INTRAMEMBRANE CHARGE MOVEMENT RESTORED IN DYSGENIC SKELETAL-MUSCLE BY INJECTION OF DIHYDROPYRIDINE RECEPTOR CDNAS
INTRAMEMBRANE CHARGE MOVEMENT RESTORED IN DYSGENIC SKELETAL-MUSCLE BY INJECTION OF DIHYDROPYRIDINE RECEPTOR CDNAS
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DOI：
10.1038/346569a0
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发表时间：
1990-08-09
期刊：
影响因子：
64.8
通讯作者：
BEAM, KG
中科院分区：
文献类型：
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作者：
ADAMS, BA;TANABE, T;BEAM, KG
骨骼肌二氢吡啶 (DHP) 受体在兴奋-收缩 (EC) 耦合中至关重要 1-4。假设受体是产生膜内电流（称为电荷运动）的电压传感器。我们现在已经使用来自具有肌发育不良突变的小鼠的肌管测试了这一假设，该突变改变了骨骼肌DHP受体基因并阻止其表达3,4,6。我们的结果表明，在肌发育不良的肌管中，电荷运动存在缺陷，但在注射携带兔骨骼肌DHP受体互补DNA的表达质粒后，电荷运动完全恢复，有力地支持了DHP受体是骨骼肌中EC耦合的电压传感器的假设。此外，我们对正常和嵌合 DHP 受体构建体获得的数据表明，具有广泛不同能力的 DHP 受体作为钙通道发挥作用并介导 EC 偶联，产生非常相似的电荷运动
THE skeletal muscle dihydropyridine (DHP) receptor is essential in excitation–contraction (EC) coupling1–4. The receptor is postulated to be the voltage sensor giving rise to the intramembrane current, termed charge movement5. We have now tested this hypothesis using myotubes from mice with the muscular dysgenesis mutation, which alters the skeletal muscle DHP receptor gene and prevents its expression3,4,6.Our results indicate that charge movement is deficient in dysgenic myotubes but is fully restored following injection of an expression plasmid carrying the rabbit skeletal muscle DHP receptor complementary DNA, strongly supporting the hypothesis that the DHP receptor is the voltage sensor for EC coupling in skeletal muscle. Additionally, our data obtained for normal and chimaeric DHP receptor constructs demonstrate that DHP receptors with widely differing abilities to function as calcium channels and to mediate EC coupling produce very similar charge movements