Giniatullin R A, Oranskaia T I, Voronin V A, Nikol'skiĭ E E
Neirofiziologiia. 1990;22(4):507-13.
The development of postsynaptic potentiation (PSP) and desensitization (DS) under the nonquantal secretion (NS) of acetylcholine (ACh) was studied using characteristics of miniature end-plate currents (MEPCs) in mice diaphragm muscle. The H-effect (the measure of the NS level) fell to zero during 3 hours after acetylcholinesterase (AChE) inhibition by armine at 20 degrees C. The MEPCs decay time constant (tau) decreased in parallel with the H-effect, though there was no reduction of the MEPCs amplitude in this case; tau did not change when NS was absent (early denervation). The maximal prolongation of tau after AChE inhibition was the same both in innervated (NS was normal) and denervated (NS was absent) muscle. The reduction of tau accelerated with the temperature rise and occurred after AChE inhibition by neostigmine. There was no changes in tau when AChE was active. It is suggested that nonquantal ACh decreases tau due to the DS development. NS induces no significant PSP after the AChE inhibition, but can do it later according to DS development, so that signs of DS may partially be masked by PSP.
利用小鼠膈神经肌肉标本的微小终板电流（MEPCs）特性，研究了乙酰胆碱（ACh）非量子释放（NS）条件下突触后电位增强（PSP）和脱敏（DS）的发展过程。在20℃条件下，用毒扁豆碱抑制乙酰胆碱酯酶（AChE）后3小时内，H效应（NS水平的度量）降至零。MEPCs的衰减时间常数（tau）与H效应平行下降，不过在此情况下MEPCs的幅度并未降低；当不存在NS时（早期去神经），tau没有变化。在AChE抑制后，tau的最大延长在有神经支配（NS正常）和去神经支配（NS不存在）的肌肉中是相同的。随着温度升高，tau的降低加速，并且在新斯的明抑制AChE后出现。当AChE有活性时，tau没有变化。提示非量子性ACh由于DS的发展而降低tau。在AChE抑制后，NS不诱导显著的PSP，但随后可根据DS的发展诱导PSP，因此DS的迹象可能会被PSP部分掩盖。
