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亚微摩尔级细胞外Ca2+活性下大鼠皮层突触体去极化的机制。使用Ca2+缓冲剂控制突触体膜电位。

Mechanism of depolarization of rat cortical synaptosomes at submicromolar external Ca2+ activity. The use of Ca2+ buffers to control the synaptosomal membrane potential.

作者信息

Schmalzing G

出版信息

Biochem J. 1985 Feb 1;225(3):671-80. doi: 10.1042/bj2250671.

DOI:10.1042/bj2250671
PMID:3977854
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1144643/
Abstract

Rat cortical synaptosomes responded to a reduction of external Ca2+ from pCa 3.5 to pCa 4.8 in the absence of MgCl2 with a slight decrease of internal K+ and an increase of Na+. The effects were prevented by tetrodotoxin or millimolar concentrations of MgCl2. Further lowering of external pCa to 7.7 with N-hydroxyethylethylenediaminetriacetate evoked a rapid fall of internal K+, which was specifically blocked by Ruthenium Red; tetrodotoxin and nifedipine were ineffective. A linear relationship was established between K+ and methyltriphenylphosphonium cation distribution ratios by varying external pCa between 4.8 and 7.7, indicating that K+ efflux resulted from a depolarization of the plasma membrane. An increase of Na+ permeability was suggested by the synaptosomes' gain of Na+ and the disappearance of the depolarization in an Na+-free sucrose medium. According to the constant field equation, the permeability ratio PNa/PK increased from 0.029 at pCa4.8 to 0.090 at pCa 7.7 with plasma membrane potentials of -74mV and -47mV, respectively. Since the plasma membrane responded to variation of external Ca2+ activities in the micromolar range with a graded and sustained depolarization, the use of Ca2+ buffers to control membrane potentials is suggested.

摘要

在没有MgCl₂的情况下,大鼠皮层突触体对细胞外Ca²⁺从pCa 3.5降至pCa 4.8的反应是细胞内K⁺略有减少,Na⁺增加。这些效应可被河豚毒素或毫摩尔浓度的MgCl₂阻止。用N-羟乙基乙二胺三乙酸将细胞外pCa进一步降至7.7会引起细胞内K⁺迅速下降,这被钌红特异性阻断;河豚毒素和硝苯地平无效。通过在4.8至7.7之间改变细胞外pCa,在K⁺与甲基三苯基鏻阳离子分布比率之间建立了线性关系,表明K⁺外流是由质膜去极化引起的。突触体对Na⁺的摄取以及在无Na⁺蔗糖培养基中去极化的消失表明Na⁺通透性增加。根据恒定场方程,在质膜电位分别为-74mV和-47mV时,通透性比率PNa/PK从pCa4.8时的0.029增加到pCa 7.7时的0.090。由于质膜对微摩尔范围内细胞外Ca²⁺活性的变化以分级和持续的去极化做出反应,因此建议使用Ca²⁺缓冲剂来控制膜电位。

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Energy transduction in intact synaptosomes. Influence of plasma-membrane depolarization on the respiration and membrane potential of internal mitochondria determined in situ.完整突触体中的能量转导。质膜去极化对原位测定的线粒体内呼吸和膜电位的影响。
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