By Susan T. Fiske, Daniel L. Schacter, Carolyn Zahn-Waxler

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Even relief from withdrawal symptoms does not account for the compulsive character of drugseeking and drug-taking behavior in addicts or for their vulnerability to relapse after detoxification (especially upon encountering drug cues and contexts). In contrast to aberrant learning theories, we suggest that no abnormality of associative learning explains the compulsive yet flexible behaviors addicts employ in their pursuit of drugs (even if abnormal associations contribute to rigid drug-taking rituals).

We now know that neural sensitization involves many long-lasting changes in NAcc-related reward circuitry. For example, behavioral sensitization is accompanied by an increase in the ability of a number of drugs to promote dopamine efflux in the NAcc (Robinson & Berridge 2000). In addition, dopamine D1 receptors on neurons in the NAcc become hypersensitive after sensitization, presumably further potentiating the mesolimbic dopamine signal (White & Kalivas 1998). However, more than dopamine is involved in reward and sensitization.

Finally, we discuss the notion that druginduced dysfunction of frontocortical systems may impair normal cognition and inhibitory control over behavior, further leading to impaired judgment and promoting impulsivity (Jentsch & Taylor 1999, Robbins & Everitt 1999b). PLEASURE, WITHDRAWAL, AND OPPONENT PROCESSES The most intuitive explanation for addiction is the traditional view that drugs are taken first because they are pleasant, but with repeated drug use homeostatic neuroadaptations lead to tolerance and dependence, such that unpleasant withdrawal symptoms ensue upon the cessation of use.

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