Drug addiction as incentive sensitization - summary of an article by Berridge & Robinson (2011)

Drug addiction as incentive sensitization
Berridge, K. C., & Robinson, T. E. (2011).
Addiction and responsibility, 21-54. The MIT Press.

Addiction and incentive sensitization

Addiction refers specifically to a pathological and arguably compulsive pattern of drug-seeking and drug-taking behaviour, which occupies an inordinate amount of an individual’s time and thoughts, and persists despite adverse consequences. Addicts find it difficult to quit taking drugs, even when they express a strong desire to do so. If they manage to abstain, addicts remain highly vulnerable to relapse for long periods of time.

Drugs themselves can change the brains of susceptible individuals in complex ways. These drug-induced changes contribute to the transition to addiction. Some of these changes, especially those related to mesolimbic sensitization, are very persistent and far outlast other changes associated with tolerance and withdrawal.

Drug-induced changes in the brain alter a number of different psychological processes in parallel, contributing to multiple symptoms of addiction. The incentive-sensitization theory of addiction holds that the most important of these psychological changes is a persistent ‘sensitization’ or hypersensitivity to the incentive motivation effects of drugs and drug-associated stimuli. Incentive sensitization produces a bias of attentional processing toward drug-associated stimuli and a pathological motivation of drug themselves.

An addictive drug is a stimulus that both potently activates the mesolimbic brain system and initiates neurobiological events that enduringly sensitize that system. The intensified ‘wanting’ for drugs is not matched by an intensification of ‘liking’ for the same drugs. This dissociation occurs because brain ‘liking’ mechanisms are somewhat separable from ‘wanting’ mechanisms, even for the same reward.

After sensitization of brain mesolimbic systems, excessive ‘wanting’ can be triggered by drug-associated cues or their mental representations. When combined with impaired executive control over behaviour, perhaps due to drug-induced prefrontal cortex dysfunction, incentive sensitization culminates in the core symptoms of addiction.

What is drug sensitization?

Incentive sensitization refers to particular neurobiological changes in brain mesolimbic dopamine systems and in related structures belonging to the same larger brain circuit that mediate the psychological function of incentive salience (wanting). Sensitization is associated with an increase in the ability of drugs to elevate dopamine neurotransmission in brain regions that receive dopamine inputs, and with changes in the physical structure of neurons in the dopamine-related circuits. It is associated with increases in ‘wanting’ for specific rewards triggered especially when the sensitized individual encounters cues related to those rewards. It is expressed in behavioural seeking and sometimes in subjective ratings of rewards.

Not all individuals are equally susceptible to sensitization. This is determined by many factors. These factors are: genetic factors, hormonal factors, gender differences, previous drug experiences, previous experiences with major stresses in life, and it is also influenced by factors related to the drug itself.

Once induced, sensitization to one drug often crosses to other drugs too. More sensitization is produced by exposure to high doses of drug than to low doses. The repeated but intermittent use of drugs induces greater sensitization than a single dose or even continuous exposure to a drug. It is further facilitated if periods of use are interspersed with periods of abstinence, and it is also influenced by the speed with which the drugs reach the brain and is facilitated by having extended access to drugs that leads to increased intake.

Once neural sensitization occurs, the brain’s mesolimbic dopamine system becomes hyper-reactive to drugs. It is not constantly hyper-reactive in a stable fashion, but can be put temporarily into a hyper-reactive state by exposure to the drug or by exposure to drug-related cues. The effects of drug cues and drugs themselves can interact, such that a small amount of drug can potentiate the influence of drug cues.

Traditional withdrawal-based explanations of addiction

The most intuitive explanation for addiction has long been simply the traditional view that drugs are taken first because they are pleasant and then after repeated drug use, drugs are taken to avoid the unpleasant withdrawal symptoms that would ensue upon the cessation of use. But, this is unlikely to be a complete explanation of addiction because: 1) Drug withdrawal actually may be much less powerful at motivating drug-taking behaviour than people generally think. They are not especially potent in motivating drug-seeking behaviour. There was no previous learning that drug intake can stop withdrawal symptoms. And even after withdrawal symptoms have stopped, the susceptibility to reinstatement continues. 2) There is no explanation of why addicts so often relapse into drug taking again even after they have long been free from withdrawal symptoms.

A better explanation comes from a distinction between ‘liking’ and ‘wanting’. Many potentially addictive drugs initially produce feelings of pleasure, encouraging users to take these drugs again. However, with the transition to addiction there sometimes appears to be a decrease in the role of drug pleasure. It can be that drugs come to be ‘wanted’ more and more even if they become ‘liked’ less and less. Repeated drug use sensitizes only the neural systems that mediate the motivational process of incentive salience (wanting), but not neural systems that mediate the pleasurable effects of drugs.

Aberrant learning as an explanation of addiction?

The nucleus accumbens (NAcc) and dopamine-related circuitry are involved in some aspect of reward learning. Drugs may alter learning processes to cause the transition to addiction. Cues that predict the availability of rewards can powerfully activate NAcc-related circuitry, sometimes even better than the reward itself. Repeated exposure to drugs of abuse facilitates some forms of learning and triggers some of the same types of neuroadaptations in reward-related neurons as seen in learning.

The transition to addiction may result from the ability of drugs to promote aberrant learning.

How does incentive-sensitization theory contrast to learning accounts of addiction?

Learning plays a role to guide aspects of addicted behaviour. It is only one part of the reward process, and probably not the one that contributes most to the pathological pursuit of drugs in addicts.

