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

机译:纳洛酮抑制尼古丁诱导的牛嗜铬细胞中受体电流和儿茶酚胺的分泌

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摘要

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.
机译:尼古丁诱导的儿茶酚胺(CA)分泌和内向离子流被阿片类药物拮抗剂纳洛酮在培养的牛嗜铬细胞中抑制。如在线实时电化学技术所检测的那样,纳洛酮以剂量依赖性(IC 50 =29μM)抑制烟碱诱导的CA分泌。在电压钳制的嗜铬细胞中,烟碱(10μM)引起-146pA的平均峰值内向电流,其被低浓度的纳洛酮(0.1μM下为42%)抑制。该拮抗剂还抑制了与烟碱样受体激活有关的总电荷流入(在0.1μM时为53%)。这提供了有力的证据,表明纳洛酮对烟碱诱导的CA分泌的调节不涉及阿片样物质受体,而是与烟碱样受体本身直接相互作用的结果,其他相关的阿片样物质也可能如此。

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