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American Psychologist
2016, Vol. 71, No. 8, 670-679
© 2016 American Psychological Association
0003-066X/16/$12.00 http://dx.doi.org/10.1037/amp0000059
Liking, Wanting, and the Incentive-Sensitization Theory of Addiction
Kent C. Berridge and Terry E. Robinson
University of Michigan
Rewards are both “liked” and “wanted," and those 2 words seem almost interchangeable.
However, the brain circuitry that mediates the psychological process of "wanting" a particular
reward is dissociable from circuitry that mediates the degree to which it is “liked.” Incentive
salience or "wanting,” a form of motivation, is generated by large and robust neural systems
that include mesolimbic dopamine. By comparison, “liking," or the actual pleasurable impact
of reward consumption, is mediated by smaller and fragile neural systems, and is not
dependent on dopamine. The incentive-sensitization theory posits the essence of drug
addiction to be excessive amplification specifically of psychological "wanting,” especially
triggered by cues, without necessarily an amplification of “liking.” This is because of
long-lasting changes in dopamine-related motivation systems of susceptible individuals,
called "neural sensitization.” A quarter-century after its proposal, evidence has continued to
grow in support the incentive-sensitization theory. Further, its scope is now expanding to
include diverse behavioral addictions and other psychopathologies.
Keywords: pleasure, desire, addiction, limbic, dopamine
It is now widely accepted that brain mechanisms that
determine how much a reward is "wanted" are dissociable
from those that determine how much the same reward is
"liked." However, that idea, which we first proposed in
1989 as a post hoc explanation for some negative results on
the role of the brain's mesolimbic dopamine system in
pleasure (Berridge, Venier, & Robinson, 1989), originally
came as a surprise even to us. At the time, we and most
other investigators generally accepted the idea that dopa-
mine mediates reward pleasure: the hedonic impact of tasty
food, addictive drugs, and many other rewards. Our early
experiment was simply intended to provide another bit of
evidence for the dopamine-pleasure hypothesis—but results
turned out otherwise.
Editor's note.
Kent C. Berridge and Terry E. Robinson received the
2016 APA Award for Distinguished Scientific Contributions for collabo-
ration. This article is based on an invited presentation at the 124th Annual
Convention of the American Psychological Association, held August 4-7,
2016, in Denver, Colorado.
Author's note. Kent C. Berridge and Terry E. Robinson, Department of
Psychology, University of Michigan.
Our research has been supported by grants from the National Institutes
of Health (DA015188 and MH63649 to Kent C. Berridge, and PO1
DA031656 to Terry E. Robinson). We thank Shannon Cole and Daniel
Castro for redrawing Figure 1.
Correspondence concerning this article should be addressed to Kent C.
Berridge or Terry E. Robinson, Department of Psychology, University of
Michigan, 530 Church Street, Ann Arbor, MI 48109-1043. E-mail:
berridge@umich.edu or ter@umich.edu
670
As background, many studies had found that brain dopa-
mine systems were activated by most rewards, and further
that manipulating dopamine altered “wanting” for rewards,
for example, changing how much animals preferred, pur-
sued, worked for, or consumed the reward (Koob & Le
Moal, 1997; Wise, 1985). Changes in “wanting” were nat-
urally interpreted to reflect corresponding changes in "lik-
ing," based on the assumption that “wanting" was propor-
tional to “liking.” Our approach to measuring pleasure
impact was different, and more similar to how, for millen-
nia, parents have asked their newborn infants whether the
taste of a particular food was enjoyable. We used a natu-
ralistic or ethological assay of sweetness pleasure, based on
affective facial expressions of “liking” (Steiner, 1973).
Sweetness elicits relaxed facial expressions and rhythmic
tongue and mouth expressions of “liking,” whereas bitter-
ness elicits "disgust" gapes and turning away. Those affec-
tive facial expressions to taste are homologous in human
infants, apes, and monkeys, and even rats (Grill & Norgren,
1978; Steiner, Glaser, Hawilo, & Berridge, 2001).
In our initial experiment, we hypothesized that depletion
of brain dopamine in rats via a neurochemical lesion would
reduce "liking" reactions for pleasant tastes, based on the
notion that dopamine mediates “liking.” We expected this
would be reflected as a reduction of hedonic orofacial
expressions elicited by sweetness. But that is not what we
found. We were surprised to find that liking reactions of rats
to sugar taste were completely normal even after depletion
of nearly all brain dopamine (Berridge et al., 1989). The
dopamine lesions did apparently abolish all motivation—the LIKING, WANTING, AND ADDICTION
rats were profoundly aphagic and no longer sought or con-
sumed food rewards, confirming what others had described.
