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Cholinergic function and alpha-bungarotoxin binding in PC12 cells

G Kemp and M Edge

Neuropsychiatry Research Program, University of Alabama at Birmingham 35294.

The cell line PC12, derived from an adrenal chromaffin cell tumor, expresses both ganglionic (C6) acetylcholine receptors (nAChR) and an alpha-bungarotoxin (BGT) binding protein of unknown function. We measured nicotinic Na+ fluxes of 180-260 nmol/mg protein X min and 0.35- 0.8 pmol [125I]BGT binding sites/mg protein; 45-65% of the [125I]BGT binding was to intracellular sites. We blocked ganglionic Na+ fluxes with reversible and irreversible inhibitors and tested whether a residual BGT-sensitive flux could be identified. No such flux was detected. These experiments place an upper limit on the amount of an undetected Na+ flux such that we question whether the BGT binding protein could act as a functional nAChR X Na+ flux and [125I]BGT binding were irreversibly inactivated by the affinity-directed antagonist 4-(N-maleimido)benzyltrimethylammonium bromide (MBTA), and the appearance of new nAChRs and BGT binding proteins was monitored. New ganglionic nAChRs appeared at a rate of 0.029 hr-1, corresponding to a steady state turnover t1/2 of 24 hr. BGT binding protein was synthesized more rapidly (K = 0.11 hr-1, t1/2 = 6.5 hr). When protein synthesis was simultaneously blocked with cycloheximide, insertion of BGT binding protein into the plasma membrane decreased to 11% of control values. Cycloheximide also induced a biphasic decline in intracellular BGT binding sites. Incubation of PC12 cells in 5 mM carbamylcholine for varying intervals resulted in a rapid 30% loss of Na+ flux activity. In contrast, the concentration of BGT binding protein did not change.

Volume 32, Issue 3, pp. 356-363, 09/01/1987
Copyright © 1987 by American Society for Pharmacology and Experimental Therapeutics




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Copyright © 1987 by the American Society for Pharmacology and Experimental Therapeutics