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在离体大鼠膈肌上制备了一种不均匀牵拉肌肉以制动,便于用微电极记录终板电位(EPP)的标本(INSMP),避免了常规制动方法带来的制动药物、台氏液Ca~(2+),Mg~(2+)浓度改变或钳压肌肉导致膜电位(MP)下降的种种干扰。INSMP的MP和小终板电位(MEPP)正常,EPP幅度高达30mV以上,是研究药物对接头作用的较好标本。在INSMP上,梭曼(5.5μM)使MEPP频率加快,串刺激(50Hz)诱发的平均串EPPs幅度及其平均ACh 量子含量减少80％和77％。小剂量三碘季铵酚和六烃季铵可部分对抗梭曼的作用。梭曼引起强直收缩抑制主要原因为终板区蓄积的ACh作用于突触前N受体、负反馈地抑制ACh 量子释放;次要原因为作用突触后N受体、使其对ACh敏感性降低。
An in vitro rat diaphragm was prepared with an inhomogeneous traction for braking to facilitate recording of endplate potentials (EPP) using a microelectrode (INSP), avoiding brake drag by conventional braking methods, The changes of Ca ~ (2 +) and Mg ~ (2+) concentration in Tyrodes solution or the interference of muscle contraction caused by the decrease of membrane potential (MP). INSMP MP and small endplate potential (MEPP) normal, EPP amplitude of up to 30mV above, is to study the effect of drugs on the joint specimens better. At INSMP, soman (5.5 μM) accelerated the MEPP frequency, and the average amplitude of string EPPs induced by string stimulation (50 Hz) and its average ACh quantum content were reduced by 80% and 77%, respectively. Small doses of triiodide quaternary ammonium phenol and hexachloroquaternary ammonium can partially antagonize the role of soman. The main reason for the inhibition of tetanic contractile induced by somatostatin is that the ACh accumulated in the terminal plate acts on the pre-synaptic N-receptor and the negative feedback inhibits the ACh’s quantum release. The secondary reason is that the post-synaptic N-receptor plays a role in ACh sensitivity reduce.