Tricyclic antidepressants block cholinergic nicotinic receptors and ATP secretion in bovine chromaffin cells

Nicotine-induced ATP secretion from chromaffin cells was blocked by imipramine and desipramine. This blocking action took place on both, fast and slow, components of ATP secretion. Exposure of chromaffin cells to nicotine (10 microM) for 4 s induced an inward current of about -155 pA. Imipramine and...

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Detalhes bibliográficos
Autores: Izaguirre, Victor, Fernández-Fernández, José Manuel, 1967-, Ceña, Valentin, González García, Carmen
Formato: artículo
Estado:Versión publicada
Fecha de publicación:1997
País:España
Recursos: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:10230/25631
Acesso em linha:http://hdl.handle.net/10230/25631
http://dx.doi.org/10.1016/S0014-5793(97)01343-4
Access Level:acceso abierto
Palavra-chave:Nicotina
Nicotine
ATP secretion
Chromaffin cell
Imipramine
Desipramine
Calcium channel
Descrição
Resumo:Nicotine-induced ATP secretion from chromaffin cells was blocked by imipramine and desipramine. This blocking action took place on both, fast and slow, components of ATP secretion. Exposure of chromaffin cells to nicotine (10 microM) for 4 s induced an inward current of about -155 pA. Imipramine and desipramine blocked, in a concentration-dependent manner, both peak inward current and total charge influx in response to nicotine. In addition, imipramine and desipramine partially (40%) blocked depolarization-induced ATP secretion and Ca2+ currents evoked by high K+. This suggests that tricyclic antidepressants block nicotine-induced ATP secretion by acting on two targets: one is the nicotinic receptor itself and the second one are voltage-dependent Ca2+ channels.