Brain Dopamine Transporter Messenger RNA and Binding Sites in Cocaine Users

Abstract

ACUTELY, COCAINE binds to the dopamine transporter (DAT) and inhibits the normal re-uptake of released dopamine from the synaptic cleft.¹ Increased synaptic dopamine in the striatum and the prefrontal cortex is believed to be critical in sustaining cocaine self-administration in animals and may underlie the subjective experience of euphoria in human users.^2,3 Results of recent postmortem experiments in human cocaine users show that chronic cocaine exposure leads to increased cocaine binding sites on the DAT in the striatum.^4,5 This perturbation could conceivably contribute to chronic cocaine-induced clinical phenomena, including binging, withdrawal anhedonia, and craving.