Fiber Type Composition of the Sternomastoid and Diaphragm Muscles of Dystrophin‐Deficient mdx Mice

AN Guido, GER Campos, HS Neto… - … Record: Advances in …, 2010 - Wiley Online Library
AN Guido, GER Campos, HS Neto, MJ Marques, E Minatel
The Anatomical Record: Advances in Integrative Anatomy and …, 2010Wiley Online Library
The muscle fiber phenotype is mainly determined by motoneuron innervation and changes
in neuromuscular interaction alter the muscle fiber type. In dystrophin‐deficient mdx mice,
changes in the molecular assembly of the neuromuscular junction and in nerve terminal
sprouting occur in the sternomastoid (STN) muscle during early stages of the disease. In this
study, we were interested to see whether early changes in neuromuscular assembly are
correlated with alterations in fiber type in dystrophic STN at 2 months of age. A …
Abstract
The muscle fiber phenotype is mainly determined by motoneuron innervation and changes in neuromuscular interaction alter the muscle fiber type. In dystrophin‐deficient mdx mice, changes in the molecular assembly of the neuromuscular junction and in nerve terminal sprouting occur in the sternomastoid (STN) muscle during early stages of the disease. In this study, we were interested to see whether early changes in neuromuscular assembly are correlated with alterations in fiber type in dystrophic STN at 2 months of age. A predominance of hybrid fast myofibers (about 52% type IIDB) was observed in control (C57Bl/10) STN. In mdx muscle, the lack of dystrophin did not change this profile (about 54% hybrid type IIDB). Pure fast type IID fibers predominated in normal and dystrophic diaphragm (DIA; about 39% in control and 30% in mdx muscle) and a population of slow Type I fibers was also present (about 10% in control and 13% in mdx muscle). In conclusion, early changes in neuromuscular assembly do not affect the fiber type composition of dystrophic STN. In contrast to the pure fast fibers of the more affected DIA, the hybrid phenotype of the STN may permit dynamic adaptations during progression of the disease. Anat Rec 293:1722–1728, 2010. © 2010 Wiley‐Liss, Inc.
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