To make sense of these paradoxical findings, we proposed
that mesolimbic dopamine systems mediate “wanting” (in
particular, a psychological process called incentive sa-
lience), but not “liking” for the same reward (Berridge et al.,
1989; T. E. Robinson & Berridge, 1993). A follow-up study
using implanted electrodes to stimulate the same mesolim-
bic systems and raise dopamine levels also failed to enhance
pleasure "liking,” despite quadrupling a rat's “wanting” to
eat food rewards (Berridge & Valenstein, 1991). In humans,
similar brain stimulation by many so-called "pleasure elec-
trodes," upon closer inspection, may also have turned on
"wanting" without “liking,” and may have not been so
pleasant after all (Berridge & Kringelbach, 2015).
In the 1990s, it was a lonely scientific position to main-
tain that dopamine did not mediate pleasure. But in about a
decade, studies of dopamine in human pleasure began to
catch up. For example, eventually it was reported that
suppressing dopamine neurotransmission in people did not
reduce their pleasure ratings of drug rewards, such as co-
caine or amphetamine, even when it reduced their desire to
consume more drug (Brauer & De Wit, 1997; Leyton,
Casey, Delaney, Kolivakis, & Benkelfat, 2005). Similarly,
dopamine suppression in ordinary people or in Parkinson's
disease was reported to not reduce pleasure ratings of tast-
ing delicious foods (Hardman, Herbert, Brunstrom, Munafò,
& Rogers, 2012; Sienkiewicz-Jarosz et al., 2013). Further,
neuroimaging studies began to report that changes in brain
dopamine neurotransmission in people was correlated more
with their subjective ratings of wanting drug and food
rewards than with their liking ratings (Evans et al., 2006;
671
Leyton, 2010; C. T. Smith, Dang, Cowan, Kessler, & Zald,
2016; Volkow et al., 2002). In sum, many studies have now
accumulated supporting our original conclusion that dopa-
mine mediates desire rather than pleasure (Salamone &
Correa, 2012), and it is now rather rare to find an affective
neuroscientist studying reward who still asserts that dopa-
mine mediates pleasure "liking."
Psychological Features of Incentive
Salience: "Wanting"
Note that our use of the word "wanting" so far is often in
quotation marks, because we use that term to refer to a partic-
ular form of desire—namely, mesolimbic incentive salience.
This type of "wanting" is often triggered in pulses by reward-
related cues or by vivid imagery about the reward (Berridge,
2012). The ordinary sense of wanting (without quotation
marks) refers to a cognitive desire with a declarative goal.
However, incentive salience "wanting" is less connected to
cognitive goals and more tightly linked to reward cues, making
those cues attention-grabbing and attractive (Anderson & Yan-
tis, 2013; Hickey & Peelen, 2015). The cues simultaneously
become able to trigger urges to obtain and consume their
rewards (Ostlund, LeBlanc, Kosheleff, Wassum, & Maidment,
2014; Peciña & Berridge, 2013; Zhou et al., 2012). "Wanting"
is mediated largely by brain mesocorticolimbic systems in-
volving midbrain dopamine projections to forebrain targets,
such as the nucleus accumbens and other parts of striatum (see
Figure 1). The intensity of the triggered urge depends both on
the cue's reward association and on the current state of
dopamine-related brain systems in an individual. This in-
teraction allows “wanting” peaks to be amplified by brain
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Prefrontal
Cortex
Striatum
Nucleus
Accumbens
Ventral
Pallidum
Wanting
Liking
Dopamine
Amygdala
Brainstem
Relative Effect
Initial
Use
Addiction
Time
"Wanting"
"Liking"
Figure 1. "Liking" and "wanting” in brain and in addiction. "Wanting" is mediated by a robust brain system
including dopamine projections (left, dark gray), whereas “liking” is mediated by a restricted brain system of
small hedonic hotspots (white; described in Berridge & Kringelbach, 2015). The incentive-sensitization theory
of addiction (right) shows how "wanting" may grow over time independently of "liking" as an individual
becomes an addict, because of sensitization of brain mesolimbic systems. (This figure was adapted by Shannon
Cole and Daniel Castro from T. E. Robinson & Berridge, 1993). This document is copyrighted by the American Psychological Association or one of its allied publishers.
