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Methods Mol Biol. 2003;233:555-70. Related Articles,
Alcohol addiction.
There is increasing evidence for a role of individual protein kinase C (PKC) isozymes in the pathology of
various diseases of the brain (1). For example, it was recently demonstrated that a mutation in PKCgamma
results in Parkinson's disease-like symptoms in rats (2). There is also evidence that alterations in the
expression of PKC isoforms may influence alcohol consumption and the behavioral responses to alcohol
and other drugs of abuse (3-7). However, the paucity of pharmacological ligands that selectively modulate
the activity of individual PKC isozymes has compelled scientists to turn to genetic methods, such as viral
gene delivery, antisense oligonucleotide, and targeted gene-deletion techniques to ascertain the function of
individual PKC isoforms in vivo. Alcohol (ethyl alcohol, or ethanol) has been shown to alter the function
and activity of numerous types of voltage- and ligand-gated ion channels in the central nervous system.
However, it is increasingly apparent that ethanol also affects multiple intracellular signaling pathways. Of
these, signaling by the PKC family of enzymes has received considerable attention. In vitro studies have
shown that acute alcohol exposure can directly inhibit or enhance PKC activity and alter the subcellular
distribution of individual PKC isozymes, whereas chronic exposure to ethanol generally leads to an up-
regulation of PKC expression and/or function (8,9). In this chapter, we discuss several methodologies for
determining ethanol consumption patterns and the behavioral effects of ethanol that are suitable for use in
PKC isoform "knockout" mice. First, we discuss two separate methods of determining voluntary ethanol
intake. We then discuss several behavioral assays for the determination of the acute effects of ethanol on
motor behavior.
Center for Alcohol and Addiction Studies, Brown University, Box G-BH, 02912,
Providence, RI, USA
Alcohol abuse.
Publication Types:
• Review
• Review, Academic