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在不均匀牵张的大鼠离体膈肌标本上,同时记录同一终板的小终板电位(MEPP),终板电位(EPP)和微电泳外源性乙酰胆碱(ACh)诱发的乙酰胆碱电位(AChP)。以AChP幅度为突触后膜兴奋性大小指标,对MEPP和EPP进行校正;以量子含量M和二项统计参数即刻可释放量子贮存n及平均量子释放机率P为突触前递质释放指标,定量观察了新霉素(neomycin)对突触前和突触后的作用。结果表明新霉素(30μmol/L,100μmol/L)作用20min,对AChP,MEPP无影响,M_l,M_x,n和P明显下降,串EPPs(50Hz)出现脱落现象,表明此浓度下的新霉素对接头的作用主要是抑制突触前诱发的递质释放,对自发释放的量子大小并无影响。其机理可能是新霉素拮抗Ca~(2+)内流,减小n和P,从而降低诱发的递质释放。
In the non-uniform distraction rat diaphragmatic muscle specimens, both MEPP, EPP and ACh-induced acetylcholine potentials (AChP ). MEPP and EPP were calibrated with the magnitude of AChP as the index of postsynaptic membrane excitability. With the quantum content M and binomial statistical parameters of immediate release quantum storage n and average quantum release probability P as presynaptic transmitter release index, The effect of neomycin on presynaptic and postsynaptic effects was quantitatively observed. The results showed that neomycin (30μmol / L, 100μmol / L) for 20min had no effect on AChP and MEPP, but M_l, M_x, n and P decreased obviously. The effect of the para-linker is primarily to inhibit the presynaptic-evoked release of the transmitter, which has no effect on the spontaneous release of the quantum size. The mechanism may be that neomycin antagonizes Ca ~ (2+) influx, reducing n and P, thereby reducing the evoked transmitter release.