Evidence of omega-conotoxin GV1A-sensitive Ca2+ channels in mammalian peripheral nerve terminals.

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.