Rats were given 45 mg/kg i.p. sodium pentobarbital 15 min prior to the intraventricular injection of 200 μCi [32P]phosphoric acid and 50 μCi [3H]glycerol. The animals were sacrificed 1 hr later, subcellular fractions were prepared from four subcortical brain regions and phospholipids were extracted. Pentobarbital significantly increased the ratio of [3H]- and [32P]-triphosphatidylinositol (TPI) to diphosphatidylinositol (DPI) in the microsomal but not synaptosomal fractions. The possible relationship of this change to nicotinic receptor activity is discussed. Pentobarbital specifically decreased 32Pi but not [3H]glycerol incorporation into synaptosomal phosphatidylinositol (PI). Thus, pentobarbital induced the opposite of the "neurotransmitter effect" on PI turnover. Pentobarbital either decreased or had no effect on the incorporation of 32Pi and [3H]glycerol into phosphatidylserine (PS), phosphatidylcholine (PC) and phosphatidylethanolamine (PE).
Bibliographical noteFunding Information:
*This study was supported in part by USPHS DA-00564 and MH-24287. t This paper is publication Department of Pharmacology, San Francisco, CA 94143. $ H. H. Loh is the recipient of an NIMH Research Scientist Award, K2-DA-70554.