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
672
BERRIDGE AND ROBINSON
states that heighten dopamine reactivity, such as stress,
emotional excitement, relevant appetites, or intoxication
(Anselme, 2016; Berridge, 2012; M. J. Robinson & Ber-
ridge, 2013). State-dependent amplification of incentive sa-
lience is one reason why many addicts find it so hard to stop
at "just one hit." In the face of an amplified urge, the one hit
may turn into many hits, or even a lost weekend. It is also
a reason why stressful states—or even happy life stresses
like winning the lottery—can promote vulnerability to re-
lapse in addiction and related disorders (Sinha, 2013). Ad-
diction is not so much about satisfaction, pleasure, need or
withdrawal, by this view, as it is about "wanting."
Ordinarily, cognitive wanting and incentive salience "want-
ing" go together, so that incentive salience can give heightened
urgency to feelings of cognitive desire. But the two forms of
wanting versus "wanting" can sometimes dissociate, so that
incentive salience can occur either in opposition to a cognitive
desire or even unconsciously in absence of any cognitive
desire. Incentive salience "wanting," in opposition to cognitive
wanting, for example, occurs when a recovering addict has a
genuine cognitive desire to abstain from taking drugs, but still
"wants" drugs, so relapses anyway when exposed to drug cues
or during vivid imagery about them. Nonconscious "wants"
can be triggered in some circumstances by subliminal stimuli,
even though the person remains unable to report any change in
subjective feelings while motivation increases are revealed in
their behavior (Childress et al., 2008; Winkielman, Berridge, &
Wilbarger, 2005).
Motivational Salience in Desire Versus Dread
For readers interested in the psychology of emotion and
motivation, we note another intriguing feature of incentive
salience. This is that “wanting” brain mechanisms can also
operate in a different neurobiological mode to generate an
active coping form of fear (Berridge & Kringelbach, 2015).
Although fear seems almost the psychological opposite of
desire in valence, fearful salience is generated by the same
mesolimbic circuitry as incentive salience. Fearful salience
also makes percepts become attention-riveting, but with a
negative threatening aspect rather than positive attraction, call-
ing out active coping responses (Richard & Berridge, 2011).
This dopamine-related fearful salience has been suggested to
contribute to human paranoia symptoms in schizophrenia
(Barch, Treadway, & Schoen, 2014; Heinz & Schlagenhauf,
2010; Howes & Kapur, 2009) and in psychostimulant-induced
psychosis (Cicero, Docherty, Becker, Martin, & Kerns, 2015).
So Where Does "Liking" Come From
in the Brain?
In contrast to the large and robust "wanting" system in
the brain, a much smaller and functionally fragile system
appears to generate intense pleasure or "liking" reactions.
Experiments in the Berridge lab have established that this
"liking" system comprises a collection of interactive
hedonic hotspots, and this hedonic circuitry may be
shared by diverse pleasures ranging from sensory food
and drug pleasures to human cultural and social pleasures
(Berridge & Kringelbach, 2015). The pleasure-generating
hotspots are anatomically tiny, neurochemically re-
stricted, and easily disrupted-perhaps a reason why
intense pleasures are relatively few and far between in
life compared with intense desires (Castro & Berridge,
2014; Mahler, Smith, & Berridge, 2007; Peciña & Ber-
ridge, 2005; K. S. Smith, Berridge, & Aldridge, 2011).
Each hedonic hotspot is nestled within its larger limbic
structure. For example, a nucleus accumbens hedonic
hotspot is only one cubic millimeter in a rat brain, and
probably about a cubic centimeter in humans. The hot-
spot constitutes only 10% of total nucleus accumbens
volume: The remaining 90% of the nucleus accumbens
lacks any ability to enhance “liking,” though still ro-
bustly causes intense “wanting."
