USE OF GEOGRAPHUTOXIN-II (MU-CONOTOXIN) FOR THE STUDY OF NEUROMUSCULAR-TRANSMISSION IN MOUSE
USE OF GEOGRAPHUTOXIN-II (MU-CONOTOXIN) FOR THE STUDY OF NEUROMUSCULAR-TRANSMISSION IN MOUSE
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DOI：
10.1111/j.1476-5381.1989.tb12034.x
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发表时间：
1989-07-01
影响因子：
7.3
通讯作者：
CHANG, CC
中科院分区：
文献类型：
--
作者：
HONG, SJ;CHANG, CC
在小鼠膈神经隔膜制备物中，研究了在存在Geographutoxin II（GTXII）的情况下的终板电位（e.p.ps）。这种毒素优先阻断肌肉Na+通道，这使得在没有烟碱受体拮抗剂或抑制乙酰胆碱释放的物质的情况下进行研究。e.p.ps GTXII消除肌肉动作电位，拮抗由克罗胺诱导的Na+通道开放产生的肌膜去极化。E.p.ps在2-4 μ g ml-1 GTXII后观察到高达19-25 mV的电压。这些浓度的GTXII并没有引起静息膜电位和频率和振幅的微小e.p.ps的可辨别的变化。较低浓度（1-2 μ g ml-1）的GTXII引起肌肉Na+通道的不完全阻断，导致夸大的“e.p.ps”，而较高浓度的GTXII（8 μ g ml-1）通过连接前效应消除e.p.ps。在GTXII后，e.p.ps对重复刺激的训练既不像筒箭毒碱处理的制剂那样向下跑，也不像低Ca 2+和/或高Mg 2+处理的制剂那样促进，并且与未处理的切割肌肉制剂的训练难以区分。在切割肌肉的准备，GTXII没有影响上升和衰减时间，振幅或下降的e.p.ps。结论GTXII是一种研究神经肌肉传递的有用试剂。该方法提供既不衰减也不修饰的信号，因为避免了改变递质释放和连接后受体反应的操作。e.p.ps
Endplate potentials (e.p.ps) were investigated in the presence of geographutoxin II (GTXII) in the mouse phrenic nerve diaphragm preparation. This toxin preferentially blocks muscle Na+ channels which allows the study of e.p.ps in the absence of nicotinic receptor antagonists or substances to depress acetylcholine release. GTXII abolished muscle action potentials and antagonized the depolarization of the muscle membrane produced by the crotamine-induced opening of Na+ channels. E.p.ps as large as 19-25 mV were observed after 2-4 .mu.g ml-1 GTXII. These concentrations of GTXII did not cause discernible changes of resting membrane potential and frequency and amplitude of miniature e.p.ps. Lower concentrations (1-2 .mu.g ml-1) of GTXII caused incomplete blockade of the muscle Na+ channel resulting in exaggerated ''e.p.ps'', while higher concentrations of GTXII (8 .mu.g ml-1) abolished e.p.ps by a prejunctional effect. Trains of e.p.ps on repetitive stimulation after GTXII neither ran down, as in tubocurarine-treated preparations, nor facilitated, as in low Ca2+ and/or high Mg2+-treated preparations, and were indistinguishable from those of untreated cut muscle preparation. In cut muscle preparations, GTXII did not affect the rise and decay times, amplitude or rundown of e.p.ps. It is concluded that GTXII is a useful agent for studying neuromuscular transmission. This method provides e.p.ps which are neither attenuated nor modified because manipulation that alter transmitter release and postjunctional receptor responses are avoided.