Central toxic effects of chronic ethanol treatment: actions on GABA and benzodiazepine recognition sites.
Prolonged ethanol treatment modifies various neurotransmitter systems. GABAergic neuronal function was particularly affected. On the other hand, clinical reports have indicated an interaction between ethyl alcohol and benzodiazepine receptors. These observations suggest a possible site of action of ethanol at the level of the GABA-benzodiazepine receptor complex. Our results showed that ethanol treatment differentially affected GABA receptor function and benzodiazepine binding sites. When [3H]GABA binding in the cerebellum, striatum and hippocampus was increased, [3H]diazepam binding remained unchanged in the same areas. The possibility of modulation of ethanol effects on GABAergic neurons through benzodiazepine receptors is discussed.
D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D000431:Ethanol / Q000633:toxicity*; D007700:Kinetics; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism; D011485:Protein Binding; D051381:Rats; D011919:Rats, Inbred Strains; D011956:Receptors, Cell Surface / Q000187:drug effects*; D011963:Receptors, GABA-A
D009419:Nerve Tissue Proteins; D011956:Receptors, Cell Surface; D011963:Receptors, GABA-A; D000431:Ethanol