Effects of alcohol and acetaldehyde on metabolism and function of neurotransmitter systems in cerebral cortical neurons in primary culture.
Effects of alcohol (ethanol) and acetaldehyde (AcAl) on the metabolism and function of gamma-amino-butyric acid (GABA)ergic and cholinergic systems were investigated using mouse cerebral cortical neurons in primary culture. Exposure to alcohol in vitro had no significant effects on the content of neuroactive amino acids as well as the activities of glutamic acid decarboxylase (GAD), GABA-transaminase (GABA-T), choline acetyltransferase (CAT) and acetylcholinesterase (AChE). In contrast, AcAl showed remarkable reductions of neuroactive amino acids content, and of CAT and AChE activities, but induced no alteration in the activities of GAD and GABA-T. [3H]Flunitrazepam [( 3H]FLN) binding and the stimulatory effect of GABA on [3H]FLN binding were found to be inhibited by in vitro exposure to both alcohol and AcAl, both of which, however, induced no changes in [3H]muscimol binding. These results suggest that the direct actions of AcAl on cholinergic systems in primary cultured neurons may be more potent than those of alcohol. The results described above also suggest that alcohol-induced neurochemical alterations in vivo may be, at least in part, caused by AcAl converted from alcohol in vivo.
D000079:Acetaldehyde / Q000494:pharmacology*; D000818:Animals; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000494:pharmacology*; D051379:Mice; D009474:Neurons / Q000187:drug effects*; D018377:Neurotransmitter Agents / Q000378:metabolism*
D018377:Neurotransmitter Agents; D000431:Ethanol; D000079:Acetaldehyde