Giniatullin R A, Khazipov R N, Oranskaia T I
Biull Eksp Biol Med. 1992 Jul;114(7):6-7.
The mechanism of shortening MEPC decay phase after initial prolongation due to acetylcholinesterase inhibition by armine and neostigmine was studied by use of two-electrode voltage-clamp at the mice diaphragm Factors which switch off non-quantal secretion of acetylcholine from the nerve (acute denervation in vitro, ouabain, high concentration of magnesium ions) only slightly reduced the prolongation of MEPC caused by AChE inhibition. So, postsynaptic potentiation of MEPC by nonquantal ACh is not significant immediately after AChE inhibition. At the same time these factors abolished the process of shortening MEPC decay phase. It is concluded, that desensitization of the postsynaptic membrane induced by nonquantal ACh is the main mechanism of the MEPC shortening and that this mechanism can compensate insufficient AChE activity.
利用双电极电压钳技术在小鼠膈肌上研究了由于阿米宁和新斯的明抑制乙酰胆碱酯酶而导致的终板电流（MEPC）衰减期在最初延长后缩短的机制。关闭神经非量子性乙酰胆碱分泌的因素（体外急性去神经、哇巴因、高浓度镁离子）仅轻微降低了由乙酰胆碱酯酶抑制引起的MEPC延长。因此，在乙酰胆碱酯酶抑制后立即，非量子性乙酰胆碱对MEPC的突触后增强作用并不显著。同时，这些因素消除了MEPC衰减期缩短的过程。得出的结论是，非量子性乙酰胆碱诱导的突触后膜脱敏是MEPC缩短的主要机制，并且该机制可以补偿乙酰胆碱酯酶活性不足。
