Calcium uptake by isolated nerve endings: evidence for a rapid component mediated by the breakdown of phosphatidylinositol.
Several physiological stimuli, including neuronal depolarization, increase the production of phosphatidate (PA) from phosphatidylinositol (PI) and increase calcium fluxes across cell membranes. To determine if breakdown of PI is required for neuronal calcium uptake, we tested inhibitors of PI-specific phospholipase C on depolarization-dependent uptake of calcium by isolated brain synaptosomes. At a concentration of 0.1 mM these inhibitors reduced calcium uptake produced by depolarization for 1 to 3 sec, but did not affect uptake due to more prolonged depolarization. Exogenous PA also stimulated calcium accumulation by synaptosomes and this uptake was not reduced by the enzyme inhibitors. These results suggest that the rapid calcium influx produced by neuronal depolarization may be mediated by the breakdown of PI.
D000818:Animals; D001921:Brain / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D002219:Carbamates / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D008297:Male; D009411:Nerve Endings / Q000378:metabolism*; D048448:Phenylcarbamates; D010664:Phenylmethylsulfonyl Fluoride / Q000494:pharmacology; D010716:Phosphatidylinositols / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013574:Synaptosomes / Q000378:metabolism
D002219:Carbamates; D048448:Phenylcarbamates; D010716:Phosphatidylinositols; C025508:2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate; D010664:Phenylmethylsulfonyl Fluoride; D002118:Calcium