Comorbidity of Schizophrenia and Cocaine Abuse: Phenomenology and Treatment

Marc L. Copersino, MA, Mark R. Serper, PhD


Medscape Psychiatry & Mental Health eJournal. 1998;3(2) 

In This Article

Neuropharmacology of Cocaine

Evidence suggests that the acute pharmacological and neurochemical actions of cocaine on endogenous reward centers generate euphoria, particularly through the stimulation of central dopamine (D) pathways. More specifically, it appears that euphoria results when dopamine reuptake is blocked by cocaine by binding directly to the reuptake site. This results in an increased D concentration in the synaptic cleft and activity of the D1 and D2 receptors.

Research has also shown that cocaine blocks reuptake of serotonin (5-HT), which may also be related to increased cortical activity. Cocaine abstinence following chronic abuse leads to hypersensitivity of dopamine receptors and has been hypothesized to cause dopamine depletion.[3] Therefore, chronic cocaine administration and schizophrenia share elements of a common pathophysiology. Serper and colleagues[4] suggested in 1995 that patients who abuse cocaine can be viewed as conducting a "natural experiment," because both dopamine and 5-HT mediate the symptoms of schizophrenia as well as underlie the reinforcing effects of cocaine.


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