Muscarinic cholinergic enhancement of inositide turnover in cerebral nerve endings is not mediated by calcium uptake

Abstract

Muscarinic cholinergic stimulation of rat cerebral nerve endings incubated with 32P i causes an enhancement of the labeling of phosphatidic acid (PA) and phosphatidylinositol (PI). The involvement of Ca 2+ in the stimulation of PA and PI labeling by carbamylcholine (CCh) was investigated. Enhancement of Ca 2+-influx with veratridine and the Ca 2+-ionophore A23187 caused a vast decrease of the labeling of the polyphosphoinositides, which was not accompanied by an enhancement of the labeling of PA and PI. The dihydropyridine Ca 2+-agonist BAY K 8644 did not affect phospholipid labeling. A23187, veratridine and BAY K 8644 did not enhance stimulation of the labeling of PA and PI by CCh. When Ca 2+ was omitted from the incubation, A23187 caused an enhancement of basal and CCh-stimulated labeling of PA and PI, possibly indicating a particular feature of A23187 unrelated to its iontophoretic properties. The Ca 2+-channel antagonists nimodipine, verapamil and flunarizine were virtually without effect on basal and CCh-stimulated labeling of PI and PA. These data support the notion that the muscarinic cholinergic inositide response is not mediated or controlled by Ca 2-flux.