EXCITATION-CONTRACTION COUPLING IN CRUSTACEAN MUSCLE

甲壳动物肌肉的兴奋-收缩耦合

• 批准号: 6243382
• 负责人: CONCHITA ZUAZAGA
• 金额: $ 9.31万
• 依托单位: UNIVERSITY OF PUERTO RICO MED SCIENCES
• 依托单位国家: 美国
• 财政年份: 1997
• 资助国家: 美国
• 起止时间: 1997-09-01 至 1999-07-27
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6243382
• 关键词: Malacostraca; action potentials; alternatives to animals in research; calcium; calcium channel; calcium flux; cyclic AMP; electron microscopy; ganglions; immunocytochemistry; membrane potentials; microelectrodes; motor neurons; muscle contraction; muscle tension; nerve threshold; neuromuscular function; neuromuscular junction; neurotransmitters; octopamine; phosphorylation; sarcoplasmic reticulum; voltage /patch clamp

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.

将细胞膜去极化的机制 细胞内Ca2+的评估，导致收缩继续 成为肌肉生理学最有趣的特征之一。 总的来说 肌肉类型这种机制受到调制，经典 例子是对心肌收缩的调节 神经递质和药物。 这一广泛的长期目标 研究是为了了解激发反应耦合 在需要细胞外CA1+收缩激活的肌肉中， 及其对神经递质和药物的调节，使用 甲壳类动物灯笼的腹腹屈肌作为模型。 该项目的具体目的是：1）使用免疫组织化学 确定神经元中前血管林和章鱼胺的存在的方法 在腹侧神经绳或肌肉纤维上的神经末端； 2）确定 如果这些物质增强了肌肉纤维中的Ca2+电流，然后开始 探索加强CA+电流的机制； 3）确定 收缩激活的阈值膜潜力，并评估 细胞外Ca2+，四卡因，尿可素和章鱼胺的影响 关于收缩激活； 4）表征非线性电荷运动 ATYA骨骼肌并确定proctolin和章鱼胺是否改变 电荷运动； 5）确定，用甘油卸下纤维 方法，CA2+通道的定位。 这些结果 实验可能会提供有关连接机制的重要见解 膜的潜力改变了这一和其他紧张的产生 Ca2+ - 依赖性肌肉。