MONOAMINE FUNCTION IN MONKEYS DURING COCAINE USE

目前尚无针对可卡因成瘾的药物治疗方法。此外，了解可卡因强化行为的机制有助于开发针对人类可卡因成瘾者的情感疗法。可卡因的药理作用是抑制突触前对包括多巴胺和5-羟色胺在内的单胺的再摄取。特定的多巴胺或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-羟色胺再摄取抑制在非人类灵长类动物中对可卡因强化的相对贡献。同时，在动物自我给药的情况下，对非人类灵长类动物进行了微透析实验。同时，在动物在用上述每种药物治疗后自我给予可卡因的情况下进行的微透析实验，将为理解药物相互作用和同时发生的神经化学变化的行为影响提供一种独特的方法。通过解决非人类灵长类动物模型中可卡因强化行为背后的神经化学机制，该项目将使人们更好地理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.