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Cocaine, reward, movement and monoamine transporters

Molecular Psychiatry volume 7, pages 21–26 (2002)Cite this article

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 However, previously-held views that DAT blockade was the sole site for cocaine reward have been replaced by a richer picture of multitransporter involvement with the rewarding and aversive actions of cocaine.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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Acknowledgements

The authors are grateful to each of the co-investigators who have contributed to this work, to helpful comments from Dr Steven Goldberg, and to financial support from the NIDA-IRP.

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  1. I Sora

    Present address: Psychopharmacology Laboratory, Tokyo Metropolitan Institute of Psychiatry, Tokyo, Japan

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  1. Molecular Neurobiology Branch, NIDA-IRP, NIH, Baltimore, 21224, MD, USA

    G R Uhl, F S Hall & I Sora

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Uhl, G., Hall, F. & Sora, I. Cocaine, reward, movement and monoamine transporters. Mol Psychiatry 7, 21–26 (2002). https://doi.org/10.1038/sj.mp.4000964

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