Depolarization-induced [3H]arachidonic acid accumulation: effects of external Ca2+ and phospholipase inhibitors

Isolated cerebellar glomeruli were prelabeled with [3H]arachidonate prior to assessment of the roles of external Ca2+ and phospholipases in the depolarization-induced accumulation of unesterified arachidonate. The glomerular particles have previously been shown to release neurotransmitters upon exposure to depolarizing conditions, calcium influx, exogenous arachidonate and added prostaglandins. It was observed that membrane depolarization caused an increased accumulation of [3H]arachidonate, which was inhibited by EGTA, verapamil or the lipase inhibitors mepacrine and dibucaine. The major effect of EGTA was expressed on the catabolism of [3H]triglycerides, while verapamil prevented the loss of radioactivity from inositol glycerophospholipids and the lipase inhibitors reduced by triglyceride and inositol glycerophospholipid catabolism.