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氯化亚锡对小鼠运动神经末梢钙内流的增强作用。

Augmentation of calcium influx by stannous chloride at mouse motor nerve terminals.

作者信息

Hattori T, Maehashi H

机构信息

Department of Dental Pharmacology, Matsumoto Dental College, Shiojiri, Japan.

出版信息

Res Commun Chem Pathol Pharmacol. 1994 May;84(2):253-6.

PMID:8091010
Abstract

Stannous chloride (SnCl2) facilitates the calcium (Ca) entry into the frog motor nerve terminals. To compare the mode of action of SnCl2 on the Ca channels in the mouse with that in the frog, we investigated the effects of SnCl2 on the inward Ca current at the nerve terminals. SnCl2 (0.1 mM) did not change the second positive component of the action potential (an outward potassium (K) current) at the terminal part of the nerve terminal. SnCl2 (0.1 mM) increased the amplitude of the prolonged negative or positive deflection (an inward Ca current) evoked by treatment with 1 mM tetraethylammonium and 0.1 mM 3,4-diaminopyridine at the terminal or preterminal part of the nerve terminal, respectively. This augmenting effect of SnCl2 was inhibited by cumulative addition of Ca channel blockers, i.e., 0.1 mM CdCl2, 5 mM NiCl2, 5 mM CoCl2, 5 mM MnCl2, or 10 mM MgCl2. From the results obtained, it has been confirmed that SnCl2 facilitates the transmitter release by enhancing the Ca influx at the nerve terminals but not by blocking the K channels and that the mode of action of SnCl2 in the mouse is identical with that in the frog.

摘要

氯化亚锡(SnCl2)可促进钙(Ca)进入青蛙运动神经末梢。为了比较SnCl2对小鼠和青蛙钙通道的作用方式,我们研究了SnCl2对神经末梢内向钙电流的影响。SnCl2(0.1 mM)不会改变神经末梢末端动作电位的第二个正向成分(外向钾(K)电流)。SnCl2(0.1 mM)分别增加了在神经末梢末端或末梢前部分用1 mM四乙铵和0.1 mM 3,4-二氨基吡啶处理所诱发的延长的负向或正向偏转(内向钙电流)的幅度。SnCl2的这种增强作用被钙通道阻滞剂(即0.1 mM CdCl2、5 mM NiCl2、5 mM CoCl2、5 mM MnCl2或10 mM MgCl2)的累积添加所抑制。从获得的结果可以证实,SnCl2通过增强神经末梢的钙内流而不是通过阻断钾通道来促进递质释放,并且SnCl2在小鼠中的作用方式与在青蛙中的相同。

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