Cocaine, reward, movement
and monoamine transporters
by
Uhl GR, Hall FS, Sora I.
Molecular Neurobiology Branch,
NIDA-IRP, NIH, Baltimore, MD 21224, USA.
Mol Psychiatry 2002 Jan;7(1):21-6

ABSTRACT

Recent evidence enriches our understanding of the molecular sites of action of cocaine reward and locomotor stimulation. Dopamine transporter blockade by cocaine appears a sufficient explanation for cocaine-induced locomotion. Variation in DAT appears to cause differences in locomotion without drug stimulation. However, previously-held views that DAT blockade was the sole site for cocaine reward have been replaced by a richer picture of multitransporter involvement with the rewarding and aversive actions of cocaine. These new insights, derived from studies of knockout mice with simultaneous deletions and/or blockade of multiple transporters, provide a novel model for the rewarding action of this heavily-abused substance and implicate multiple monoamine systems in cocaine's hedonic activities.

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Monoamines, cocaine and rats
A disease of the reward centers?
Cocaine highs and the olfactory tubercle
Does cocaine use damage the pleasure centers?
Dopamine/noradrenaline vs serotonin releasers to treat cocaine dependence

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