PACEMAKER POTENTIALS OF SEROTONERGIC DORSAL RAPHE NEURONS - CONTRIBUTION OF A LOW-THRESHOLD CA-2+ CONDUCTANCE
PACEMAKER POTENTIALS OF SEROTONERGIC DORSAL RAPHE NEURONS - CONTRIBUTION OF A LOW-THRESHOLD CA-2+ CONDUCTANCE
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DOI：
10.1002/syn.890010611
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发表时间：
1987-01-01
期刊：
影响因子：
2.3
通讯作者：
AGHAJANIAN, GK
中科院分区：
文献类型：
--
作者：
BURLHIS, TM;AGHAJANIAN, GK
中缝背核的神经元表现出内在的起搏电位(逐渐的棘波去极化斜坡)，使它们能够在没有突触相互作用的情况下维持自发的节律活动。在这些细胞中观察到去极化前电位(PP)，这似乎触发了起搏周期接近尾声的尖峰。本研究在大鼠中缝背核脑片上进行，目的是(1)确定PP的离子性质，(2)研究其时间和电压依赖的特性，以及(3)研究α1激动剂苯肾上腺素和5-羟色胺(5-HT)对潜在电导的可能调节。在电流钳下的细胞内记录过程中，PPS被二价阳离子完全可逆地阻断，表明引起PPS的电流中有很大一部分是由钙离子携带的。Ni2+特异性地抑制PP，但不影响高阈值(−40 mV)钙峰或钙激活的钾电导。PP的激活阈值约为−60 mV。超极化激发可以时间和电压依赖的方式去除PP的失活(失活)，最大PPS伴随着−90 mV的超极化脉冲，失活开始发生在−65和−75 mV之间。单电极电压钳实验表明，在−60和−50 mV之间存在一个负斜率电导区域，对应于PP的活化范围。本研究的结果与PP的低阈值钙电导一致，它的作用是使膜电位在起搏周期结束时反弹到动作电位阈值；苯肾上腺素和5-羟色胺都不直接影响这一内向电流。
Neurons of the dorsal raphe nucleus exhibit intrinsic pacemaker potentials (gradual interspike depolarizing ramps) enabling them to sustain spontaneous rhythmic activity in the absence of synaptic interactions. A depolarizing prepotential (PP) has been observed in these cells, which appears to trigger the spike toward the end of the pacemaker cycle. The purposes of this study, carried out in the rat dorsal raphe nucleus brain slice preparation, were to (1) determine the ionic nature of the PP, (2) investigate its time‐ and voltage‐dependent properties, and (3) investigate the possible modulation of the underlying conductance by the α1‐agonist phenylephrine and by serotonin (5‐HT), agents that modify dorsal raphe pacemaker activity. During intracellular recording under current clamp, PPs were completely and reversibly blocked by divalent cations indicating that Ca2+carries a significant portion of the current causing the PPs. Ni2+specifically inhibited the PP with no effect on high‐threshold (−40 mV) Ca2+spikes or the Ca2+activated K+conductance in these neurons. Activation threshold for the PP was found to be approximately −60 mV. Priming by hyperpolarization allowed removal of inactivation (de‐inactivation) of the PP in a time‐ and voltage‐dependent manner, with maximal PPs accompanying hyperpolarizing pulses to −90 mV and the de‐inactivation beginning to occur between −65 and −75 mV. Single‐electrode voltage‐clamp experiments demonstrated a region of negative‐slope conductance between −60 and −50 mV, which corresponds to the range of PP activation. The results of this study are consistent with a lowthreshold Ca2+conductance underlying the PP whose role is to enable the membrane potential to rebound to action potential threshold at the end of the pacemaker cycle; neither phenylephrine nor 5‐HTdirectlyaffected this inward current.