omega-Agatoxin IVA blocks nicotinic receptor channels in bovine chromaffin cells

We have studied the contribution of P-type voltage-dependent Ca2+ channels to both catacholamine (CA) and ATP secretion from bovine chromaffin cells induced by high K+ or nicotine using omega-agatoxin IVA, a selective blocker of P-type voltage-dependent Ca2+ channels. We found that high K+ (75 mM) i...

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Detalles Bibliográficos
Autores: Granja, Ricardo, Fernández-Fernández, José Manuel, 1967-, Izaguirre, Victor, González García, Carmen, Ceña, Valentin
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:1995
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:10230/25632
Acceso en línea:http://hdl.handle.net/10230/25632
http://dx.doi.org/10.1016/0014-5793(95)00149-4
Access Level:acceso abierto
Palabra clave:Canals de potassi
Nicotina
Calcium channel
P-type
Nicotinic receptor
omega-Agatoxin IVA
Secretion
Chromaffin cell
Descripción
Sumario:We have studied the contribution of P-type voltage-dependent Ca2+ channels to both catacholamine (CA) and ATP secretion from bovine chromaffin cells induced by high K+ or nicotine using omega-agatoxin IVA, a selective blocker of P-type voltage-dependent Ca2+ channels. We found that high K+ (75 mM) induced the release of about 13% of norepinephrine, 5% epinephrine and 11% ATP, and that omega-agatoxin (100 nM) did not affect this secretion. However, both nicotine-induced CA and ATP secretion were significantly blocked (about 50%) by omega-agatoxin IVA (100 nM). In addition, this toxin also reversibly blocked (about 70%) the inward current induced by nicotine in bovine chromaffin cells. The results suggest that, besides its known action of blocking P-type voltage-dependent channels, omega-agatoxin is a potent and reversible blocker of the nicotinic receptor channel in chromaffin cells, and that this action would explain the blockade of nicotine-induced secretion.

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