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Electrical stimulation delays reinnervation in denervated rat muscle
Author(s) -
PinheiroDardis Clara M.,
Erbereli Bruna T.,
GigoBenato Davilene,
Castro Paula A.T.S.,
Russo Thiago L.
Publication year - 2017
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.25589
Subject(s) - reinnervation , neuromuscular junction , myod , muscle atrophy , denervation , myogenin , medicine , endocrinology , biology , stimulation , myocyte , acetylcholine receptor , myogenic regulatory factors , microbiology and biotechnology , anatomy , receptor , skeletal muscle , neuroscience , myogenesis
It 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. Methods Denervated 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. Results ES 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. Discussion ES can delay the reinnervation process by modulating factors related to NMJ stability and organization, and inducing dysfunction, hypoexcitability, and muscle atrophy. Muscle Nerve 56 : E108–E118, 2017