Abstract
Cocaine exerts its behavioral actions mainly through inhibition of dopamine reuptake. However, cocaine is a weak and non-selective inhibitor of the monoamine transporters. In addition, many dopamine reuptake inhibitors do not produce psychotropic effects in drug-experienced volunteers. On the other hand, previous evidence indicates more potent effects of cocaine. For example, low nanomolar cocaine regulates dopamine D2 receptor signaling. In planarians, low nanomolar levels of cocaine produces environmental place conditioning. These signaling and behavioral actions of cocaine could not be mediated through the inhibition of monoamine transporters. Furthermore, previous a study describes 16 nM cocaine binding in rat striatal synaptosomes suggesting the existence of a high-affinity receptor for cocaine. However, the identity of such receptor is unknown.
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