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铵和氯的排出:脊髓运动神经元中的超极化突触抑制

Ammonium and chloride extrusion: hyperpolarizing synaptic inhibition in spinal motoneurons.

作者信息

Lux H D

出版信息

Science. 1971 Aug 6;173(3996):555-7. doi: 10.1126/science.173.3996.555.

Abstract

The reversal potential of postsynaptic inhibition shifts toward resting membrane potentials in cat spinal motoneurons after intravenous infusion of ammonium salts(1 to 3 millimoles per kilogram of body weight). Simultaneously, the depolarizing action of intracellularly injected chloride ions on the inhibitory membrane is enhanced and recovery therefrom is prolonged. Passive membrane properties remain unaltered. The results indicate a blocking of active extrusion of chloride which normally maintains a high ionic gradient for hyperpolarizing inhibition.

摘要

静脉注射铵盐(每千克体重1至3毫摩尔)后,猫脊髓运动神经元中突触后抑制的反转电位向静息膜电位偏移。同时,细胞内注入氯离子对抑制性膜的去极化作用增强,且恢复时间延长。被动膜特性保持不变。结果表明,正常情况下维持超极化抑制的高离子梯度的氯离子主动外排被阻断。

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