Neural influence on experimental myotonia.
A transitory myotonic state, lasting for less than 24 hours, was induced in rats within 2 hours of the intraperitoneal injection of 2,4-dichlorophenoxyacetic acid. Neuromuscular blockade, nerve block, nerve section, and cordotomy had no effect on the established myotonic state. However, muscle that had been denervated progressively lost its capacity for a myotonic response to subsequent injections of 2,4-dichlorophenoxyacetic acid. After 10 to 12 days denervation, the injection of 2,4-dichlorophenoxyacetic acid produced a brief increase in the number of fibrillations, but typical myotonic discharges were no longer detectable. Unlike denervation, cordotomy did not impair the capacity of the paralyzed limbs to develop in response to 2,4-dichlorophenoxyacetic acid. While myotonia is the result of a primary defect in the muscle membrane, these experiments indicate the innervation is necessary to maintain the muscle membrane in a state that will support myotonia. We hypothesize that an alteration in ionic conductance secondary to denervation is the critical factor in preventing myotonia.
D015084:2,4-Dichlorophenoxyacetic Acid; D000818:Animals; D008297:Male; D009132:Muscles / Q000294:innervation / Q000503:physiopathology; D009222:Myotonia / Q000139:chemically induced / Q000503:physiopathology*; D009224:Myotonia Congenita / Q000503:physiopathology; D009420:Nervous System / Q000503:physiopathology*; D051381:Rats; D012584:Sciatic Nerve / Q000503:physiopathology; D013116:Spinal Cord / Q000503:physiopathology
D015084:2,4-Dichlorophenoxyacetic Acid