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The influence of skeletal muscle reinnervation on experimentally induced myotonia.

Abstract
Earlier studies have shown that prior denervation of muscle prevents myotonia induced by 2,4-dichlorophenoxy acetic acid (2,4-D) both in vivo and in vitro. This work studied the effect of reinnervation on 2,4-D myotonia. Twenty Sprague-Dawley rats were injected with 2,4-D at specific intervals following unilateral sciatic nerve crushing; the gastrocnemius muscle on both sides was studied electromyographically to assess myotonia and to document denervation and reinnervation. All the rats gradually became amyotonic following denervation; myotonia reappeared during reinnervation. Myotonic discharges were no longer detectable 1 week after nerve crushing, but returned completely within 3 weeks. Blocking axoplasmic transport with colchicine had essentially the same effect on myotonia. A reciprocal temporal relationship was noted between the occurrence of fibrillations and myotonic discharges. These findings substantiate the view that innervation is essential to maintain the muscle membrane in a state that will support myotonic discharges.
AuthorsA Al-Sulaiman, S Al-Rajeh, V Iyer
JournalMuscle & nerve (Muscle Nerve) Vol. 9 Issue 4 Pg. 364-6 (May 1986) ISSN: 0148-639X [Print] United States
PMID2423870 (Publication Type: Journal Article)
Chemical References
  • 2,4-Dichlorophenoxyacetic Acid
  • Sodium
  • Potassium
Topics
  • 2,4-Dichlorophenoxyacetic Acid
  • Animals
  • Axonal Transport
  • Cell Membrane Permeability
  • Disease Models, Animal
  • Electromyography
  • Male
  • Muscles (innervation)
  • Myotonia (chemically induced, physiopathology)
  • Potassium (metabolism)
  • Rats
  • Rats, Inbred Strains
  • Sodium (metabolism)

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