Journal
MUSCLE & NERVE
Volume 47, Issue 6, Pages 823-834Publisher
WILEY-BLACKWELL
DOI: 10.1002/mus.23813
Keywords
Kennedy disease; motor dysfunction; muscle dysfunction; neuromuscular disease; skeletal muscle; testosterone
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Funding
- National Institutes of Health [R01 NS045195, DK095210]
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Introduction Testosterone (T) induces motor dysfunction in transgenic (Tg) mice that overexpress wild-type androgen receptor (AR) in skeletal muscles. Because many genes implicated in motor neuron disease are expressed in skeletal muscle, mutant proteins may act in muscle to cause dysfunction in motor neuron disease. Methods We examined contractile properties of the extensor digitorum longus (EDL) and soleus (SOL) muscles in vitro after 5 and 3 days of T treatment in motor-impaired Tg female mice. Results Both muscles showed deficits in tetanic force after 5 days of T treatment, without losses in muscle mass, protein content, or fiber number. After 3 days of T treatment, only SOL showed a deficit in tetanic force comparable to that of 5 days of treatment. In both treatments, EDL showed slowed twitch kinetics, whereas SOL showed deficits in the twitch/tetanus ratio. Conclusions These results suggest calcium-handling mechanisms in muscle fibers are defective in motor-impaired mice. Muscle Nerve 47: 823834, 2013
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