MONOAMINE FUNCTION IN MONKEYS DURING COCAINE USE

没有药物治疗存在可卡因成瘾。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。可卡因的药理作用是抑制突触前单胺的再摄取，包括多巴胺和血清素。在药物滥用动物模型中，特异性多巴胺或5 -羟色胺再摄取抑制剂可减弱可卡因的自我给药。该项目将探索多巴胺和血清素再摄取抑制对非人类灵长类动物可卡因增强的相对贡献。同时，在非人类灵长类动物身上进行了微透析实验，同时动物自行给药。与此同时，微透析实验将为理解药物相互作用的行为影响和同时发生的神经化学变化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的神经化学机制，该项目将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.