Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Physiol Res. 2009;58(6):763-784. doi: 10.33549/physiolres.931865.
There are two principal mechanisms of acetylcholine (ACh) release from the resting motor nerve terminal: quantal and non-quantal (NQR); the former being only a small fraction of the total, at least at rest. In the present article we summarize basic research about the NQR that is undoubtedly an important trophic factor during endplate development and in adult neuromuscular contacts. NQR helps to eliminate the polyneural innervation of developing muscle fibers, ensures higher excitability of the adult subsynaptic membrane by surplus polarization and protects the RMP from depolarization by regulating the NO cascade and chloride transport. It shortens the endplate potentials by promoting postsynaptic receptor desensitization when AChE is inhibited during anti-AChE poisoning. In adult synapses, it can also activate the electrogenic Na(+)/K(+)-pump, change the degree of synchronization of quanta released by the nerve stimulation and affects the contractility of skeletal muscles.
乙酰胆碱(ACh)从静止运动神经末梢释放有两种主要机制:量子和非量子(NQR);前者至少在休息时只是总释放量的一小部分。在本文中,我们总结了关于 NQR 的基础研究,NQR 无疑是终板发育和成年神经肌肉接触过程中的一个重要营养因子。NQR 有助于消除发育中肌纤维的多神经元支配,通过过剩极化确保成年亚突触膜更高的兴奋性,并通过调节 NO 级联和氯离子转运来防止 RMP 去极化。当 AChE 抑制剂在抗 AChE 中毒时,它可以通过促进突触后受体脱敏来缩短终板电位。在成年突触中,它还可以激活生电性 Na(+)/K(+)-泵,改变神经刺激释放量子的同步程度,并影响骨骼肌的收缩性。