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.
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Authors | A Al-Sulaiman, S Al-Rajeh, V Iyer |
Journal | Muscle & nerve
(Muscle Nerve)
Vol. 9
Issue 4
Pg. 364-6
(May 1986)
ISSN: 0148-639X [Print] United States |
PMID | 2423870
(Publication Type: Journal Article)
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Chemical References |
- 2,4-Dichlorophenoxyacetic Acid
- Sodium
- Potassium
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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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