Brown E E, Fibiger H C
Department of Psychiatry, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
Psychopharmacology (Berl). 1993;113(1):123-30. doi: 10.1007/BF02244344.
The reinforcing properties of cocaine can readily become associated with salient environmental stimuli that acquire secondary reinforcing properties. This type of classical conditioning is of considerable clinical relevance, as intense drug craving can be evoked by the presentation of stimuli previously associated with the effects of cocaine. Given the large body of evidence that implicates the amygdaloid complex in the learning of stimulus-reward associations, the present experiments examined the effects of quinolinic acid lesions of the amygdala on cocaine-induced conditional locomotion and conditioned place preference (CPP). Destruction of the amygdala did not affect basal or cocaine-induced locomotion, suggesting that the amygdala does not mediate the unconditioned psychomotor stimulant effects of this drug. Preconditioning lesions also failed to affect cocaine-induced conditional locomotion. Specifically, exposure of both lesioned and non-lesioned rats to a cocaine-paired environment produced significant conditional increases in locomotion. This lack of effect was contrasted by a complete blockade of cocaine-induced CPP by the amygdaloid lesions. These data demonstrate that cocaine-induced stimulus-reward conditioning can be differentially affected by lesions of the amygdala.
可卡因的强化特性很容易与具有二级强化特性的显著环境刺激联系起来。这种经典条件作用具有相当大的临床相关性，因为呈现先前与可卡因效应相关的刺激可诱发强烈的药物渴望。鉴于大量证据表明杏仁核复合体参与刺激-奖赏关联的学习，本实验研究了杏仁核喹啉酸损伤对可卡因诱导的条件性运动和条件性位置偏爱（CPP）的影响。杏仁核的破坏不影响基础运动或可卡因诱导的运动，这表明杏仁核不介导该药物的非条件性精神运动兴奋作用。预处理损伤也未能影响可卡因诱导的条件性运动。具体而言，将损伤组和未损伤组大鼠暴露于与可卡因配对的环境中，均产生了显著的条件性运动增加。与这种无影响形成对比的是，杏仁核损伤完全阻断了可卡因诱导的CPP。这些数据表明，杏仁核损伤可对可卡因诱导的刺激-奖赏条件作用产生不同影响。