The most influential type of ‘learning hypothesis’ suggest that compulsivity arises in addiction because drugs facilitate the learning of especially strong automatic stimulus-response (S-R) habits, and by their nature these habits confer compulsivity to behaviour.

Instead, this article argues that a confusion may be involved in calling a pure habit ‘compulsive’. Automatic S-R habits do not become compulsive merely by virtue of being extremely well learned. The defining feature of habits is that they tend to be performed autonomously, without having to think about them. Automatic habits appear only when there is no countervailing purpose to act otherwise. Not matter how many times an action is repeated, repetition cannot by itself make a habit compulsive. For an action to acquire compulsive properties requires something motivational. A compulsive psychological trait is characterized by pathological motivation.

Beyond compulsion, addictive behaviour also displays a high degree of targeted flexibility, which requires a completely different explanatory mechanism from S-R habits, and which again suggests a motivational component.

S-R associations involved in habits are responsible for the automatized habits and rituals involved in consuming drugs once they have been obtained.

How does learning interact with incentive sensitization?

The central thesis of the incentive-sensitization theory of addiction is that repeated exposure to potentially addictive drugs can, in a way that is not reducible to learning, persistently change brain cells and circuits in susceptible individuals and under particular circumstances. After this has developed, the expression of sensitization is powerfully modulated by learning.

The sensitized brain circuits normally regulate the attribution of incentive salience to stimuli, a process involved in motivated behaviour. The nature of these neuro-adaptions is to render these brain circuits hypersensitive in a way that results in pathological levels of incentive salience being attributed to drugs and drug-associated cues.

Learning is an important contributor to the operation of incentive salience mechanisms. The specific 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 objects of pathological desire via associations to that object gained from past experiences and also modulates the expression of neural sensitization at particular places or times.

Pathological motivation arises from the sensitized and non-associative adaptions in brain circuits that mediate incentive-motivational processes. Learning can modulate the expression of those changes. Contextual control may provide an additional mechanism for why addicts will ‘want’ drugs most particularly when they are in drug-associated contexts.

Incentive sensitization can sometimes spill over to other objects.

Other addictions?

There is some reason to believe that over-activation of brain of brain dopamine circuits can overpower certain human cases of excessive ‘wanting’ to have sex, binge eat, and so forth. It is not known whether sensitization-type states ever emerge in any brains in the absence of the person having taken any drugs.

Sensitization or sensitization-like processes might contribute to cases of pathological motivation for gambling, sex, food, and other addictions, but no evidence exists yet.

Relation of incentive sensitization to cognitive dysfunction

Myriad other brain changes contribute to addiction as well. For example, damage or dysfunction in cortical mechanisms can underlie cognitive choice and decision making.

Impairment in 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.

Unpacking some issues that remain

The nature of incentive salience as a ‘wanting’ module

Incentive salience is a ‘wanting’ module. It is just one of several types of what is meant by the word ‘wanting’. It is psychologically most visible in its cue-triggered ‘wanting’ and motivational magnet effects that cause individuals to be strongly attracted to particular reward stimuli. ‘Wanting’ can occur even in the absence of conscious awareness of the reward.

Utility comes in several forms. These are: 1) Predicted, the expectation of how much a future reward will be liked. 2) Decision, what we decide to do. 3) Experienced, what most people think of the term reward. 4) Remembered, the memory of how good a previous reward was in the past. In this framework, incentive salience ‘wanting’ is a pure form of decision utility.

In incentive salience, ‘wants’ are bound closely to precepts. It is typically triggered as a phasic pulse or relatively brief peak upon encountering a reward or a physical reminder of the reward (a cue). It doesn’t require a clear cognition of what is wanted and does not even need to be consciously experienced as a feeling of wanting.

Incentive salience is mediated chiefly by subcortical brain mechanisms.

Incentive salience can be viewed as a motivational transform of a brain signal corresponding to the perceived object of desire or its mental representation. When attributed to a stimulus representation, incentive salience transforms mere memory shapes, smells, or sounds into attractive and attention-riveting incentives.

An incentive stimulus has several distinguishing psychological features. These are: 1) Incentive saliences gives a ‘motivational magnet’ property to stimuli it is attributed to and makes those stimuli attractive and potently able to elicit approach toward them. 2) Stimuli attributed with incentive salience are ‘wanted’, people will work to get them. 3) Incentive salience triggers momentary peaks of intense motivation to obtain a cued reward, often manifest as a ‘surge’ in the instrumental action required to obtain the reward.

Can ‘wanting’ be compulsive?

A motive or want does not qualify as compulsive or addictive in character or purport unless it contravenes or violates a contrary. A compulsive ‘want’ or motive seems self-contradictory.

The possibility of a compulsive ‘want’ arises from the dissociation among components of desire. A person has some choice over the cognitively prized goal but not so much choice over the ‘wanted’ target of incentive salience. If desire is not unitary, one can ‘want’ one thing at the same time as one cognitively wants a different thing.

The dominant cognitive desired need not necessarily switch in every case and sensitized ‘wanting’ can act in the absence of a strong cognitive desire. ‘Wanting’ can act against a dominant cognitive intention or desire. When ‘wanting’ is strong enough, it can take on compulsive properties.

The neural mesolimbic mechanisms for ‘wanting’ seems to involve a synergy between dopamine levels and the external presence of a reward-related event or object. This seems separable from the cortex and other neural systems that mediate much stable cognitive goals and steady-state performance.