首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Muscarinic and beta-adrenergic depression of the slow Ca2(+)-activated potassium conductance in hippocampal CA3 pyramidal cells is not mediated by a reduction of depolarization-induced cytosolic Ca2+ transients.
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Muscarinic and beta-adrenergic depression of the slow Ca2(+)-activated potassium conductance in hippocampal CA3 pyramidal cells is not mediated by a reduction of depolarization-induced cytosolic Ca2+ transients.

机译:在海马CA3锥体细胞中缓慢的Ca2(+)激活钾电导的毒蕈碱和β-肾上腺素的抑制不是由去极化诱导的胞质Ca2 +瞬变的减少介导的。

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摘要

Combined intracellular and microfluorometric recording techniques were used to evaluate whether the inhibition by cholinergic or adrenergic transmitters of the Ca2(+)-activated potassium current (IAHP) in hippocampal CA3 pyramidal cells was mediated by an alteration of depolarization-induced change in cytosolic free Ca2+ concentration [(Ca2+]i). Low concentrations of isoproterenol (1-10 microM) and muscarine (0.25-1 microM) reversibly abolished IAHP without affecting concomitant Ca2+ transients or the steady-state [Ca2+]i. Only after application of higher concentrations of muscarine, [Ca2+]i increased; in the presence of potassium channel blockers, muscarine depressed Ca2+ currents and concomitant Ca2+ transients. These observations provide direct evidence that the inhibition of IAHP by isoproterenol and muscarine are not mediated by an alteration of Ca2+ dynamics.
机译:结合细胞内和微荧光记录技术来评估海马CA3锥体细胞中Ca2(+)激活的钾电流(IAHP)的胆碱能或肾上腺素递质的抑制是否是由去极化诱导的胞质游离Ca2 +改变的改变介导的浓度[(Ca2 +] i)。低浓度的异丙肾上腺素(1-10 microM)和毒蕈碱(0.25-1 microM)可逆地废除IAHP,而不会影响伴随的Ca2 +瞬变或稳态[Ca2 +] i。仅在施用较高浓度的毒蕈碱后,[Ca2 +] i升高;在钾通道阻滞剂的存在下,毒蕈碱抑制了Ca2 +电流并伴随着Ca2 +瞬变。这些观察结果提供直接证据,表明异丙肾上腺素和毒蕈碱对IAHP的抑制作用不是由Ca2 +动力学的改变介导的。

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