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Previous Article | Next Article
The Journal of Neuroscience, December 1, 2000, 20(23):8701-8709
Involvement of the Extracellular Signal-Regulated Kinase Cascade for Cocaine-Rewarding Properties
Emmanuel Valjent1, 2, Jean-Christophe Corvol3, Christiane Pagès1, Marie-Jo Besson1, Rafael Maldonado2, and Jocelyne Caboche1 1 Laboratoire de Neurochimie-Anatomie, Institut des Neurosciences, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7624, Université Pierre et Marie Curie, 75005 Paris, 2 Laboratori de Neurofarmacologia, Facultat de Cienciès de la Salut i de la Vida, Universidad Pompeu Fabra, E-08003 Barcelona, Spain, and 3 Institut National de la Santé et de la Recherche Médicale U 114, Chaire de Neuropharmacologie, Collège de France, 75231, Paris Cedex 05, France
A central feature of drugs of abuse is to induce gene expression in discrete brain structures that are critically involved in behavioral responses related to addictive processes. Although extracellular signal-regulated kinase (ERK) has been implicated in several neurobiological processes, including neuronal plasticity, its role in drug addiction remains poorly understood. This study was designed to analyze the activation of ERK by cocaine, its involvement in cocaine-induced early and long-term behavioral effects, as well as in gene expression. We show, by immunocytochemistry, that acute cocaine administration activates ERK throughout the striatum, rapidly but transiently. This activation was blocked when SCH 23390 [a specific dopamine (DA)-D1 antagonist] but not raclopride (a DA-D2 antagonist) was injected before cocaine. Glutamate receptors of NMDA subtypes also participated in ERK activation, as shown after injection of the NMDA receptor antagonist MK 801. The systemic injection of SL327, a selective inhibitor of the ERK kinase MEK, before cocaine, abolished the cocaine-induced ERK activation and decreased cocaine-induced hyperlocomotion, indicating a role of this pathway in events underlying early behavioral responses. Moreover, the rewarding effects of cocaine were abolished by SL327 in the place-conditioning paradigm. Because SL327 antagonized cocaine-induced c-fos expression and Elk-1 hyperphosphorylation, we suggest that the ERK intracellular signaling cascade is also involved in the prime burst of gene expression underlying long-term behavioral changes induced by cocaine. Altogether, these results reveal a new mechanism to explain behavioral responses of cocaine related to its addictive properties.
Key words: cocaine; ERK; Elk-1; c-fos expression; striatum; dopamine receptors; reward
Copyright © 2000 Society for Neuroscience 0270-6474/00/20238701-09$05.00/0
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