Muscarinic receptor modulation of slow afterhyperpolarization and phasic firing in rat supraoptic nucleus neurons
Muscarinic receptor modulation of slow afterhyperpolarization and phasic firing in rat supraoptic nucleus neurons
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DOI：
10.1523/jneurosci.1240-04.2004
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发表时间：
2004-09-01
影响因子：
5.3
通讯作者：
Bourque, CW
中科院分区：
文献类型：
--
作者：
Ghamari-Langroudi, M;Bourque, CW
本文研究了体外培养的大鼠大细胞神经分泌细胞（MNCs）的慢后超极化（sAHP）。用Cs+阻断去极化后电位（DAP），用apamin阻断中等后超极化（mAHP），将sAHP与其他后电位分离。sAHP振幅随活动的增加而递增（类似于每增加1倍脉冲数3 mV），当放电停止时，以2秒的时间常数呈指数衰减。sAHP与膜电导增加，其幅度与电压呈线性变化，在K+平衡电位反转。sAHP被Cd~（2+）阻断，但不被中电导型和大电导型Ca~（2+）依赖性K~+（K-Ca）通道阻断剂-的sAHP可逆抑制毒蕈碱，阿托品拮抗的效果，表明参与毒蕈碱胆碱能受体。毒蕈碱不影响动作电位，DAP，或在MNCs的mAHP的钙依赖性功能，表明选择性调制的K-Ca通道引起的sAHP。毒蕈碱抑制的sAHP增强高原电位，并增加平均放电率和持续时间的后放电，随后从阈值附近的电压引起的尖峰列车。同样，频率和持续时间的自发阶段性爆发，生理激活的加压素释放的MNCs的特点增强了毒蕈碱。因此，MNCs表达介导sAHP的apamin和电压不敏感的K-Ca通道。sAHP的活性依赖性和动力学使其以衰减平台电位振幅的方式掩蔽DAP。毒蕈碱抑制的sAHP提供了一个有效的机制，促进阶段性放电的MNCs。
A slow posttrain afterhyperpolarization (sAHP) was studied in rat magnocellular neurosecretory cells (MNCs) in vitro. The sAHP was isolated from other afterpotentials by blocking the depolarizing afterpotential (DAP) with Cs+ and the medium afterhyperpolarization (mAHP) with apamin. The sAHP amplitude increased logarithmically with activity (similar to3 mV per e-fold increase in number of impulses) and, when firing stopped, decayed exponentially with a time constant of 2 sec. The sAHP was associated with increased membrane conductance, and its amplitude varied linearly with voltage, reversing at the K+ equilibrium potential. The sAHP was blocked by Cd2+ but not by charybdotoxin or iberiotoxin, blockers of intermediate- and big-conductance-type Ca2+-dependent K+ (K-Ca) channels. The sAHP was reversibly inhibited by muscarine, an effect antagonized by atropine, indicating involvement of muscarinic cholinergic receptors. Muscarine did not affect Ca2+-dependent features of action potentials, DAPs, or the mAHP in MNCs, indicating selective modulation of K-Ca channels causing the sAHP. Muscarinic inhibition of the sAHP enhanced plateau potentials and increased the mean firing rate and duration of afterdischarges that followed spike trains evoked from voltages near threshold. Similarly, the frequency and duration of the spontaneous phasic bursts that characterize physiologically activated vasopressin-releasing MNCs were enhanced by muscarine. MNCs thus express apamin- and voltage-insensitive K-Ca channels that mediate an sAHP. The activity dependence and kinetics of the sAHP cause it to mask DAPs in a manner that attenuates the amplitude of plateau potentials. Muscarinic inhibition of the sAHP provides an effective mechanism for promoting phasic firing in MNCs.