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The Journal of Neuroscience, July 15, 2001, 21(14):5297-5303

The cAMP-Protein Kinase A Signal Transduction Pathway Modulates Ethanol Consumption and Sedative Effects of Ethanol

Gary Wand1, 2, Michael Levine1, 3, Larry Zweifel1, William Schwindinger5, and Ted Abel4

Departments of 1 Medicine, 2 Psychiatry, and 3 Pediatrics, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, 4 Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, and 5 Weis Center for Research, The Geisinger Clinic, Danbury, Pennsylvania 17822

Ethanol and other drugs of abuse modulate cAMP-PKA signaling within the mesolimbic reward pathway. To understand the role of the cAMP-PKA signal transduction in mediating the effects of ethanol, we have studied ethanol consumption and the sedative effects of ethanol in three lines of genetically modified mice. We report that mice with the targeted disruption of one Gsalpha allele as well as mice with reduced neuronal PKA activity have decreased alcohol consumption compared with their wild-type littermates. Genetic reduction of cAMP-PKA signaling also makes mice more sensitive to the sedative effects of ethanol, although plasma ethanol concentrations are unaffected. In contrast, mice with increased adenylyl cyclase activity resulting from the transgenic expression of a constitutively active form of Gsalpha in neurons within the forebrain are less sensitive to the sedative effects of ethanol. Thus, the cAMP-PKA signal transduction pathway is critical in modulating sensitivity to the sedative effects of ethanol as well as influencing alcohol consumption.

Key words: alcohol; sedation; adenylyl cyclase; protein kinase A; cAMP; alcoholism

Copyright © 2001 Society for Neuroscience  0270-6474/01/21145297-07$05.00/0


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