Donaldson S K, Goldberg N D, Walseth T F, Huetteman D A
Department of Physiology, School of Medicine, University of Minnesota, Minneapolis 55455.
Proc Natl Acad Sci U S A. 1988 Aug;85(15):5749-53. doi: 10.1073/pnas.85.15.5749.
Excitation-contraction coupling in skeletal muscle is known to be under absolute control of plasmalemma voltage, but the steps from transverse (T)-tubule depolarization to Ca2+ release from the sarcoplasmic reticulum have not been elucidated. The effect of changing T-tubule membrane potential on inositol 1,4,5-trisphosphate (InsP3) stimulation of Ca2+ release from the sarcoplasmic reticulum was studied to explore a possible role for InsP3 as a chemical signal in excitation-contraction coupling. InsP3 was microinjected into peeled rabbit skeletal muscle fibers at a pipette concentration of 0.5 microM; Ca2+ release from the sarcoplasmic reticulum was monitored as an isometric tension transient. The response to 0.5 microM InsP3 was significantly larger when T-tubules were in a depolarized state than when they were in a polarized state, and this difference in response was independent of the ionic composition of the bathing solutions or the method for depolarizing the T-tubules. Thus, T-tubule depolarization may sensitize the sarcoplasmic reticulum to a preexisting low concentration of InsP3 and greatly reduce the need for InsP3 production. Plasmalemma voltage control of the stimulatory effects of InsP3 may have relevance for mechanisms in excitable nonmuscle cells.
已知骨骼肌中的兴奋 - 收缩偶联完全受质膜电压控制，但从横管（T管）去极化到肌浆网释放Ca2+的具体步骤尚未阐明。本研究通过改变T管膜电位对肌醇1,4,5 - 三磷酸（InsP3）刺激肌浆网释放Ca2+的影响，来探索InsP3作为兴奋 - 收缩偶联中化学信号的可能作用。将浓度为0.5微摩尔的InsP3以微量注射的方式注入剥离的兔骨骼肌纤维；将肌浆网释放Ca2+作为等长张力瞬变进行监测。当T管处于去极化状态时，对0.5微摩尔InsP3的反应明显大于其处于极化状态时，且这种反应差异与浴液的离子组成或使T管去极化的方法无关。因此，T管去极化可能使肌浆网对预先存在的低浓度InsP3敏感，并大大减少对InsP3产生的需求。质膜电压对InsP3刺激作用的控制可能与可兴奋非肌肉细胞中的机制有关。