Hedonic hotspots exist in limbic prefrontal cortex, in
orbitofrontal and insula regions, where they may correspond
to human sites that code sensory and higher pleasures (Krin-
gelbach, 2010; Kringelbach, O'Doherty, Rolls, & Andrews,
2003; Small, Zatorre, Dagher, Evans, & Jones-Gotman,
2001). Other hotspots are buried deeper in subcortical brain
structures. Each hedonic hotspot has the special ability
when neurochemically stimulated, such as by opioid or
endocannabinoid neurotransmitters (the brain's natural
heroin-like and marijuana-like signals), to amplify “liking”
reactions, and so make sweetness appear even more enjoy-
able. Dopamine stimulations even in hedonic hotspots, by
contrast, always fail to enhance "liking" (Berridge & Krin-
gelbach, 2015; K. S. Smith et al., 2011)—the role of dopa-
mine seems restricted to "wanting."
Especially crucial to the normal capacity for pleasure
may be a particular hedonic hotspot located in the ventral
pallidum, which lies at the base of the subcortical fore-
brain (K. S. Smith & Berridge, 2007). In addition to
enhancing "liking" for intense pleasure, this ventral pal-
lidal hotspot is the only known site in the brain where a
small lesion eliminates normal pleasure, and reverses the
hedonic impact of sweet sensation from “liked” to, “dis-
gust" (so that afterward, sucrose elicits bitterness-typical
gapes and related negative expressions (Berridge & Krin-
gelbach, 2015; Ho & Berridge, 2014).
Addiction Distorts “Wanting" Versus “Liking”
Our discovery that “wanting” and “liking” are mediated
by dissociable brain systems took us halfway toward the
incentive-sensitization theory of addiction (T. E. Robinson
& Berridge, 1993, 2008). The other half of the journey came
from the discovery around the same time that brain dopa-
mine systems can be enduringly “sensitized” by many drugs This document is copyrighted by the American Psychological Association or one of its allied publishers.
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
LIKING, WANTING, AND ADDICTION
of abuse (cocaine, amphetamine, heroin, alcohol, nicotine,
etc.), not just stimulated while those drugs are actually on
board (T. E. Robinson & Becker, 1986). Mesolimbic sen-
sitization happens especially if the drugs are taken repeat-
edly, and at high doses spaced apart (e.g., in weekend
binges; Kalivas & Stewart, 1991; Post, 1980; T. E. Robin-
son & Becker, 1986). Once induced, sensitization is very
long lasting, and possibly even permanent.
Early research on sensitization in the T. E. Robinson lab
focused particularly on dopamine neurons, and increases in
release of dopamine, but it is now clear that mesolimbic
sensitization changes other neurotransmitters and neurons
as well. For example, drug sensitization also alters gluta-
mate neurons that project from cortex to nucleus accumbens
(Wolf, 2010), which interact with dopamine there, and
similarly are receiving attention as potential targets of future
addiction therapies (e.g. Creed, Pascoli, & Lüscher, 2015;
Roberts-Wolfe & Kalivas, 2015). Sensitization also changes
the physical structure of mesolimbic neurons, such as alter-
ing the shape and number of tiny spines on dendrites of
neurons in nucleus accumbens, which act as their "receiving
antennae" for incoming signals (T. E. Robinson & Kolb,
2004; Singer et al., 2009; Steketee & Kalivas, 2011). Ini-
tially, the main experimental evidence for mesolimbic sen-
sitization by drugs came from studies in rodents, but now
sensitization is well-documented in humans as well (Boi-
leau et al., 2007; Paulson & Robinson, 1995; M. J. F.
Robinson, Fischer, Ahuja, Lesser, & Maniates, 2016;
Vezina & Leyton, 2009).
Functionally, mesolimbic sensitization renders brain
"wanting" systems hyperreactive to drug cues and contexts,
thus conferring more intense incentive salience on those
cues or contexts. Consequently, addicts have stronger cue-
triggered urges and intensely "want" to take drugs (see
Figure 1). “Liking," by contrast, need not increase with
sensitization, and may even decrease. Sensitized "wanting"
can persist for years, even if the person cognitively does not
want to take drugs, does not expect the drugs to be very
pleasant, and even long after withdrawal symptoms have
subsided (Berridge & Robinson, 2011; T. E. Robinson &
Berridge, 2003, 2008). Thus, the central tenet of the
incentive-sensitization theory is that addiction becomes
compulsive when mesolimbic systems become sensitized
and hyperreactive to the incentive motivational properties of
drug cues (Childress et al., 2008; Ostlund et al., 2014;
Witteman et al., 2015; Zhou et al., 2012). This theory of
addiction is specifically meant to explain individuals who
have near-compulsive levels of urge to take drugs, and who
remain vulnerable to a persisting risk of relapse even after a
significant period of drug abstinence.
