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Acetylcholine receptors and neuronal nitric oxide synthase distribution at the neuromuscular junction of regenerated muscle fibers
Author(s) -
Minatel Elaine,
Neto Humberto Santo,
Marques Maria Julia
Publication year - 2001
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 - 10.1002/1097-4598(200103)24:3<410::aid-mus1014>3.0.co;2-0
Subject(s) - dystrophin , acetylcholine receptor , medicine , endocrinology , nitric oxide synthase , neuromuscular junction , acetylcholine , skeletal muscle , nitric oxide , lidocaine hydrochloride , chemistry , regeneration (biology) , receptor , biology , microbiology and biotechnology , neuroscience , lidocaine
We investigated whether the changes in acetylcholine receptor (AChR) distribution and neuronal nitric oxide synthase (nNOS) expression reported for the skeletal muscle of mdx mice were a consequence of muscle fiber regeneration rather than of the absence of dystrophin. Degenerative‐regenerative changes in muscle fibers of the sternomastoid muscle of normal mice were induced by injecting lidocaine hydrochloride. Twenty‐one days later, AChRs were labeled with alpha‐bungarotoxin and nNOS with anti‐nNOS antibody, and observed under a confocal microscope. AChRs were distributed in continuous branches in normal fibers. Regenerated fibers showed disruption of AChRs distribution similar to that seen in muscle of mdx mice. This suggests that changes in AChRs distribution seen in mdx mice were probably a consequence of muscle fiber degeneration and regeneration, rather than a symptom of dystrophin deficiency. Conversely, there were no changes in nNOS distribution and expression in normal regenerated fibers, suggesting that the decrease in nNOS expression reported for mdx mice might be attributed to the absence of dystrophin. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 410–416, 2001