MONOAMINE FUNCTION IN MONKEYS DURING COCAINE USE

描述没有药物治疗可卡因成瘾。此外，了解可卡因强化行为的机制有助于开发人类可卡因成瘾者的情感疗法。皮质醇可抑制突触前单胺（包括多巴胺和5-羟色胺）的再摄取。特异性多巴胺或5-羟色胺单胺再摄取抑制剂可以减弱药物滥用动物模型中可卡因的自我给药。这个项目将探索多巴胺和5-羟色胺再摄取抑制对非人类灵长类可卡因强化的相对贡献。同时，在非人灵长类动物中进行了动物自我给药的微透析实验。结合，微透析实验进行，而动物自我管理可卡因治疗后，与上述药物将提供一个独特的方法来了解药物相互作用和并发的神经化学变化的行为影响。通过解决非人类灵长类动物模型中可卡因强化行为的神经化学机制，该项目将更好地了解特定神经递质系统与可卡因滥用的关系。

DESCRIPTION No pharmacological therapy exists for cocaine addiction. Further, understanding of the mechanism of cocaine-reinforced behavior could aid in the development of an affective therapy for human cocaine addicts. Cocaine acts pharmacologically to inhibit presynaptic reuptake of monoamines including dopamine and serotonin. Specific dopamine or serotonin monoamine reuptake inhibitors can attenuate cocaine self- administration in animal models of drug abuse. This project will explore the relative contributions of dopamine and serotonin reuptake inhibition to cocaine-reinforced in non-human primates. In conjunction, microdialysis experiments performed while animals self-administer in non-human primates. In conjunction, microdialysis experiments performed while animals self-administer cocaine following treatments with each of the above drugs will provide a unique approach to understanding the behavioral effects of drug interactions and concurrent neurochemical changes. By addressing the neurochemical mechanisms that underlie cocaine-reinforced behavior in a non-human primate model, this project will afford greater understanding of the relationship of specific neurotransmitter systems to cocaine abuse.