We present a brief overview of the incentive sensitization theory of addiction.

This posits that addiction is caused primarily by drug-induced sensitization in the brain mesocorticolimbic systems
that attribute incentive salience to reward-associated stimuli. If rendered hypersensitive, these
systems cause pathological incentive motivation (‘wanting’) for drugs. We address some current
questions including: what is the role of learning in incentive sensitization and addiction? Does
incentive sensitization occur in human addicts? Is the development of addiction-like behaviour in
animals associated with sensitization? What is the best way to model addiction symptoms using
animal models? And, finally, what are the roles of affective pleasure or withdrawal in addiction?

At some time in their life, most people try a potentially
addictive drug (e.g. alcohol). However, few become
addicts. Addiction implies a pathological and compulsive
pattern of drug-seeking and drug-taking behaviours,
which occupies an inordinate amount of an individual’s
time and thoughts, and persists despite adverse
consequences (Hasin et al. 2006). Addicts also find it
difficult to reduce or terminate drug use, even when
they desire to do so. Finally, addicts are highly
vulnerable to relapse even after long abstinence and
well after symptoms of withdrawal have disappeared.
Thus, a key question in addiction research is: what is
responsible for the transition to addiction in those few
susceptible individuals?
Over the last 20 years or so there has been increasing
recognition that drugs change the brain of addicts in
complex and persistent ways, so persistent that they
far outlast other changes associated with tolerance
and withdrawal. It is important to identify the brain
changes that cause the transition to addiction from
casual or recreational drug use, and the features that
make particular individuals especially susceptible to the
transition (Robinson & Berridge 1993; Nestler 2001;
Hyman et al. 2006; Kalivas & O’Brien 2008). Persistent
drug-induced changes in the brain alter a number of
psychological processes, resulting in various symptoms
of addiction. We suggested in the incentive sensitization
theory of addiction, originally published in
1993, that the most important of these psychological
changes is a ‘sensitization’ or hypersensitivity to the
incentive motivational effects of drugs and drug-associated
stimuli (Robinson & Berridge 1993). Incentive sensitization
produces a bias of attentional processing
towards drug-associated stimuli and pathological
motivation for drugs (compulsive ‘wanting’). When
combined with impaired executive control over
behaviour, incentive sensitization culminates in the
core symptoms of addiction (Robinson & Berridge
1993, 2000, 2003). Incentive sensitization has drawn
considerable interest in the past 15 years and, therefore,
we thought it worthwhile to update our perspective.
We present here a brief and idiosyncratic overview
of this view of addiction and raise some current issues

The central thesis of the incentive sensitization theory
of addiction (Robinson & Berridge 1993) is that
repeated exposure to potentially addictive drugs can,
in susceptible individuals and under particular circumstances,
persistently change brain cells and circuits
that normally regulate the attribution of incentive
salience to stimuli, a psychological process involved in
motivated behaviour. The nature of these ‘neuroadaptations’
is to render these brain circuits hypersensitive
(‘sensitized’) in a way that results in pathological levels
of incentive salience being attributed to drugs and
drug-associated cues. Persistence of incentive sensitization
makes pathological incentive motivation
(wanting) for drugs last for years, even after the
discontinuation of drug use. Sensitized incentive
salience can be manifest in behaviour via either implicit
(as unconscious wanting) or explicit (as conscious
craving) processes, depending on circumstances.
Finally, the focus on drugs in particular in addicts is

