NEURONAL PLASTICITY AND DRUG-ADDICTION

Addictive drugs act as a discriminative stimulus and induce positive r einforcement. In concert with psychomotor stimulatory effects these ac tions are responsible for their habit-forming action in experimental a nimals and humans. Factors such as genetic predisposition, stress, pha rmacological pretreatment and social context may deteriorate a previou sly controllable behaviour into compulsive drug-seeking dominated by t he uncontrollable desire to take a drug (craving). The introduction of concepts of neuronal plasticity in addiction research has lead to imp ortant therapeutical consequences. Novel compounds and new regimes for drug treatment to prevent activity-dependent long-term changes, or to facilitate extinction in drug-sensitized neuronal systems, are emergi ng; Recently anti-craving substances have been registered for relapse prophylaxis in weaned alcoholics in various European countries (acampr osate) and the United States (naltrexone). Acamprosate and the opioid antagonist naltrexone most likely reduce alcohol abuse through differe nt neuronal mechanisms. A synopsis of data from behavioural and molecu lar studies suggests the involvement of long-lasting adaptations in br ain-reinforcement systems through which conditioned cues can, even aft er several years of drug abstinence, reinstate a former acquired addic tive behaviour.