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乌贼巨大神经纤维施万细胞膜电位的肽能调节。

Peptidergic modulation of the membrane potential of the Schwann cell of the squid giant nerve fibre.

作者信息

Evans P D, Reale V, Villegas J

出版信息

J Physiol. 1986 Oct;379:61-82. doi: 10.1113/jphysiol.1986.sp016241.

Abstract

The effects of a range of neuropeptides were investigated on the membrane potential of the Schwann cells of the giant nerve fibre of the tropical squid. Vasoactive intestinal peptide (VIP) produced a dose-dependent, long-lasting hyperpolarization of the Schwann-cell membrane potential. Among peptides structurally related to VIP, similar effects were produced by peptide histidine isoleucine (PHI) but not by secretin and glucagon. Substance P and somatostatin also hyperpolarized the Schwann-cell membrane potential but via receptor systems distinct from those activated by VIP. Methionine enkephalin ([Met]-enkephalin) blocked the actions of all the above peptides as well as the effects of DL-octopamine and carbachol. The actions of [Met]-enkephalin upon the VIP responses were antagonized by naloxone. VIP produces its effects on the Schwann-cell membrane potential via a receptor system that is independent from those described previously which mediate the effects of carbachol and DL-octopamine. However, VIP can potentiate the effects of the latter systems. The actions of VIP on the Schwann cell are unlikely to be mediated via changes in adenosine 3',5'-cyclic monophosphate (cyclic AMP) levels and are insensitive to changes in the level of extracellular calcium in the superfusate. The actions of VIP are, however, potentiated in the presence of low concentrations of lithium ions suggesting that the VIP receptor may mediate its effects by inducing the hydrolysis of polyphosphatidylinositols in the Schwann-cell membrane. Evidence is presented for the existence of an endogenous VIP-like component in the normal hyperpolarizing action of giant-axon activity on the membrane potential of the Schwann cell.

摘要

研究了一系列神经肽对热带鱿鱼巨大神经纤维施万细胞膜电位的影响。血管活性肠肽(VIP)可使施万细胞膜电位产生剂量依赖性的持久超极化。在与VIP结构相关的肽中,肽组氨酸异亮氨酸(PHI)产生了类似的效应,但促胰液素和胰高血糖素则没有。P物质和生长抑素也使施万细胞膜电位超极化,但通过与VIP激活的受体系统不同的受体系统。甲硫氨酸脑啡肽([Met]-脑啡肽)阻断了上述所有肽的作用以及DL-章鱼胺和卡巴胆碱的效应。[Met]-脑啡肽对VIP反应的作用可被纳洛酮拮抗。VIP通过一种受体系统对施万细胞膜电位产生作用,该受体系统独立于先前描述的介导卡巴胆碱和DL-章鱼胺效应的受体系统。然而,VIP可增强后一种系统的效应。VIP对施万细胞的作用不太可能通过3',5'-环磷酸腺苷(环AMP)水平的变化介导,并且对灌流液中细胞外钙水平的变化不敏感。然而,在低浓度锂离子存在的情况下,VIP的作用会增强,这表明VIP受体可能通过诱导施万细胞膜中多磷脂酰肌醇的水解来介导其效应。有证据表明,在巨轴突活动对施万细胞膜电位的正常超极化作用中存在内源性VIP样成分。

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