离体大鼠膈肌标本上梭曼引起终板区持续性去极化的机理分析

Mechanisms of sustained depolarization induced by soman in endplate of isolated rat diaphragm

在离休大鼠膈肌标本上，细胞内记录终板区微电泳给乙酰胆碱（ＡＣｈ）的电位，以ＡＣｈ电位幅度为突触后反应性指标，观察了梭曼中毒后间接串刺激产生终板区持续性去极化反应的性质并分析了其产生的机理。持续性去极化过程中不仅串终板电位消失，ＡＣｈ电位也消失，持续性去极化之后ＡＣｈ逐渐恢复。在正常大鼠和肉毒毒素Ａ中毒大鼠膈肌标本上，梭曼中毒后，串ＡＣｈ电位（５－１０Ｈｚ）也可诱发与持续性去极化性质相同的去极化反应，结果表明，持续性去极化主要是突触后Ｎ型ＡＣｈ受体对高浓度ＡＣｈ的一种反应，不支持突触前ＡＣｈ“再生性”释放的假说。

On isolated nonuniform stretched muscle preparation (INSMP) of rat diaphragm, it was found that the sustained depolarization (SD) in endplate area is the predominant response to repetitive stimu1ation after soman intoxication. Both the microelectrode intracellular recording and the extracellular acetylcholine (ACh) iontophoresis were used to investigate the mechanism of SD.The amplitude of ACh potential was used as the criterion of N-ACh receptor to ACh. ACh potential as well asendplate potential could not be recorded during SD.ACh potential restored gradually after SD. A large depolarization response with 70 % duration dependent of the number ofiontophoresis pulse could be recorded in response to iontophoresis at 5-l0 Hz(1～58). After soman (5.5 μmol·L-1), it turned out to be a longlasting depolarization with 70% duration of 3.23±s 0.7s (n=6) independent of the number ofiontophoresis pulse. This response was the same asendplate potential induced SD in nature. On INSMPfrom rats pretreated with Botulinunl toxin A, in whichpresynaptic ACh release has been blocked, SD couldalso be recorded in response to 5-10 Hz AChiontophoresis after soman (5.5 μmol·L-1). It is con-cluded that SD is the result of postsynaptic responsesto ACh accumulated in the synaptic cleft after inhibi-tion of acetvlcholinesterase. The present results do notsupport the hypothesis that SD is the result ofpresynaptic“regenerative release”of ACh.