Randle J C, Bourque C W, Renaud L P
Am J Physiol. 1986 Sep;251(3 Pt 2):R569-74. doi: 10.1152/ajpregu.1986.251.3.R569.
Intracellular data were obtained from 35 supraoptic nucleus neurosecretory neurons maintained in vitro in intra-arterially perfused explants of rat hypothalamus. Addition of norepinephrine, phenylephrine, or methoxamine, but not isoproterenol (30-200 microM), consistently induced membrane depolarization, bursting activity, and an associated prolongation in action potential duration, effects that were reversibly antagonized by the alpha 1-antagonist prazosin. Norepinephrine-evoked depolarizations demonstrated no consistent change in membrane resistance and were reduced both by membrane hyperpolarization and by raising extracellular K+. Norepinephrine shortened the time course of spike hyperpolarizing afterpotentials and increased the magnitude of late depolarizing afterpotentials. It is proposed that one of norepinephrine's actions on supraoptic neurons involves K+ channels, perhaps by modulation of a transient K+ current known as A current.
细胞内数据取自35个视上核神经分泌神经元，这些神经元在体外由大鼠下丘脑动脉内灌注的外植体维持。加入去甲肾上腺素、苯肾上腺素或甲氧明，但不加入异丙肾上腺素（30 - 200微摩尔），持续诱导膜去极化、爆发活动以及动作电位持续时间的相关延长，这些效应可被α1拮抗剂哌唑嗪可逆性拮抗。去甲肾上腺素诱发的去极化未显示膜电阻有一致变化，且在膜超极化和细胞外钾离子浓度升高时均降低。去甲肾上腺素缩短了动作电位超极化后电位的时间进程，并增加了晚期去极化后电位的幅度。有人提出，去甲肾上腺素对视上核神经元的作用之一涉及钾离子通道，可能是通过调节一种称为A电流的瞬时钾离子电流来实现的。