A sensitized dopamine system is not always hyperactive,
but it is hyperreactive to drug cues and contexts. That
hyperreactivity produces pulses of heightened dopamine
release, brain activations, and motivation that last seconds
673
or minutes (T. E. Robinson & Berridge, 2008; Tindell,
Berridge, Zhang, Peciña, & Aldridge, 2005). Drug contexts
powerfully gate the ability of both drugs themselves and of
discrete cues to elicit sensitized neural hyperreactivity (Ley-
ton & Vezina, 2013; T. E. Robinson, Browman, Crombag,
& Badiani, 1998). This means that surges of intense "want-
ing" are most likely to be triggered when drug cues are
encountered (or imagined) in contexts previously associated
with taking drugs.
Sensitization in Human Addiction
Laboratory neuroimaging studies have shown that even
the oral administration of relatively low doses of amphet-
amine can produce mesolimbic sensitization in people with-
out a history of drug use (Boileau et al., 2006; Leyton &
Vezina, 2013). Furthermore, in nondependent cocaine users,
the ability of self-administered cocaine (taken by the intra-
nasal route) to increase dopamine levels in the ventral
striatum is positively correlated with amount of lifetime
cocaine use, suggesting past use sensitized their dopamine
systems (Cox et al., 2009). However, there is reason to
expect even stronger sensitization from higher street-typical
doses, or by intravenous or smoking routes of consumption
(which deliver drugs to the brain more rapidly than swal-
lowing or snorting), based on animal studies (Allain, Mi-
nogianis, Roberts, & Samaha, 2015). Indeed, addicts tend to
prefer to smoke or inject drugs, because those routes deliver
drugs to the brain more rapidly. Consequently, real-life
addicts may have greater mesolimbic sensitization than so
far demonstrated by laboratory studies in nonusers.
Do human addicts actually show the brain hyperreactivity
to drug cues that is posited by incentive sensitization? The
short answer is “yes.” There have been many reports over
the past 10 years that mesolimbic brain responses to drug
cues, such as viewing photos of drug paraphernalia or of
other people taking drugs, are enhanced in individuals with
addiction (Kühn & Gallinat, 2011). Furthermore, “more
years of cocaine use [are] associated with greater activation
to cocaine cues in ventral striatum" (Prisciandaro et al.,
2014), indicating progressively intense sensitization. Simi-
lar findings have been reported with alcohol use (Claus,
Ewing, Filbey, Sabbineni, & Hutchison, 2011).
We note as a caveat that most reports of such hyperreac-
tivity used functional MRI (fMRI) measures, which do not
directly measure dopamine, but rather oxygenated blood
signals (BOLD), which are used to infer neural activity.
However, recent research confirms that dopamine release
does cause striatal BOLD activations (Ferenczi et al., 2016),
supporting the interpretation that fMRI hyperreactivity to
drug cues in addicts reflects a higher dopamine surge, and
indicates incentive sensitization. Further, several studies
that have used more direct PET measures of dopamine
release in people (i.e., via dopamine displacement of radio- This document is copyrighted by the American Psychological Association or one of its allied publishers.
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
674
BERRIDGE AND ROBINSON
active raclopride from D2 receptors) also confirm that drug
cues do trigger higher increases in dopamine release, and in
fact, “the greater the cue-induced dopamine release the
greater the craving" to take more drugs (Leyton & Vezina,
2013, p. 2004). These intense cue-triggered neural signa-
tures are very much what one would expect based on the
incentive-sensitization theory of addiction.
