肌细胞的收缩功能2013.ppt

骨骼肌Skeletal Muscle 肌纤维=肌细胞 运动神经元：其轴突支配肌纤维 运动单位Motor Unit = 一个运动神经元a motor neuron + 肌纤维 muscle fibers Ca 2+ 通道的开放和Ach 的释放 末梢钮扣: 含有上千个囊泡， Ach 存在其中。 The axon terminal is enlarged into the terminal button. Each terminal button contains thousands of vesicles that store Ach. 动作电位可触发末梢钮扣处的电压门控钙离子通道打开。钙离子内流可引起Ach 以出胞方式释放。 Propagation of action potential the terminal triggers the opening of Ca 2+ channels in the terminal button. It permits Ca 2+ to diffuse into the terminal button from extracellular fluid, which in turn causes the release of Ach by exocytosis from the vesicles. 终板电位 End plate potential Ach 与运动终板上受体结合，诱导Na+ - K+，化学门控通道开放。 Binding of Ach with the receptor site in the motor end-plate induces the opening of channels . 钠进多于钾出，使运动终板去极化，产生终板电位（EPP）（终板膜本身无电压门控钠通道，故不会产生动作电位） 形成局部电流后可使邻近肌膜产生动作电位。 More Na+ moves inward than K+ outward, bringing about a depolarization of the motor end plate -----This potential is known as end-plate potential (EPP). Local current can reach the threshold of adjacent muscle fiber membrane） and bring about an action potential. 乙酰胆碱酯酶Acetylcholinesterase 运动终板表面含乙酰胆碱酯酶，可分解突触间隙游离的ACh 。 The surface of the motor end plate contains the enzymes acetylcholinesterase, which can break downfree Ach in the cleft. As the concentration of free ACh falls because of its breakdown by acetylcholinesterase, less ACh is available to bind to the receptors. When receptors no longer contain bound Ach, the ion channels in the end plate close. The depolarized end plate returns to its resting potential and can respond to the subsequent arrival of ACh. 有机磷农药中毒 有机磷农药中毒一般认为是抑制了胆碱酯酶的活性，造成组织中乙酰胆碱的积聚，其结果引起胆碱能受体活性紊乱， 而使有胆碱能受体的器官功能发生障碍。凡由脏器平滑肌、腺体、汗腺等兴奋而引起的症状，与毒蕈中毒所引起的症状相似，则称为毒蕈样症状； 凡由交感神经节和横纹肌活动异常所引起的症状，与烟碱中毒所引起的症状相似，故称烟碱样症状。 症状 副交感神经和分布于汗腺的交感神经节后纤维的胆碱能受体兴奋，表现腺体分泌增加，可见大汗、流涎和支气管分泌物增多。虹膜括约肌收缩使瞳孔缩小，胃肠平滑肌兴奋引起恶心、呕吐、腹泻、腹痛。心血管系统受抑制而致心跳缓慢，血压下降。 以上症状与毒蕈中毒症状相似故称毒蕈碱样 症状 运动神经肌肉连接点胆碱能受体兴奋，表现肌肉纤维颤动或抽搐，晚期则见肌无力或麻痹。交感神经节前纤维和支配肾上腺髓质交感神经胆碱能受体兴奋可见血压上升、心率加快、体温升高等症状，这与烟碱中毒的症状相似，称烟碱样作