Premium
Neural regulation of acetylcholinesterase‐associated collagen Q in rat skeletal muscles
Author(s) -
Trinkaus Miha,
Pregelj Peter,
Trkov Saša,
Sketelj Janez
Publication year - 2008
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2008.05328.x
Subject(s) - denervation , soleus muscle , chemistry , stimulation , neuromuscular junction , acetylcholinesterase , endocrinology , acetylcholine receptor , medicine , skeletal muscle , microbiology and biotechnology , anatomy , biology , receptor , biochemistry , neuroscience , enzyme
Acetylcholinesterase‐associated collagen Q is expressed also outside of neuromuscular junctions in the slow soleus muscle, but not in fast muscles. We examined the nerve dependence of muscle collagen Q expression and mechanisms responsible for these differences. Denervation decreased extrajunctional collagen Q mRNA levels in the soleus muscles and junctional levels in fast sternomastoid muscles to about one third. Cross‐innervation of denervated soleus muscles by a fast muscle nerve, or electrical stimulation by ‘fast’ impulse pattern, reduced their extrajunctional collagen Q mRNA levels by 70–80%. In contrast, stimulation of fast muscles by ‘slow’ impulse pattern had no effect on collagen Q expression. Calcineurin inhibitors tacrolimus and cyclosporin A decreased collagen Q mRNA levels in the soleus muscles to about 35%, but did not affect collagen Q expression in denervated soleus muscles or the junctional expression in fast muscles. Therefore, high extrajunctional expression of collagen Q in the soleus muscle is maintained by its tonic nerve‐induced activation pattern via the activated Ca 2+ ‐calcineurin signaling pathway. The extrajunctional collagen Q expression in fast muscles is independent of muscle activation pattern and seems irreversibly suppressed. The junctional expression of collagen Q in fast muscles is partly nerve‐dependent, but does not encompass the Ca 2+ ‐calcineurin signaling pathway.