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去神经支配小鼠肌肉的乙酰胆碱和钾挛缩中的力与膜电位

Force and membrane potential in acetylcholine and potassium contractures of denervated mouse muscles.

作者信息

Lorković H

出版信息

Pflugers Arch. 1985 May;404(1):50-5. doi: 10.1007/BF00581490.

DOI:10.1007/BF00581490
PMID:4011399
Abstract

Depolarization and contracture force (P) provoked by acetylcholine (ACh) and by K ions were studied in bundles dissected from mouse soleus muscles that had been denervated for 4-7 days. Cl-free solutions were used. The muscle fibres were depolarized by solutions containing 150 mM K or 10 microM ACh to nearly zero mV resulting in maximum P (Pmax). Threshold P was produced when the membrane was depolarized to more than about -60 mV by both agents. 50% Pmax was produced by [K] causing the membrane to depolarize to -42 mV, whereas a potential more positive than -20 mV was required for 50% Pmax to be produced when ACh was used. The rate of depolarization was always higher for ACh than for K. Pretreatment by 0.05 microM ACh (about threshold for P) did not affect the P-[K] relation appreciably showing that ACh did not "stabilize" the membrane. Nearly equal P was provoked by successive applications of just suprathreshold agent concentrations when the order of application was ACh----K but not with the reverse order. Hypertonicity (by addition of 300 mM sucrose to all solutions) caused PACh to decrease and PK to increase. It was concluded that the ACh receptors are located in the surface membrane of the muscle fibres, not in the T-system membranes.

摘要

在从已去神经4 - 7天的小鼠比目鱼肌中分离出的肌束中,研究了乙酰胆碱(ACh)和钾离子(K)引发的去极化和挛缩力(P)。使用了无氯溶液。含有150 mM K或10 microM ACh的溶液可使肌纤维去极化至接近零mV,从而产生最大P(Pmax)。当两种试剂使膜去极化至超过约 -60 mV时,产生阈值P。[K]使膜去极化至 -42 mV时产生50% Pmax,而使用ACh时,产生50% Pmax需要比 -20 mV更正的电位。ACh引起的去极化速率总是高于K。用0.05 microM ACh(约为P的阈值)预处理对P-[K]关系没有明显影响,表明ACh并未使膜“稳定”。当施加顺序为ACh----K时,连续应用刚好高于阈值的试剂浓度所引发的P几乎相等,但顺序相反时则不然。高渗性(通过在所有溶液中添加300 mM蔗糖)导致PACh降低而PK升高。得出的结论是,ACh受体位于肌纤维的表面膜中,而非T系统膜中。

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本文引用的文献

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