title: Evidence of omega-conotoxin GV1A-sensitive Ca2+ channels in mammalian peripheral nerve terminals.
abstract: The existence of omega-conotoxin GV1A (omega-CgTx)-sensitive, voltage-sensitive Ca2+ channels (VSCCs) in mammalian peripheral nerves was investigated in the guinea pig ileum myenteric plexus longitudinal smooth muscle preparation (GPI). omega-CgTx (0.01-1.0 microM) reduced the electrically stimulated GPI twitch height, failed to modify exogenously applied acetylcholine (ACh) contractions, and inhibited Ca2+-dependent KCl-stimulated ACh release as measured by chemiluminescence. The 1,4-dihydropyridine VSCC antagonist (-) 202-791 (0.1-1.0 microM) inhibited the GPI twitch height, reduced contractions to exogenous ACh, but failed to affect ACh release. In the rat aorta, a nerve free preparation, omega-CgTx failed to affect contractions to KCl which were inhibited by (-) 202-791 and potentiated by the VSCC agonist (+) 202-791. The results provide evidence of neuronal N type VSCCs in mammalian peripheral cholinergic nerve terminals.
authors.affiliation: Biomedical Defence Section, Defence Research Establishment Suffield, Ralston, Alberta, Canada.
authors.forename: P M
authors.initials: PM
authors.lastname: Lundy
authors.forename: R
authors.initials: R
authors.lastname: Frew
mesh_terms: D000109:Acetylcholine / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects*; D006168:Guinea Pigs; D007082:Ileum / Q000187:drug effects / Q000294:innervation / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D008978:Mollusk Venoms / Q000494:pharmacology*; D009119:Muscle Contraction / Q000187:drug effects; D010525:Peripheral Nerves / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D051381:Rats; D020866:omega-Conotoxin GVIA
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D008978:Mollusk Venoms; D020866:omega-Conotoxin GVIA; D000109:Acetylcholine