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Keywords:

  • Kennedy disease;
  • motor dysfunction;
  • muscle dysfunction;
  • neuromuscular disease;
  • skeletal muscle;
  • testosterone

ABSTRACT

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: 823–834, 2013