EXCITATION-CONTRACTION COUPLING IN CRUSTACEAN MUSCLE

将细胞膜去极化与细胞外膜去极化耦合的机制， 导致收缩的细胞内Ca 2+的评估继续进行 是肌肉生理学最有趣的特征之一。 在所有 肌肉类型这种机制是受调制，经典的 例如， 神经递质和药物。 这一广泛的长期目标 研究的目的是了解兴奋-收缩耦合 在需要细胞外Ca 1+来激活收缩的肌肉中， 以及通过神经递质和药物的调节， 腹腹屈肌的甲壳动物Atya lanipes作为模型。 该项目的具体目标是：1）使用免疫组织化学 测定神经元中的普罗托林和章鱼胺的存在的方法 在腹神经索或肌肉纤维上的神经末梢; 2）确定 如果这些物质增强肌纤维中的Ca 2+电流并开始 探讨Ca+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Ca ~（2+）、丁卡因、普罗托林和章鱼胺 收缩激活; 4）表征非线性电荷运动， Atya骨骼肌，并确定是否proctolin和章鱼胺改变 电荷运动; 5）测定，用甘油使纤维脱管， 方法，钙离子通道的定位。 的结果予以 实验可能会提供重要的洞察机制， 膜电位的变化，以产生张力，在这和其他 Ca 2+依赖性肌肉。

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.