Muscarinic cholinergic stimulation of phosphatidylinositol turnover in isolated rat superior cervical sympathetic ganglia

Lapetina, E.G.; Brown, W.E.; Michell, R.H.

Journal of Neurochemistry 26(3): 649-651

1976


ISSN/ISBN: 0022-3042
PMID: 177736
DOI: 10.1111/j.1471-4159.1976.tb01530.x
Accession: 005946104

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Abstract
In ganglia incubated without any additions phosphatidylinositol incorporated about one-fifth of the total 32P which went into phospholipids, and it therefore had a higher specific radioactivity than the majority of the other lipids. When ganglia were incubated with acetylcholine and eserine, which would stimulate both the nicotinic and muscarinic populations of cholinergic receptors, the labeling of phosphatidylinositol was almost doubled. Treatment with bethanechol (carbamyl .beta.-methylcholine), an agonist whose effects are almost entirely on muscarinic cholinergic receptors, produced the same response as acetylcholine. In experiments with tubocurarine and atropine, which are the classical antagonists for, respectively, nicotinic and muscarinic receptors, only blockade of the phosphatidylinositol response by atropine was observed. Tubocurarine had no significant effect on phosphatidylinositol labeling either in stimulated or unstimulated ganglia. These results suggested that the effects on phosphatidylinositol metabolism were controlled via muscarinic receptors. The effect of propylbenzilylcholine mustard, a compound which produced highly specific and essentially irreversible blockade of the muscarinic receptors of gastrointestinal smooth muscle, was tested. The increase in phosphatidylinositol labeling in cholinergically stimulated ganglia was also prevented by this antagonist.

Muscarinic cholinergic stimulation of phosphatidylinositol turnover in isolated rat superior cervical sympathetic ganglia