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The Journal of Neuroscience, October 1, 1998, 18(19):7996-8002

Decreased Presynaptic Sensitivity to Adenosine after Cocaine Withdrawal

Olivier Manzoni^{1, 2}, Didier Pujalte¹, John Williams², and Joël Bockaert¹

¹ Centre National de la Recherche Scientifique, Unité Propre de Recherches 9023, 34094 Montpellier Cedex 05, France, and ² Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201.

The nucleus accumbens (NAc) is a site mediating the rewarding properties of drugs of abuse, such as cocaine, amphetamine, opiates, nicotine, and alcohol ( ). Acute cocaine has been shown to decrease excitatory synaptic transmission mediated by the cortical afferents to the NAc (), but the effects of long-term cocaine treatment and withdrawal have not been explored. Here, we report that long-term (1 week) withdrawal from chronic cocaine reduced the potency of adenosine to presynaptically inhibit glutamate (Glu) release by activating adenosine A1 receptors. Adenosine A1 receptors were not desensitized, because the potency of the metabolically stable adenosine analog N⁶-cyclopentyl-adenosine was unchanged after chronic cocaine withdrawal. When adenosine transporters were blocked, the potency of adenosine to inhibit Glu release from naive and cocaine-withdrawn NAc slices was similar. These results suggest that one of the long-term consequences of cocaine withdrawal is an augmented uptake of adenosine. This long-lasting change expressed at the presynaptic excitatory inputs to the medium spiny output neurons in the NAc may help identify new therapeutic targets for the treatment of drug abuse.

Key words: nucleus accumbens; chronic cocaine; adenosine; transporter; withdrawal; drug abuse

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Copyright © 1998 Society for Neuroscience  0270-6474/98/18197996-07$05.00/0

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