Why the study?
Does myostatin deficiency increase the number of axons and motor units in mouse tibialis anterior muscle?
Does myostatin deficiency increase the number of axons and motor units in mouse tibialis anterior muscle?
Myostatin deficiency in mice is associated with increased total and motor axons innervating the tibialis anterior muscle, suggesting myostatin's role in neuromuscular interrelationships.
Answers are grounded in this paper and cite their sources.
Should not change clinical practice; extends preclinical evidence linking myostatin to motor axon and unit regulation.
INTRODUCTION: Myostatin (Mstn) is a secreted protein that acts as a negative regulator of skeletal muscle mass. However, a critical evaluation of neuromuscular aspects of hypertrophied muscles induced by Mstn deficiency has not been done. METHODS: We compared the tibialis anterior muscle-nerve interrelationships in wild-type and Mstn-null mice of both genders by immunohistochemical analyses, which allowed us to count the number of total axons and motor axons and estimate the size of motor units and the innervation ratio of the tibialis anterior muscle (TAm). RESULTS: There was an increase in the number of total axons and motor axons, and higher values in both the motor unit size and the innervation ratio of Mstn-null TAm compared with those of wild-type TAm. CONCLUSIONS: We found that myostatin is involved either directly in the control of neuromuscular interrelationships or indirectly through its effect on muscle size.
No takes yet. Share an insight, caveat, or question.
Gay et al. (2011) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: