首页> 美国卫生研究院文献>The Journal of Physiology >Peptidergic modulation of the membrane potential of the Schwann cell of the squid giant nerve fibre.
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Peptidergic modulation of the membrane potential of the Schwann cell of the squid giant nerve fibre.

机译:鱿鱼巨神经纤维雪旺细胞膜电位的前肽调节。

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摘要

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.
机译:研究了一系列神经肽对热带鱿鱼巨大神经纤维雪旺细胞膜电位的影响。血管活性肠肽(VIP)对雪旺氏细胞膜电位产生剂量依赖性的持久超极化作用。在结构上与VIP相关的肽中,类似的作用是由肽组氨酸异亮氨酸(PHI)产生的,而不是由促胰液素和胰高血糖素产生的。 P物质和生长抑素也使雪旺氏细胞膜电位超极化,但通过不同于VIP激活的受体系统。蛋氨酸脑啡肽([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作用。纳洛酮拮抗[Met]-脑啡肽对VIP反应的作用。 VIP通过独立于前述介导卡巴胆碱和DL-章鱼胺作用的受体系统,对雪旺细胞膜电位产生作用。但是,VIP可以增强后一种系统的效果。 VIP对雪旺细胞的作用不太可能通过3',5'-环一磷酸腺苷(环AMP)水平的变化来介导,并且对超融合液中细胞外钙水平的变化不敏感。但是,在低浓度的锂离子存在下,VIP的作用增强了,这表明VIP受体可能通过诱导雪旺细胞膜中的多磷脂酰肌醇的水解来介导其作用。证据表明在巨轴突活性对雪旺氏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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