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钠离子通道的异常表达加速了非洲爪蟾胚胎骨骼肌中钾离子通道的发育。

Na+ channel mis-expression accelerates K+ channel development in embryonic Xenopus laevis skeletal muscle.

作者信息

Linsdell P, Moody W J

机构信息

Department of Zoology, University of Washington, Seattle 98195.

出版信息

J Physiol. 1994 Nov 1;480 ( Pt 3)(Pt 3):405-10. doi: 10.1113/jphysiol.1994.sp020370.

Abstract
  1. The normal developmental pattern of voltage-gated ion channel expression in embryonic skeletal muscle cells of the frog Xenopus laevis was disrupted by introduction of cloned rat brain Na+ channels. 2. Following injection of channel mRNA into fertilized eggs, large Na+ currents were observed in muscle cells at the earliest developmental stage at which they could be uniquely identified. Muscle cells normally have no voltage-gated currents at this stage. 3. Muscle cells expressing exogenous Na+ channels showed increased expression of at least two classes of endogenous K+ currents. 4. This increase in K+ current expression was inhibited by the Na+ channel blocker tetrodotoxin, suggesting that increased electrical activity caused by Na+ channel mis-expression triggers a compensatory increase in K+ channel expression. 5. Block of endogenous Na+ channels in later control myocytes retards K+ current development, indicating that a similar compensatory mechanism to that triggered by Na+ channel mis-expression operates to balance Na+ and K+ current densities during normal muscle development.
摘要
  1. 克隆大鼠脑钠通道的导入破坏了非洲爪蟾胚胎骨骼肌细胞中电压门控离子通道表达的正常发育模式。2. 将通道mRNA注射到受精卵中后,在肌肉细胞最早可被明确识别的发育阶段观察到了大的钠电流。在此阶段,肌肉细胞通常没有电压门控电流。3. 表达外源钠通道的肌肉细胞显示至少两类内源性钾电流的表达增加。4. 钠通道阻滞剂河豚毒素抑制了钾电流表达的这种增加,这表明由钠通道错误表达引起的电活动增加触发了钾通道表达的代偿性增加。5. 在后期对照肌细胞中阻断内源性钠通道会延缓钾电流的发育,这表明在正常肌肉发育过程中,存在一种与钠通道错误表达触发的机制类似的代偿机制,用于平衡钠电流和钾电流密度。

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