Androgen receptors in muscle fibers induce rapid loss of force but not mass: Implications for spinal bulbar muscular atrophy. Issue 6 (30th April 2013)

• Record Type: Journal Article
• Authors: Oki, Kentaro; Wiseman, Robert W.; Breedlove, S. Marc; Jordan, Cynthia L.
• Is Part Of: Muscle & nerve. Volume 47:Issue 6(2013:Jun.)
• Page Start: 823
• Page End: 834
• Publication Date: 2013-04-30
• Subjects: Neuromuscular diseases -- Periodicals; Muscles -- Periodicals; Nerves -- Periodicals; 616.74
• DOI: 10.1002/mus.23813
• Languages: English
• ISSNs: 0148-639X

Abstract

<abstract abstract-type="main"> <title>ABSTRACT</title> <sec id="mus23813-sec-0001" sec-type="section"> <title>Introduction</title> <p>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.</p> </sec> <sec id="mus23813-sec-0002" sec-type="section"> <title>Methods</title> <p>We examined contractile properties of the extensor digitorum longus (EDL) and soleus (SOL) muscles <italic>in vitro</italic> after 5 and 3 days of T treatment in motor‐impaired Tg female mice.</p> </sec> <sec id="mus23813-sec-0003" sec-type="section"> <title>Results</title> <p>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.</p> </sec> <sec id="mus23813-sec-0004" sec-type="section"> <title>Conclusions</title> <p>These results suggest calcium‐handling mechanisms in muscle fibers are defective in motor‐impaired mice. Muscle Nerve 47: 823–834, 2013</p> </sec> </abstract>