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This study investigated the hypothesis that increases in monoaminergic neurotransmitter levels in the brain of chronically treated rats might be due to a redistribution of vesicular monoamine transporter type 2 (VMAT2) protein from the synaptic vesicles where it concentrates the monoamines into storage vesicles. Vervet monkeys were tested for self-administration of cocaine under a progressive ratio schedule of reinforcement. Four separate groups of vervet monkeys (M(age) = 8.0 +/- 0.1 years, range = 4-10 years) were exposed for one year to daily treatment with an i.v. infusion of cocaine (10 mg/kg body wt/hour) or saline for one hour. Since cocaine self-administration is known to produce a 30 to 50% increase in tyrosine hydroxylase (TH) expression and a 30% increase in dopamine transporter (DAT) levels in the caudate putamen (CP), we measured changes in the respective levels of TH and VMAT2 after 4, 8, and 12 months of chronic treatment. DAT levels increased by 16.2% after 8 months and 19.4% after 12 months in CP. TH levels increased by 37.5% after 8 months and 34.7% after 12 months. VMAT2 levels in the CP were significantly increased (32.6% at 8 months and 28.4% at 12 months), in the nucleus accumbens (45.5% at 8 months and 33.3% at 12 months), and in the amygdala (35.8% at 8 months and 33.9% at 12 months), and in the striatum (43.9% at 12 months). Evidence is presented indicating that the observed VMAT2 increases in the CP and amygdala were due to the actions of cocaine. The data indicate that the hypothesis of a redistribution of VMAT2 from synaptic to storage vesicles due to chronic cocaine treatment may be the most reasonable explanation for the observed
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