Chronic ethanol intake and synaptosomal glutamate binding activity.
The studies presented above add further support to the notion that one of ethanol's most important sites of activity may be the plasma membrane of cells. In addition, they provide an example of how ethanol's effects on these membranes may affect the function of protein molecules associated with nerve cell membranes such as the receptive sites for the putative excitatory neurotransmitter L-glutamic acid. The result of chronic ethanol administration is an apparently enhanced sensitivity to glutamate action in the CNS as measured by either the increases in L-glutamate binding activity or the increased Ca2+ mobilization as a result of glutamate interaction with the synaptosomal membranes. Both of these processes exhibit an enhancement of the maximum response with little or no change in the KD for binding of L-glutamic acid to its receptor site. Finally, it was demonstrated by means of in vivo experiments that there is an apparent sensitization to glutamate during the induction of ethanol dependence, and that this enhanced sensitivity may be causally linked to some of the signs of the post withdrawal CNS hyperexcitability.
D000437:Alcoholism / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D000431:Ethanol / Q000494:pharmacology*; D005971:Glutamates / Q000378:metabolism*; D006801:Humans; D007608:Kainic Acid / Q000494:pharmacology; D007700:Kinetics; D010433:Pentylenetetrazole / Q000494:pharmacology; D051381:Rats; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism*
D005971:Glutamates; D000431:Ethanol; D007608:Kainic Acid; D002118:Calcium; D010433:Pentylenetetrazole