Professor Barry Everitt

My research is in the general area of behavioural neuroscience and is concerned with the neural and psychological mechanisms underlying learning, memory and motivation. My major research focus is the neuropsychology of drug addiction and is funded by the Medical Research Council. There are several key themes to this research: (i) the impact of learning on drug addiction – both its development and its persistence. For example, individuals who initially take drugs do so voluntarily (in psychological terms it is ‘goal-directed’); subsequently, prolonged bouts of drug taking, in some individuals, result in a loss of control over drug intake and in time it becomes a compulsive habit that is extremely difficult to relinquish. We have shown that this transition from initial, voluntary drug use to the compulsive drug taking, addicted state occurs through the progressive engagement of different pavlovian and instrumental learning systems in the brain and we are continuing to investigate this issue at a cellular and systems level. (ii) Only a small proportion of individuals who take drugs go on to become addicted and they can be considered as vulnerable. Research in our laboratory has shown that behavioural impulsivity is a vulnerability characteristic for addiction: impulsive individuals more readily escalate their cocaine intake and are those most likely to develop compulsive drug seeking and taking, which persists in the face of adverse outcomes. Impulsivity, we have shown, is associated with reduced levels of the D2 subtype of dopamine receptor in a specific brain area, the nucleus accumbens. (iii) Drug cues – stimuli that have become associated with the effects of self-administered drugs through pavlovian conditioning (these include not only the paraphernalia used by drug addicts, but specific places and even people) – also exert a powerful control over addictive behaviour. These cues elicit drug craving and they can precipitate relapse to a drug-taking habit in otherwise abstinent individuals. We have studied extensively the neural systems underlying these pavlovian influences on drug seeking. (iv) When individuals retrieve drug-associated memories, for example when they are exposed to drug-associated stimuli, the retrieved memory enters a labile state from which it must be restored, or reconsolidated through a new round of protein synthesis in the brain. This means that maladaptive drug-associated memories can be disrupted when they are made labile at retrieval. In our recent research we have shown both the underlying neural and cellular mechanisms involved, and also that disrupting such maladaptive memories can prevent subsequent drug seeking and relapse. Thus, disrupting drug memories in a clinical setting might provide a future treatment for drug addiction – and also other neuropsychiatric disorders characterized by intrusive and maladaptive memories, such as post-traumatic stress disorder.