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Details

Autor(en) / Beteiligte
Titel
Biochemical and Neurotransmitter Changes Implicated in Alcohol-Induced Brain Damage in Chronic or ‘Binge Drinking’ Alcohol Abuse
Ist Teil von
  • Alcohol and alcoholism (Oxford), 2009-03, Vol.44 (2), p.128-135
Ort / Verlag
England: Oxford University Press
Erscheinungsjahr
2009
Link zum Volltext
Quelle
Applied Social Sciences Index & Abstracts (ASSIA)
Beschreibungen/Notizen
  • The brain damage, which occurs after either chronic alcoholization or binge drinking regimes, shows distinct biochemical and neurotransmitter differences. An excessive amount of glutamate is released into specific brain regions during binge drinking (in excess of 4- to 5-fold of the normal basal concentration) that is not evident during periods of excessive alcohol consumption in chronic alcohol abusers. Increases in glutamate release are only observed during the initial stages of withdrawal from chronic alcoholism (∼2- to 3-fold) due to alterations in the sensitivities of the NMDA receptors. Such changes in either density or sensitivity of these receptors are reported to be unaltered by binge drinking. When such excesses of glutamate are released in these two different models of alcohol abuse, a wide range of biochemical changes occur, mediated in part by increased fluxes of calcium ions and/or activation of various G-protein-associated signalling pathways. Cellular studies of alveolar macrophages isolated from these two animal models of alcohol abuse showed enhanced (binge drinking) or reduced (chronic alcoholization) lipopolysaccharide (LPS)-stimulated NO release. Such studies could suggest that neuroadaptation occurs with the development of tolerance to alcohol's effects in both neurotransmitter function and cellular processes during chronic alcoholization that delay the occurrence of brain damage. In contrast, ‘binge drinking’ induces immediate and toxic effects and there is no evidence of an increased preference for alcohol as seen after withdrawal from chronic alcoholization.

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