develop
normal behavioral sensitization in their drug
treatment environment; they simply do not ex-
press it in a different environment that has never
been paired with drug administration.73 Sec-
ondly, neural sensitization has been described
under conditions that preclude the in uence of
contextual stimuli on the neurobiological ex-
pression of the drug response. For example, evi-
dence for neural sensitization to a number of
drugs has been reported using striatal tissue
slices in vitro and in anaesthetized animals.46,77 81
It appears, therefore, that repeated exposure to
amphetamine may induce neural sensitization
non-associatively, but whether the consequences
of neural sensitization are expressed at a particu-
lar place or time is determined to a lar
