Llados F T
J Neurol Sci. 1985 Jul;69(3):171-82. doi: 10.1016/0022-510x(85)90131-5.
An experimental myopathy was induced in frog skeletal muscle incubated in vitro with the calcium ionophore A23187. This myopathy could be prevented if Ca2+ ions in the incubating medium were replaced by either Mg2+ or Co2+ ions. Similarly, preincubation of the preparation with acetylcholine (ACh) receptor blockers such as d-tubocurarine (d-TC) or alpha-bungarotoxin (alpha-BuTX) prevented the development of muscle damage. In muscles that had been previously denervated or treated with botulinum toxin (BTX) the ionophore failed to induce morphological alterations. These results suggest that spontaneous transmitter release, greatly increased by the ionophore A23187, triggers Ca2+ influx into the muscle fibres at the endplate region. Elevated levels of intracellular Ca2+ presumably activate proteolytic systems leading to myofilament disassembly.
用钙离子载体A23187在体外孵育青蛙骨骼肌，诱发了实验性肌病。如果将孵育培养基中的Ca2+离子替换为Mg2+或Co2+离子，这种肌病是可以预防的。同样，用乙酰胆碱（ACh）受体阻滞剂如d-筒箭毒碱（d-TC）或α-银环蛇毒素（α-BuTX）对标本进行预孵育，可防止肌肉损伤的发生。在先前已去神经支配或用肉毒杆菌毒素（BTX）处理过的肌肉中，离子载体未能诱发形态学改变。这些结果表明，离子载体A23187极大地增加了自发递质释放，触发了终板区域Ca2+流入肌纤维。细胞内Ca2+水平升高可能激活蛋白水解系统，导致肌丝解体。
