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大蝎毒素和iberiotoxin可消除肠肌丛神经元中的缓慢超极化后电位,但蜂毒明肽则不能。

Charybdotoxin and iberiotoxin but not apamin abolish the slow after-hyperpolarization in myenteric plexus neurons.

作者信息

Kunze W A, Bornstein J C, Furness J B, Hendriks R, Stephenson D S

机构信息

Department of Physiology, University of Melbourne, Parkville, Victoria, Australia.

出版信息

Pflugers Arch. 1994 Oct;428(3-4):300-6. doi: 10.1007/BF00724511.

DOI:10.1007/BF00724511
PMID:7529400
Abstract

Myenteric neurons of guinea-pig ileum were studied with intracellular microelectrodes. The specific toxins charybdotoxin, iberiotoxin and apamin were used to characterize the prolonged after-hyperpolarizations of AH neurons in this preparation. Charybdotoxin and iberiotoxin blocked prolonged after-hyperpolarizations in 23 of 24 AH neurons, but apamin had no effect on 5 of 5 AH neurons. Abolition of the after-hyperpolarizations was accompanied by depolarization and increases in input resistances of those AH neurons affected, but the shapes of action potentials were unchanged. The excitability of the AH neurons was enhanced as shown by an increase in the number of action potentials evoked by a 500-ms depolarizing current pulse or by a train of 15-ms depolarizing current pulses (10Hz). The other class of myenteric neurons, S neurons, was also investigated. The 19 S neurons studied fired action potentials only at the start of a 500 ms depolarization, but the toxins had no effect on this behaviour or on their other properties. Intracellular injection of Neurobiotin into the neurons studied and subsequent immunohistochemical staining to localise the calcium-binding protein, calretinin, indicated that all major classes of S neurons were included in the sample. Thus, the prolonged after-hyperpolarizations in AH neurons may be due to opening of a large-conductance (BK) calcium-dependent potassium channel, but similar channels play little or no role in regulation of the excitability of S neurons.

摘要

采用细胞内微电极对豚鼠回肠的肠肌间神经元进行了研究。使用特异性毒素——蝎毒素、iberiotoxin和蜂毒明肽来表征该标本中AH神经元延长的超极化后电位。蝎毒素和iberiotoxin阻断了24个AH神经元中23个的延长超极化后电位,但蜂毒明肽对5个AH神经元中的5个没有影响。超极化后电位的消除伴随着受影响的AH神经元的去极化和输入电阻的增加,但动作电位的形状未改变。500毫秒去极化电流脉冲或一串15毫秒去极化电流脉冲(10赫兹)诱发的动作电位数量增加,表明AH神经元的兴奋性增强。还对另一类肠肌间神经元,即S神经元进行了研究。所研究的19个S神经元仅在500毫秒去极化开始时发放动作电位,但毒素对这种行为或它们的其他特性没有影响。向所研究的神经元内注射神经生物素,随后进行免疫组织化学染色以定位钙结合蛋白钙视网膜蛋白,表明样本中包括了所有主要类型的S神经元。因此,AH神经元中延长的超极化后电位可能是由于大电导(BK)钙依赖性钾通道的开放,但类似的通道在调节S神经元的兴奋性方面作用很小或没有作用。

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