Oligodendrocyte myelin glycoprotein (OMgp) in rat hippocampus is depleted by chronic ethanol consumption

Hanayo Okamoto, Kagawa University, Japan
Takanori Miki, Kagawa University, Japan
Kyoung-Youl Lee, Kagawa University, Japan
Toshifumi Yokoyama, Kagawa University, Japan
Hiromi Kuma, Kagawa University, Japan
Zhi-Yu Wang, Kagawa University, Japan
He Gu, Kagawa University, Japan
Hong-Peng Li, Kagawa University, Japan
Yoshiki Matsumoto, Kagawa University, Japan
Satriotomo Irawan, Kagawa University, Japan
Kuldip S. Bedi, Bond University
Yu Nakamura, Kagawa University, Japan
Yoshiki Takeuchi, Kagawa University, Japan

Article comments

Okamoto, Hanayo, Miki, Takanori, Lee, Kyoung-Youl, Yokoyama, Toshifumi, Kuma, Hiromi, Wang, Zhi-Yu, Gu, He, Li, Hong-Peng, Matsumoto, Yoshiki, Irawan, Satriotomo, Bedi, Kuldip S., Nakanmura, Yu and Takeuchi, Yoshiki (2006) Oligodendrocyte myelin glycoprotein (OMgp) in rat hippocampus is depleted by chronic ethanol consumption is published in Neuroscience Letters, Volume 406, Issue 1-2, October 2006, pp. 76-80.
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2006 HERDC submission

Abstract

The hippocampal formation has been shown to be particularly vulnerable to the neurotoxic effects of chronic ethanol consumption. It was hypothesized that this damage was due to the disruption of the expression of neurotrophic factors and certain other proteins within the hippocampus. By using real-time reverse transcription-polymerase chain reaction (RT-PCR) techniques, this study aimed to determine whether chronic ethanol consumption could alter the mRNA expression level of brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF), and oligodendrocyte myelin glycoprotein (OMgp) in the hippocampus. Wistar male rats received an unrestricted access to a liquid diet containing 5% (v/v) ethanol as the sole source of fluid from 10 to 29 weeks of age. Control rats had unlimited access to a liquid diet containing an isocaloric amount of sucrose. We found that chronic ethanol consumption did not cause significant changes in the levels of mRNA for BDNF and GDNF. However, OMgp mRNA showed a significant deficit in ethanol-treated animals. It is suggested that this deficit may be related to the demyelination that is commonly observed in human alcoholics and that this may contribute to the functional and cognitive deficits. Copyright © 2007 Elsevier