EXCITATION-CONTRACTION COUPLING IN CRUSTACEAN MUSCLE

将细胞膜的去极化与细胞的 继续评估导致收缩的细胞内钙离子 是肌肉生理学最耐人寻味的特征之一。总而言之， 肌肉类型这种机制是受调制的，经典的 例如，通过以下方式调节心肌收缩 神经递质和药物。这方面的广泛、长期目标 研究是为了了解兴奋-收缩耦合 在需要细胞外CA1来激活收缩的肌肉中， 以及神经递质和药物对它的调节，使用 以甲壳类的腹腹屈肌阿提亚毛腿为模型。 该项目的具体目标是：1)使用免疫组织化学 测定神经细胞中原胆碱和章鱼胺含量的方法 在腹神经索或肌纤维上的神经末梢；2)确定 如果这些物质增强肌肉纤维中的钙电流并开始 探讨钙电流增强的机制；3)确定 收缩激活的阈值膜电位，并评估 细胞外钙、丁卡因、原胆碱和章鱼胺的作用 关于收缩激活；4)刻画了电荷的非线性运动 检测骨骼肌，确定原胡萝卜素和章鱼胺是否改变 电荷运动；5)测定，用甘油使纤维脱管 方法：钙通道的定位。这些研究的结果 实验可能会提供重要的洞察，让我们了解 膜电位的变化会在这个和其他地方产生张力 依赖于钙离子的肌肉。

The mechanism which couples depolarization of the cell membrane to the evaluation of intracellular Ca2+ which results in contraction continues to be one of the most intriguing features of muscle physiology. In all muscle types this mechanism is subject to modulation, the classical example being the regulation of myocardial contraction by neurotransmitters and drugs. The broad, long-term objectives of this research are to gain an understanding of excitation-contraction coupling in muscles that require extracellular Ca1+ for contractile activation, and its modulation by neurotransmitters and drugs, using the ventroabdominal flexor muscle of the crustacean Atya lanipes as a model. The specific aims of the project are to: 1) use immunohistochemical methods to determine the presence of proctolin and octopamine in neurons in the ventral nerve cord or nerve endings on muscle fibers; 2) determine if these substances enhance Ca2+ currents in muscle fibers and begin to explore the mechanism by which Ca+ currents are enhanced; 3) determine the threshold membrane potential for contractile activation, and assess the effects of extracellular Ca2+, tetracaine, proctolin and octopamine on contractile activation; 4) characterize nonlinear charge movement in Atya skeletal muscle and determine whether proctolin and octopamine alter charge movement; 5) determine, detubulating the fibers with the glycerol method, the localization of the Ca2+ channels. The results of these experiments may provide important insights into the mechanisms that link membrane potential changes to the generation of tension in this and other Ca2+- dependent muscles.