Electrical stimulation delays reinnervation in denervated rat muscle

被引:12
作者
Pinheiro-Dardis, Clara M. [1 ]
Erbereli, Bruna T. [1 ]
Gigo-Benato, Davilene [1 ]
Castro, Paula A. T. S. [2 ]
Russo, Thiago L. [1 ]
机构
[1] Univ Fed Sao Carlos UFSCar, Dept Fisioterapia, Fisioterapia Neurol LaFiN, Km 235,CP 676, BR-13565905 Sao Carlos, SP, Brazil
[2] Univ Fed Sao Carlos, DFisio, Lab Muscle Plast, Sao Carlos, SP, Brazil
基金
巴西圣保罗研究基金会;
关键词
muscle atrophy; neurology; neuromuscular junction; neurorehabilitation; physiotherapy; FUNCTIONAL RECOVERY; PERIPHERAL-NERVE; GENE-EXPRESSION; ATROPHY; REPAIR; REGENERATION; RECEPTORS; FORCE; MUSK; NCAM;
D O I
10.1002/mus.25589
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
IntroductionIt is not clear if electrical stimulation (ES) can affect muscle reinnervation. This study aimed to verify if ES affects neuromuscular recovery after nerve crush injury in rats. MethodsDenervated muscles were electrically stimulated daily for 6 or 14 days. Neuromuscular performance and excitability, and muscle morphology were determined. Muscle trophism markers (atrogin-1, MuRF-1, and myoD), as well as neuromuscular junction (NMJ) organization (muscle-specific receptor tyrosine kinase [MuSK], cytoplasmic protein downstream of kinase-7 [Dok-7], nicotinic ACh receptor [nAChR], and neural cell adhesion molecule [N-CAM]) were assessed. ResultsES impaired neuromuscular recovery at day 14 postdenervation. Muscle hypoexcitability was accentuated by ES at 6 and 14 days postdenervation. Although ES reduced the accumulation of atrogin-1, MuRF1, and myoD mRNAs, it increased muscle atrophy. Gene expression of MuSK, Dok-7, nAChR, and the content of N-CAM protein were altered by ES. DiscussionES can delay the reinnervation process by modulating factors related to NMJ stability and organization, and inducing dysfunction, hypoexcitability, and muscle atrophy. Muscle Nerve56: E108-E118, 2017
引用
收藏
页码:E108 / E118
页数:11
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