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兰尼碱对大鼠颈上神经节交感神经元动作电位后超极化的影响。

Effects of ryanodine on the spike after-hyperpolarization in sympathetic neurones of the rat superior cervical ganglion.

作者信息

Kawai T, Watanabe M

机构信息

Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Nagoya City University, Japan.

出版信息

Pflugers Arch. 1989 Mar;413(5):470-5. doi: 10.1007/BF00594175.

DOI:10.1007/BF00594175
PMID:2544853
Abstract

Effects of ryanodine on sympathetic neurones of the rat superior cervical ganglion were investigated by means of intracellular recording. Ryanodine (1 microM) significantly shortened the after-hyperpolarization (AH) following the spike evoked by current injection or pre-ganglionic stimulation without affecting the configuration of the spikes. The shortening of AH caused by ryanodine was dose-dependent at concentrations between 0.1 and 1 microM and was slowly recovered by washing the tissue over 1 h. A partial inhibition of the apamin-sensitive slow component of AH was the maximal effect obtained at 1 microM. Although the input membrane resistance was not changed, ryanodine evoked repetitive discharges at long intervals in response to long depolarizing current pulses applied across the cell membrane. Ryanodine (5 microM) did not depress the Ca-spike but shortened the following AH in a lesser degree than that following the normal spike. Spontaneous small fluctuations of the resting membrane potential were occasionally observed under normal conditions. They were facilitated by caffeine and abolished by ryanodine. Caffeine also enhanced the slow component of the AH but did not affect it in the presence of ryanodine. These results suggest that ryanodine inhibits Ca release from intracellular store sites. The released Ca may contribute to generating the long-lasting AH and to regulating the excitability of rat sympathetic neurones.

摘要

采用细胞内记录法研究了ryanodine对大鼠颈上神经节交感神经元的作用。Ryanodine(1微摩尔)显著缩短了电流注入或节前刺激诱发的锋电位后的超极化后电位(AH),而不影响锋电位的形态。Ryanodine引起的AH缩短在0.1至1微摩尔的浓度范围内呈剂量依赖性,且通过在1小时内冲洗组织可缓慢恢复。在1微摩尔时获得的最大效应是对AH的蜂毒明肽敏感慢成分的部分抑制。尽管输入膜电阻未改变,但Ryanodine在细胞膜上施加长去极化电流脉冲时,会以较长间隔诱发重复放电。Ryanodine(5微摩尔)不抑制Ca锋电位,但缩短随后的AH,其程度小于正常锋电位后的AH。在正常条件下偶尔会观察到静息膜电位的自发小波动。它们被咖啡因促进,被Ryanodine消除。咖啡因也增强了AH的慢成分,但在存在Ryanodine的情况下对其没有影响。这些结果表明,Ryanodine抑制细胞内储存部位的Ca释放。释放的Ca可能有助于产生持久的AH并调节大鼠交感神经元的兴奋性。

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