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[乙酰胆碱酯酶抑制条件下量子成分、膜电位和胆碱能受体密度对大鼠终板电流时间进程的影响]

[Effect of the quantal composition, membrane potential and cholinoreceptor density on the temporal flow of the end plate current in the rat under conditions of acetylcholinesterase inhibition].

作者信息

Giniatullin R A, Shvetsov A B

出版信息

Neirofiziologiia. 1992;24(3):269-79.

PMID:1513401
Abstract

The factors determining the decay of multiquantal end plate currents (EPC) were studied in the diaphragm muscle of rat by the comparison of EPC and miniature EPC (MEPC) amplitude--temporal characteristics. The decay of EPC (quantal content 25-100) was 1.2 times slower than the decay of MEPC when AChE was active. The AChE inhibition by armine or neostigmine made this difference 10-100 times higher. In most synapses the decay of multiquantal EPC can be approximated by a sum of two or three exponents. It depended on the quantal content and 3-exponential EPC could be transformed in 2-exponential and later to monoexponential ones if increasing concentration of magnesium ions. A slow component of EPCs (but not of MEPC) decay was highly sensitive to concentration of magnesium ions and had 3 times higher dependence of the membrane potential value than that one of MEPC. The irreversible blocking of receptors by alpha-bungarotoxin (alpha-BuTX) accelerated the decay of MEPC but the decay of multiquantal EPC changed in two phases: it was prolonged at the beginning of alpha-BuTX action followed by its acceleration, but never the time of the decay of EPC had achieved the apparent open time of ACh-activated ionic channels. It is suggested that during the multiquantal EPC generation not only the synchronization of opening but the kinetic of ACh-activated channels is changed, probably by blocking of this channels by high concentrations of endogenous ACh.

摘要

通过比较终板电流(EPC)和微小终板电流(MEPC)的幅度 - 时间特性,研究了大鼠膈肌中决定多量子终板电流衰减的因素。当乙酰胆碱酯酶(AChE)活性存在时,EPC(量子含量为25 - 100)的衰减比MEPC的衰减慢1.2倍。用毒扁豆碱或新斯的明抑制AChE使这种差异增大10 - 100倍。在大多数突触中,多量子EPC的衰减可用两个或三个指数之和来近似。它取决于量子含量,并且如果增加镁离子浓度,三指数EPC可转变为二指数EPC,随后再转变为单指数EPC。EPC(而非MEPC)衰减的慢成分对镁离子浓度高度敏感,并且其对膜电位值的依赖性是MEPC的3倍。α-银环蛇毒素(α-BuTX)对受体的不可逆阻断加速了MEPC衰减,但多量子EPC的衰减在两个阶段发生变化:在α-BuTX作用开始时延长,随后加速,但EPC衰减的时间从未达到ACh激活离子通道的明显开放时间。有人提出,在多量子EPC产生过程中,不仅通道开放的同步性发生变化,而且ACh激活通道的动力学也发生变化,这可能是由于高浓度内源性ACh对这些通道的阻断所致。

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