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The Journal of Neuroscience, January 24, 2007, 27(4):791-795; doi:10.1523/JNEUROSCI.4152-06.2007

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Brief Communications
Phasic Dopamine Release Evoked by Abused Substances Requires Cannabinoid Receptor Activation

Joseph F. Cheer, Kate M. Wassum, Leslie A. Sombers, Michael L. A. V. Heien, Jennifer L. Ariansen, Brandon J. Aragona, Paul E. M. Phillips, and R. Mark Wightman

Department of Chemistry and Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-3290

Correspondence should be addressed to R. Mark Wightman, Department of Chemistry and Neuroscience Center, Campus Box 3290, Venable Hall, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-3290. Email: rmw{at}unc.edu

Transient surges of dopamine in the nucleus accumbens are associated with drug seeking. Using a voltammetric sensor with high temporal and spatial resolution, we demonstrate differences in the temporal profile of dopamine concentration transients caused by acute doses of nicotine, ethanol, and cocaine in the nucleus accumbens shell of freely moving rats. Despite differential release dynamics, all drug effects are uniformly inhibited by administration of rimonabant, a cannabinoid receptor (CB₁) antagonist, suggesting that an increase in endocannabinoid tone facilitates the effects of commonly abused drugs on subsecond dopamine release. These time-resolved chemical measurements provide unique insight into the neurobiological effectiveness of rimonabant in treating addictive disorders.

Key words: rimonabant; dopamine; cocaine; nicotine; ethanol; cyclic voltammetry

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Received July 18, 2006; revised Dec. 14, 2006; accepted Dec. 14, 2006.

Correspondence should be addressed to R. Mark Wightman, Department of Chemistry and Neuroscience Center, Campus Box 3290, Venable Hall, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-3290. Email: rmw{at}unc.edu

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