[Possible alterations in brain neural network by ethanol].
Advances in the neurosciences over the past two decades have elucidated that alcoholism is a chronic and easily recurring disorder, which is based on brain damage induced by long-term ethanol consumption.  Researchers have identified neural circuits that subsume the actions of ethanol and they have also elaborated many of the intracellular signalling pathways that follow receptor activation by ethanol, suggesting a substantial difference between the addicted brain and non-addicted brain.  However, most of the molecular biological changes, which are likely based on the transition from occasional drinking to alcohol dependence, remain to be elucidated.  This review summarizes the findings on the biological background of alcoholism concerning the brain rewarding system, its related receptors, and the second messenger-mediated signal transduction system within the cells, especially focusing on the cyclic AMP signaling pathway calcium (Ca2+) system in neurons.  In addition, our studies with neural stem cells are introduced to indicate future directions of research on the pathophysiology of alcoholism.
Yamamoto
Megumi
M
Department of Neuropsychiatry, Sapporo Medical University School of Medicine, Minami 1 Nishi 16, Chuo-ku, Sapporo 060-8543, Japan.
Ukai
Wataru
W
Tateno
Masaru
M
Saito
Toshikazu
T
D000437:Alcoholism / Q000209:etiology*; D000818:Animals; D001921:Brain / Q000187:drug effects*; D002118:Calcium / Q000502:physiology; D002454:Cell Differentiation / Q000187:drug effects; D000242:Cyclic AMP / Q000502:physiology; D000431:Ethanol / Q000009:adverse effects*; D006801:Humans; D009415:Nerve Net / Q000187:drug effects*; D015290:Second Messenger Systems / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects; D013234:Stem Cells / Q000166:cytology
D000431:Ethanol; D000242:Cyclic AMP; D002118:Calcium