Labeling of rat brain synaptosomal phosphatidyl serine in the after state of acute alcoholic intoxication and in the withdrawal state.
The synaptosomal phosphatidyl serine labeling by 14-C-serine after elimination of a single dose of 6 g EtOH/kg b.w. and after a prolonged ethanol period (8-11 g EtOH/kg b.w. for 8 days) was studied in vivo. In both experimental groups the 14-C-labeling of the phosphatidyl serine is decreased as compared with the controls. There is a great deal of evidence which implicates that phosphatidyl serine plays a major role in neural excitation providing ion exchanges sites which control the sodium current, known to be sensitive to ethanol. These ethanol induced changes in phosphatidyl serine labeling may be reflected functionally in the impulse conduction and increased sensitivity in the withdrawal state. These changes are suggested to be consequences of the primary membrane fluidity increasing properties of ethanol.
D000435:Alcoholic Intoxication / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000648:ultrastructure; D002250:Carbon Radioisotopes; D006801:Humans; D008297:Male; D010718:Phosphatidylserines / Q000378:metabolism*; D051381:Rats; D013375:Substance Withdrawal Syndrome / Q000378:metabolism*; D013574:Synaptosomes / Q000378:metabolism*
D002250:Carbon Radioisotopes; D010718:Phosphatidylserines