ACETYLCHOLINE SENSITIVITY OF BIPHASIC CA2-MUSCLE END-PLATE( MOBILIZATION INDUCED BY NICOTINIC RECEPTOR ACTIVATION AT THE MOUSE SKELETAL)

Authors
Citation
K. Dezaki et I. Kimura, ACETYLCHOLINE SENSITIVITY OF BIPHASIC CA2-MUSCLE END-PLATE( MOBILIZATION INDUCED BY NICOTINIC RECEPTOR ACTIVATION AT THE MOUSE SKELETAL), British Journal of Pharmacology, 123(7), 1998, pp. 1418-1424
Citations number
27
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
0007-1188
Volume
123
Issue
7
Year of publication
1998
Pages
1418 - 1424
Database
ISI
SICI code
0007-1188(1998)123:7<1418:ASOBCE>2.0.ZU;2-I
Abstract
1 Acetylcholine (ACh) was locally applied onto the endplate region in a mouse phrenic nerve-diaphragm muscle preparation to measure intracel lular free calcium ([Ca2+](i)) entry through nicotinic ACh receptors ( AChRs) by use of Ca2+-aequorin luminescence. 2 ACh (0.1-3 mM, 20 mu l) elicited biphasic elevation of [Ca2+](i) (fast and slow Ca2+ mobiliza tion) in muscle cells. The peak amplitude of the slow Ca2+ mobilizatio n (not accompanied by twitch tension) was concentration-dependently in creased by ACh, whereas that of the fast component (accompanied by twi tch tension) reached a maximum response at a lower concentration (0.1 mM) of applied ACh. 3 A pulse of nicotinic agonists, (-)-nicotine (10 mM) and 1,1-dimethyl-4-phenyl-piperazinium (10 mM), but not a muscarin ic agonist pilocarpine (10 mM), also elicited a biphasic Ca2+ signal. 4 Even though ACh release from motor nerve endings was blocked by botu linum toxin (5 mu g, bolus i.p. before isolation of the tissue), the g eneration of both a fast and slow Ca2+ component caused by ACh applica tion was observed. 5 These results strongly suggest that ACh locally a pplied onto the endplate region of skeletal muscle induces a slow Ca2 signal reflecting Ca2+ entry through a postsynaptic nicotinic AChR, w hich has a low sensitivity to transmitter ACh.