Changes in Ca2+-dependent protein kinase C isoforms induced by chronic ethanol treatment in mice

• Published in: Neuroscience letters 2001-07, Vol.307 (2), p.85-88
• Main Authors: NARITA, Minoru, TAMAKI, Hiroko, KOBAYASHI, Misato, SOMA, Miho, NARITA, Michiko, SUZUKI, Tsutomu
• Format: Article
• Language: English
• Subjects: Alcohol-Induced Disorders, Nervous System - enzymology; Alcohol-Induced Disorders, Nervous System - pathology; Alcohol-Induced Disorders, Nervous System - physiopathology; Alcoholism and acute alcohol poisoning; Animals; Biological and medical sciences; Brain - drug effects; Brain - enzymology; Brain - physiopathology; Brain Chemistry - drug effects; Brain Chemistry - physiology; Calcium - metabolism; Calcium Signaling - drug effects; Calcium Signaling - physiology; Ethanol - pharmacology; Frontal Lobe - drug effects; Frontal Lobe - enzymology; Frontal Lobe - physiopathology; Male; Medical sciences; Mice; Mice, Inbred C57BL; Nucleus Accumbens - drug effects; Nucleus Accumbens - enzymology; Nucleus Accumbens - physiopathology; Olfactory Pathways - drug effects; Olfactory Pathways - enzymology; Olfactory Pathways - physiopathology; Protein Isoforms - drug effects; Protein Isoforms - metabolism; Protein Kinase C - drug effects; Protein Kinase C - metabolism; Toxicology
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(01)01939-5

Protein kinase C (PKC) has been shown to regulate ethanol sensitivity. The goal of the present study was to ascertain whether chronic in vivo ethanol treatment could affect PKC isoforms in the mouse brain. We measured the protein level of membrane-bound PKC isoforms following chronic ethanol treatment using Western blotting. The protein level of membrane-bound PKCalpha and PKCgamma isoforms, which are defined as Ca2+-dependent PKC isoforms (cPKC), in the limbic forebrain during chronic ethanol treatment was significantly increased, whereas the levels of both were significantly decreased in the frontal cortex. By contrast, there was no change in PKCepsilon, a Ca2+-independent PKC isoform, in both areas. These findings suggest that the change in membrane-bound cPKC in the limbic forebrain and frontal cortex may play substantial roles for the development of ethanol dependence.