produced by an interaction between incentive salience

mechanisms with associative learning mechanisms that
normally direct motivation to specific and appropriate
targets. Learning specifies the object of desire, but it is
important to note that learning per se is not enough for
pathological motivation to take drugs. Thus, we argue
that pathological motivation arises from sensitization of
brain circuits that mediate Pavlovian conditioned
incentive motivational processes (i.e. incentive sensitization).
However, it is important to emphasize that
associative learning processes can modulate the
expression of neural sensitization in behaviour at
particular places or times (and not others), as well as
guide the direction of incentive attributions. This is why
behavioural sensitization is often expressed only in
contexts in which the drugs have previously been
experienced (Stewart & Vezina 1991; Anagnostaras &
Robinson 1996; Robinson et al. 1998), and may
reflect the operation of an ‘occasion-setting’ type of
mechanism (Anagnostaras et al. 2002). Learning might
be viewed as layered onto basic sensitization processes
in a top-down fashion, similar to how learning regulates
the expression of such non-associative motivation
processes as stress and pain. The contextual control
over the expression of sensitization provides an
additional mechanism that accounts for why addicts
‘want’ drugs most particularly when they are in drugassociated
Finally, by spreading beyond the associative focus of
wanting on drug targets, incentive sensitization can also
sometimes spill over in animals or humans to other
targets, such as food, sex, gambling, etc. (Mitchell &
Stewart 1990; Fiorino & Phillips 1999a,b; Taylor &
Horger 1999; Nocjar & Panksepp 2002). For example,
treatment with dopaminergic medications in some
patient populations can lead to a ‘dopamine dysregulation
syndrome’ (DDS) that is manifest not only by
compulsive drug use but also sometimes by ‘pathological
gambling, hypersexuality, food bingeing . and
punding, a form of complex behavioral stereotypy’
(Evans et al. 2006, p. 852).
(a) Incentive sensitization: more than just
It has become popular to refer to addiction as a ‘learning
disorder’ (Hyman 2005), but we think that this phrase
may be too narrow to fit reality. Learning is only one
part of the process and probably not the one that
contributes most to the pathological pursuit of drugs.
The most influential type of ‘learning hypothesis’
suggests that drugs promote the learning of strong
‘automatized’ stimulus–response (S–R) habits, and it is
then supposed that by their nature S–R habits confer
compulsivity to behaviour (Tiffany 1990; Berke &
Hyman 2000; Everitt et al. 2001; Hyman et al. 2006).
However, it is difficult to imagine how any influence
of drugs on learning processes alone could confer
compulsivity on behaviour, unless an additional
motivational component was also involved, and S–R
habits by definition are not modulated by motivational
factors (Robinson & Berridge 2003). Do automatic
S–R habits really become compulsive merely by virtue
of being extremely well learned? We have doubts.
Strong S–R habits do not necessarily lead to compulsive
behaviour: activities such as tying shoes, brushing
teeth, etc. are not performed compulsively by most
people, even after being performed more than 10 000
times. Additional motivational processes seem needed
to explain why an addict waking up in the morning with
no drug spends the day engaging in a complex and
sometimes new series of behaviours, such as scamming,
stealing and negotiating, all seemingly motivated
to procure drug. Addicts do what they have to do and
go where they have to go to get drugs, even if actions
and routes that have never been performed before are
required. Such focused yet flexible behaviour in
addiction shows pathological motivation for drugs
that cannot be explained by evoking S–R habits.
Indeed, a strict S–R habit theory would require the
addict, upon waking up in the morning with no drug
available, to engage ‘automatically’ in exactly the same
old sequence of habitual actions they used previously to
get drugs, whether the actions were currently effective
or not. Yet addicts in the real world are not S–R
automatons; they are, if nothing else, quite resourceful.
On the other hand, everyone must agree that S–R
habits probably contribute to the automatized
behaviours and rituals involved in consuming drugs
once obtained (Tiffany 1990), and it has been shown
that treatment with drugs facilitates the development
of S–R habits in animals (Miles et al. 2003; Nelson &
Killcross 2006), perhaps via recruitment of the dorsal
striatum (Everitt et al. 2001; Porrino et al. 2007). We
also note that habits may be especially prominent in
standard animal self-administration experiments,
where only a single response is available to be
performed (e.g. press a lever) thousands of times in a
very impoverished environment to earn injections of
drugs. Thus, we think studies on how drugs promote
the learning of S–R habits will provide important
information about the regulation of drug consumption
behaviour in addicts, but this is not the core problem
in addiction.
(b) Relation of incentive sensitization to cognitive
The incentive sensitization theory focuses on sensitization-
induced changes in incentive motivational processes
and related changes in the brain, but we have
acknowledged that other brain changes contribute
importantly to addiction too, including damage or
dysfunction in cortical mechanisms that underlie cognitive
choice and decision making (Robinson & Berridge
2000, 2003). Many studies have documented that
changes in ‘executive functions’, involving howalternative
outcomes are evaluated and decisions and choices made,
occur in addicts and animals given drugs (Jentsch &
Taylor 1999; Rogers & Robbins 2001; Bechara et al.
2002; Schoenbaum & Shaham 2008). We agree that the
impairment of executive control plays an important
role in making bad choices about drugs, especially when
combined with the pathological incentive motivation
for drugs induced by incentive sensitization.

In conclusion, addiction involves drug-induced
changes in many different brain circuits, leading to
complex changes in behaviour and psychological
function.We have argued that the core changes leading
to addiction occur when incentive sensitization
combines with defects in cognitive decision making
and the resulting ‘loss of inhibitory control over
behaviour and poor judgement, combined with sensitization
of addicts’ motivational impulses to obtain
and take drugs, makes for a potentially disastrous
combination’ (Robinson & Berridge 2003, pp. 44–46).
Thus, bolstered by the evidence that has accumulated
over recent years, we remain confident in concluding
‘that at its heart, addiction is a disorder of aberrant
incentive motivation due to drug-induced sensitization
of neural systems that attribute salience to particular
stimuli. It can be triggered by drug cues as a learned
motivational response of the brain, but it is not a disorder
of aberrant learning per se. Once it exists, sensitized
wanting may compel drug pursuit whether or not an
addict has any withdrawal symptoms at all. And
because incentive salience is distinct from pleasure or
liking processes, sensitization gives impulsive drug
wanting an enduring life of its own’ (Robinson &
Berridge 2003).

For further information:Addiction_Theory2