CALCITONIN-GENE-RELATED PEPTIDE POTENTIATES NICOTINIC ACETYLCHOLINE RECEPTOR-OPERATED SLOW CA2-PLATES( MOBILIZATION AT MOUSE MUSCLE END)

Citation
Sy. Salim et al., CALCITONIN-GENE-RELATED PEPTIDE POTENTIATES NICOTINIC ACETYLCHOLINE RECEPTOR-OPERATED SLOW CA2-PLATES( MOBILIZATION AT MOUSE MUSCLE END), British Journal of Pharmacology, 125(2), 1998, pp. 277-282
Citations number
29
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Pharmacology & Pharmacy",Biology
ISSN journal
0007-1188
Volume
125
Issue
2
Year of publication
1998
Pages
277 - 282
Database
ISI
SICI code
0007-1188(1998)125:2<277:CPPNAR>2.0.ZU;2-V
Abstract
1 The involvement of calcitonin gene-related peptide (CGRP) in the non -contractile slow Ca2+ mobilization induced by prolonged nicotinic sti mulation was investigated by measurement of [Ca2+](i) levels in mouse single muscle cells (flexor digitorum brevis; FDB) loaded with a Ca2indicator fluo-3 using confocal laser scanning microscopy. 2 CGRP (3-3 0 nM) potentiated acetylcholine (ACh, 1 mu M)-elicited slow Ca2+ mobil ization in a concentration-dependent manner. 3 The potentiation by CGR P of the slow Ca2+ component was greatly depressed by a competitive ni cotinic antagonist (+)-tubocurarine (5 mu M). The Ca2+ channel blocker nitrendipine (1 mu M) affected neither ACh responses nor the CGRP pot entiation. 4 The slow Ca2+ component was completely abolished by reduc ing [Ca2+](0) from 2.5 to 0.25 mM whereas the fast component was not a ffected. The CGRP-induced potentiation of slow Ca2+ signal was also de pressed by decreasing [Ca2+](0). 5 Isoproterenol (30 mu M) and 8-bromo -adenosine 3',5'-cyclic monophosphate (1 mM) potentiated the ACh-elici ted slow Ca2+ response. The potentiation by CGRP of the slow Ca2+ comp onent was completely abolished by a protein kinase-A inhibitor H-89 (1 mu M). 6 These findings indicate that CGRP potentiates the nicotinic ACh receptor-operated slow Ca2+ signal via the activation of protein k inase-A system at the skeletal muscle endplates.