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Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells

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Detalhes bibliográficos
Resumo:Nicotine-induced catecholamine (CA) secretion and inward ionic currents were inhibited by the opioid antagonist naloxone in cultured bovine chromaffin cells. Naloxone inhibited nicotine-induced CA secretion, as detected by an on-line real-time electrochemical technique, in a dose-dependent manner (IC50=29 [mu]M). In voltage-clamped chromaffin cells, nicotine (10 [mu]M) evoked an average peak inward current of -146 pA that was inhibited by low concentrations of naloxone (42% at 0.1 [mu]M). The antagonist also inhibited total charge influx associated with nicotinic receptor activation (53% at 0.1 [mu]M). This provides strong evidence that naloxone modulation of nicotine-induced CA secretion does not involve opioid receptors but results from the direct interaction with the nicotinic receptor itself, which might also be the case for other related opioid compounds.
Autores principais:Tomé, Ângelo R.
Outros Autores:Izaguirre, Victor; Rosário, Luís M.; Ceña, Valentín; González-García, Carmen
Assunto:Opioids Nicotinic receptor Currents Catecholamine secretion Patch-clamp
Ano:2001
País:Portugal
Tipo de documento:artigo
Tipo de acesso:acesso aberto
Instituição associada:Universidade de Coimbra
Idioma:inglês
Origem:Estudo Geral - Universidade de Coimbra
Descrição
Resumo:Nicotine-induced catecholamine (CA) secretion and inward ionic currents were inhibited by the opioid antagonist naloxone in cultured bovine chromaffin cells. Naloxone inhibited nicotine-induced CA secretion, as detected by an on-line real-time electrochemical technique, in a dose-dependent manner (IC50=29 [mu]M). In voltage-clamped chromaffin cells, nicotine (10 [mu]M) evoked an average peak inward current of -146 pA that was inhibited by low concentrations of naloxone (42% at 0.1 [mu]M). The antagonist also inhibited total charge influx associated with nicotinic receptor activation (53% at 0.1 [mu]M). This provides strong evidence that naloxone modulation of nicotine-induced CA secretion does not involve opioid receptors but results from the direct interaction with the nicotinic receptor itself, which might also be the case for other related opioid compounds.

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