[“非量子”乙酰胆碱对突触后膜敏感性的影响:乌阿巴因的作用和外源性乙酰胆碱对这些作用的模仿]。

Neirofiziologiia = Neurophysiology Pub Date : 1992-01-01
R A Giniatullin, T I Oranskaia, R N Khazipov
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引用次数: 0

摘要

通过乌阿巴因研究乙酰胆碱酯酶抑制后“非量子”乙酰胆碱引起的突触后增强(PSP)和脱敏(DS)的发展,乌阿巴因是一种已知的调节乙酰胆碱非量子分泌水平的药物(先升高后降低)。AChE激活时,瓦巴因对MEPC参数无影响。在AChE抑制后,瓦巴因最初增加MEPC (tau)的衰减时间常数,即引起突触后增强(PSP)。这种效果随着抑制乙酰胆碱和应用瓦阿因之间的时间而增加。PSP阶段之后,由于脱敏(DS)的发展,mepc衰变缩短,这一过程比对照组更为明显。在AChE抑制前应用瓦巴因,对tau蛋白无影响。因此PSP和DS都不是在这样的条件下发展起来的。外源性乙酰胆碱ACh (20 nmol/l)与乙酰胆碱AChE抑制剂同时施用,部分阻止了MEPC衰减的缩短,但降低了MEPC的振幅。在MEPCs缩短后,外源ACh (50 nmol/l)倾向于返回tau的初始值。由此可见,非量子化乙酰胆碱抑制乙酰胆碱后在突触后膜上产生PSP和DS,且在停止非量子化乙酰胆碱分泌后,DS持续存在较长时间。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Effects of "non-quantal" acetylcholine on the sensitivity of the postsynaptic membrane: action of ouabain and imitation of these effects by exogenous acetylcholine].

Development of postsynaptic potentiation (PSP) and desensitization (DS) caused by "non-quantal" acetylcholine after acetylcholinesterase inhibition was studied by means of ouabain, an agent known to modulate (initially increase and then decrease) the level of non-quantal secretion of ACh. Ouabain had no effect on the MEPC parameters when AChE was active. After AChE inhibition ouabain initially increased the decay time constant of MEPC (tau), i.e. caused postsynaptic potentiation (PSP). This effect of ouabain grew with time between inhibition of AChE and application of ouabain. The PSP stage was followed by shortening of MEPCs decay, due to the development of desensitization (DS), and that process was more pronounced than in control. Applied before AChE inhibition, ouabain had no effect on tau. Thus neither PSP nor DS developed under those conditions. Exogenous ACh (20 nmol/l) applied simultaneously with inhibitor of AChE partially prevented the shortening of MEPCs decay, but decreased the amplitude of MEPC. Applied after MEPCs shortening, exogenous ACh (50 nmol/l) tended to return the initial value of tau. It is concluded that nonquantal ACh produces PSP and DS on the postsynaptic membrane after inhibition of ACh and that the DS persists after cessation of nonquantal secretion for a long time.

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