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.
