PMID: 8613952Apr 1, 1996Paper

Diversity of nicotinic acetylcholine receptors in rat hippocampal neurons. IV. Regulation by external Ca++ of alpha-bungarotoxin-sensitive receptor function and of rectification induced by internal Mg++

The Journal of Pharmacology and Experimental Therapeutics
R Bonfante-CabarcasE X Albuquerque

Abstract

Applying the whole-cell mode of the patch-clamp technique to cultured hippocampal neurons, we demonstrated that extracellular Ca++ modulates the activation and inactivation of type IA nicotinic currents, ie., the currents subserved by alpha-bungarotoxin (alpha-BGT)-sensitive, alpha-7-containing nicotinic acetylcholine receptors (nAChRs). The rundown profile of acetylcholine (ACh)-induced type IA currents that were obtained using patch pipettes filled with F(-)-based internal solution had two components: the first component of rundown was counteracted by a more physiological internal solution containing an organic anion (malate or aspartate), suggesting energy dependence; the second component exhibited dependence on concentration of CaCl2 added to the external solution ([Ca++]o), with rundown minimized at 0.32 mM. The inward rectification of Ach-elicited type IA currents, induced by intracellular Mg++ was augmented by lowering [Ca++]o (from 2 to 0.32 mM). Moreover, extracellular Ca++ (0.01-10 mM) acted in a concentration-dependent manner (IC50 = 0.26 mM) to decrease the cooperativity induced by ACh (nH was reduced from 2.7 to 1). Extracellular Ca++ (EC50 = 0.1 mM) also increased the efficacy of ACh, but exposure to [Ca++]o from ...Continue Reading

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