[甲状腺毒性肌病肌纤维的运动神经支配]。

V M Kazakov
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引用次数: 0

摘要

在病人和实验动物中也发现了类似的神经支配变化。一些前端轴突出现退化。最明显的特征是远端轴突分支增加。没有发现真正神经再生的迹象。前终轴突、终轴突和++超终轴突的新侧支通常以附加神经末梢的形式在同一肌纤维上结束。实验动物的运动端板平均直径的减小并不取决于它们的退化,而是由于远端轴突未成熟的轴突分支导致新的小运动端板的形成。终板乙酰胆碱酯酶活性降低。提示骨骼肌中甲状腺激素的过量扰乱了环核苷酸系统和肌肉收缩机制,分别与它和轴浆运输有关。末梢肌内神经支配的变化表明,运动终板结构中乙酰胆碱酯酶活性降低,可能是由于甲状腺激素过量引起轴浆电流紊乱,导致肌纤维神经营养调节紊乱所致。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Motor innervation of muscle fibers in thyrotoxic myopathy].

In patients and test animals similar changes in innervation have been revealed. Degeneration of some preterminal axons has been shown. The most manifested feature's increased ramification of distal axons. No signs of real reinnervation have been found. New collateral branches of preterminal, terminal and ++ultra-terminal axons usually have their ends at the same muscle fiber in the form of additional nervous terminals. Decreased average diameter of motor end-plates, revealed in the test animals, depends not on their degeneration, but on formation of new small motor end plates as a result of immature axonal ramification of distal axons. Acetylcholinesterase activity in the end-plates is decreased. A suggestion is made that excess of thyroid hormones in the skeletal muscle disturbs both the system of cyclic nucleotides and mechanisms of muscular contraction, connected with it and axoplasmic transport, respectively. The changes of the terminal intramuscular innervation revealed, structures of the motor end-plates with a decrease of acetylcholinesterase activity are supposed to result from disturbances of neurotrophic regulation of the muscle fibers because of the disturbances of the axoplasmic current as the excess of thyroid hormones.

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