Electrical activity and postsynapse formation in adult muscle:: γ-AChRs are not required
Electrical activity and postsynapse formation in adult muscle:: γ-AChRs are not required
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DOI：
10.1006/mcne.2000.0911
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发表时间：
2000-12-01
影响因子：
3.5
通讯作者：
Brenner, HR
中科院分区：
文献类型：
--
作者：
Hashemolhosseini, S;Moore, C;Brenner, HR
骨骼肌纤维不会接受外来运动轴突的超神经支配，除非它们被麻痹，这表明瘫痪使它们能够接受神经支配，例如，通过上调突触外的伽马-AChRs和/或集聚蛋白受体Musk的表达。为了研究这些参数在麻痹介导的突触诱导中的作用，我们使支配神经肌肉突触形成的运动神经元因子集聚蛋白的异位表达依赖于支配的成人肌肉纤维中多西环素的给药。作为对多西环素诱导的集聚蛋白分泌的反应，成体纤维确实形成了异位突触后特化，即使它们是电活跃的，缺乏胎儿AChRs，并且表达正常低水平的麝香。这些数据表明，麻痹和与之相关的变化不是集聚蛋白诱导的突触后形成所必需的。他们认为，瘫痪的肌肉通过释放使运动神经突起接触肌肉纤维并分泌集聚蛋白的因子来诱导突触的形成。
Skeletal muscle fibers will not accept hyperinnervation by foreign motor axons unless they are paralyzed, suggesting that paralysis makes them receptive to innervation, e.g., by upregulating extrasynaptic expression of gamma -AChRs and/or of the agrin receptor MuSK. To examine the involvement of these parameters in paralysis-mediated synapse induction, ectopic expression of agrin, a factor from motor neurons controlling neuromuscular synapse formation, was made dependent on the administration of doxycycline in innervated adult muscle fibers. In response to doxycycline-induced agrin secretion, adult fibers did form ectopic postsynaptic specializations, even when they were electrically active, lacked fetal AChRs, and expressed normal low levels of MuSK. These data demonstrate that paralysis and changes associated with it are not required for agrin-induced postsynapse formation. They suggest that paralyzed muscle induces synapse formation via the release of factors that make motor neurites contact muscle fibers and secrete agrin.