Disentangling Reports of Mesolimbic Suppression
Versus Sensitization in Addiction
As another caveat, it is only fair to note that some studies
have reported nearly the opposite of sensitized brain re-
sponses as described in the Sensitization in Human Addic-
tion section that is, neural suppression or blunted rise in
dopamine displacement elicited when an addict takes a
drug. Suppressed brain responses are typically not to the
drug cues that trigger urges, but rather to drugs themselves
once actually taken, such as amphetamine or methylpheni-
date (Volkow, Koob, & McLellan, 2016). However, we
caution that two points need to be considered before jump-
ing to a conclusion that addicts have too little brain dopa-
mine, as some have suggested. First, suppression of drug-
elicited brain activation to drugs is by no means a universal
finding. For example, as mentioned, sensitized or increased
dopamine rises elicited by exposure to a drug are also
sometimes reported. For instance, alcohol is reported to
elicit greater dopamine release in the striatum of alcoholics
than in social drinkers (Yoder et al., 2016). Still, suppres-
sion of drug-induced dopamine is found often enough in
addicts to have led some observers to suggest that the
essence of addiction is primarily too-little dopamine in
nucleus accumbens and striatum (Volkow et al., 2016). That
dopamine-deficit suggestion is quite a contrast to incentive
sensitization, and is often wrapped together implicitly with
the older assumption that lower dopamine causes reduced
pleasure and that addicts simply seek pleasure (despite the
emerged consensus that the dopamine pleasure hypothesis
not true). Second, however, partial compensations to exces-
sive dopamine stimulation may occur in the brain after
heavy drug use, which at least for a while can mask the
expression of neural sensitization. We would agree that
compensatory neural suppressions (e.g., receptor downregu-
lation) do accompany heavy drug use, while drug-taking
continues. Suppressions produce tolerance to drug highs
(and to the aversive effects of some addictive drugs—which
permits the person to take higher doses, inducing even more
tolerance). Neural suppressions also produce withdrawal for
a while, once the drug is finally stopped.
However, even the same investigators that report suppres-
sion of responses to drugs often also report the same addicts
show intense neural hyperactivations-not suppressions—to
the drug cues that trigger urges to take drugs. That is, com-
pensatory suppressions of drug-elicited reactions as conse-
quences of overstimulation need not contradict incentive sen-
sitization as the primary mechanism for the compulsive
craving in addiction, consistent with incentive sensitization.
Further, many tolerance-related neural suppressions are merely
temporary. Suppressions are partial compensatory responses to
the high levels of mesolimbic stimulation induced by drugs,
essentially a temporary cellular effort by neurons to turn down
their levels of neurochemical overstimulation. Sensitization
and tolerance can develop simultaneously in the same brain
while drug is being taken, because they have parallel mech-
anisms involving different intracellular signaling cascades.
But many tolerance/withdrawal suppressions are apt to fade
within weeks if drug-taking is stopped. By contrast the
neural changes that cause incentive sensitization do not fade
over months of drug abstinence if anything, sensitization
grows for some time during abstinence (Paulson & Robin-
son, 1995), a phenomenon sometimes called “incubation of
drug craving," which is an increase in relapse vulnerability
after a month or so of drug abstinence (Pickens et al., 2011).
Incubation of craving is impossible to explain by a neural
suppression or withdrawal view of addiction, because those
fade, over a month of abstinence, but is entirely plausible in
light of incentive sensitization. Finally, suppression of neu-
ral responses to drugs may occur mostly in test situations
that are very different from situations in which drugs were
usually taken such as while in a neuroimaging scanner in
a hospital setting (Leyton & Vezina, 2013). By contrast,
neural suppression may be converted into sensitized hyper-
reaction when neuroimagers take efforts to provide realistic
drug-related cues and contexts during the neuroimaging test
(Leyton & Vezina, 2013). Early animal studies showed that
giving a drug in a test environment in which it never before
was experienced can completely prevent the expression of
sensitization, even when it clearly has been induced. By
contrast, a previously drug-associated context enables the
sensitized response to fully reappear again when drug is
retaken (T. E. Robinson et al., 1998). That is, sensitized
"wanting" urges are much more likely to occur in drug-
associated contexts than in biomedical neuroimaging situa-
tions. Recent neuroimaging evidence indicates that drug-
related contexts gate sensitized brain reactions in humans as
well (Leyton & Vezina, 2013). Therefore, it may be crucial
that PET studies of drug-elicited brain responses take steps
to better recreate drug-related contexts and cues in order to
reveal sensitized hyperreactive brain responses to drugs that
would occur in real-life drug situations, and which may
underlie addictive urges to take more drugs. Of course, how
addicts perceive contexts is likely complex, so it might help
to let addicts also actively engage in their drug-taking rituals
(e.g., preparing lines of cocaine to sniff, or preparing an
injection), or to experience diverse drug-related auditory,
smell, taste, or other sensations in order to unmask sensi-
tized hyperreactivity in mesolimbic systems (Cox et al.,
2009). It might also be useful to test with the same drug an/n Need 2 Copies->
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