Effect of ethanol on mouse brain microsomal phospholipid turnover

In an investigation of the effects of chronic and acute ethanol administration on phospholipid synthesis, mice subjected to chronic or acute ethanol administration were intraventricularly injected with 1,332 kBq of 2-3H-glycerol (3H-glycerol) and 4,070 kBq of 32P-phosphoric acid 15 min after the ethanol injection. One hour later, mice were sacrificed, and brain microsomes were prepared for analysis of incorporation of radioactivity into phospholipids. Chronic ethanol treatment significantly decreased incorporation of 3H-glycerol and 32P-phosphoric acid into phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol plus phosphatidylserine. However, acute ethanol treatment had no marked effect on incorporation of 3H-glycerol or 32P-phosphoric acid into any of these phospholipids. On the other hand, chronic ethanol administration had no significant effect on incorporation of the radioisotopes into triphosphoinositide (TPI) or diphosphoinositide (DPI) in microsomal fractions, or the 3H- and 32P-TPI/DPI ratios. However, acute ethanol administration decreased the incorporation of 3H-glycerol into DPI and TPI, but did not change the TPI/DPI ratio; it also significantly increased the 32P-TPI/DPI ratio and decreased 32P-phosphoric acid incorporation into DPI but did not significantly affect 32P-phosphoric acid incorporation into TPI. Chronic ethanol administration is thought to have altered the turnover of phospholipids in the microsomal membrane, thereby affecting both the levels and turnover of neurotransmitters. In addition, the change of labeled TPI/DPI ratio observed after acute ethanol treatment may reflect nicotinic receptor activity in the mouse brain.