EXCITATION/CONTRACTION COUPLING IN CRUSTACEAN MUSCLE

将细胞膜的去极化与细胞的 导致收缩的细胞内钙离子升高继续 是肌肉生理学最耐人寻味的特征之一 肌肉类型这种机制受到调制的影响，这是一个经典的例子 是神经递质对心肌收缩的调节作用 毒品。这项研究的广泛、长期目标是获得 对肌肉兴奋-收缩偶联的理解 细胞外钙离子对收缩的激活作用及其调节作用 神经递质和药物，使用腹腹屈肌 甲壳类动物阿提亚·拉尼普斯作为模特。该项目的具体目标是 1)使用免疫组织化学方法确定是否存在 原胡萝卜素和章鱼胺在腹神经核或神经中的神经元 肌肉纤维上的末端；2)确定这些物质是否增强钙 并开始探索钙离子在肌纤维中的作用机制 电流增强；3)确定膜的阈值电位 收缩激活，并评估细胞外钙离子的作用， 丁卡因、原甲酚和章鱼胺对收缩活动的影响；4) 表征ATYA骨骼肌中的非线性电荷运动和 确定原蛋白和章鱼胺是否改变电荷运动；5) 测定，用甘油法脱管纤维， 钙离子通道的定位。这些实验的结果可能 对连接膜电位的机制提供了重要的见解 这种和其他钙离子依赖的张力产生的变化 肌肉。

The mechanism which couples depolarization of the cell membrane to the elevation of intracellular Ca2+ which results in contraction continues to be one of the most intriguing features of muscle physiology.l 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 Ca2+ 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 athe ventral nerve cored 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 Ca2+ 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 protolin 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.