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锡离子对青蛙运动神经末梢递质诱发释放的加速作用。

Acceleration by stannous ion of the evoked release of transmitter from motor nerve endings in the frog.

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

Brain Res. 1988 Nov 8;473(1):157-60. doi: 10.1016/0006-8993(88)90328-9.

Abstract

Stannous ion (Sn2+, 30 microM) increased the amplitude of endplate potential (EEP) in the frog sartorius muscle, although the amplitude of miniature endplate potential (MEPP) or acetylcholine potential evoked by iontophoretic application of acetylcholine was unchanged. Sn2+ (10-100 microM) dose-dependently increased the quantal content of the EPP. MEPP frequency was not altered by 30 microM Sn2+. These findings indicate that Sn2+ may increase the EPP as a result of acceleration of the transmitter release evoked by nerve impulses.

摘要

亚锡离子(Sn2+,30微摩尔)可增加青蛙缝匠肌终板电位(EEP)的幅度,尽管微终板电位(MEPP)的幅度或离子电渗法施加乙酰胆碱所诱发的乙酰胆碱电位未发生变化。Sn2+(10 - 100微摩尔)剂量依赖性地增加了终板电位(EPP)的量子含量。30微摩尔的Sn2+未改变MEPP频率。这些发现表明,Sn2+可能是由于加速神经冲动诱发的递质释放而增加EPP。

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