Suppression of myotonia in dystrophic chicken muscle by phenytoin.
We describe myotonic electromyographic activity in muscles of genetically dystrophic chickens and show that this activity is antagonized in vivo by doses of phenytoin (DPH) that improve righting ability. To test the possibility that the in vivo effects of DPH can be accounted for by a direct action on skeletal muscle we studied posterior latissimus dorsi fibers in vitro at 23 degrees C with intracellular microelectrodes. Compared to normal fibers, fibers from untreated dystrophic chicks had larger diameters, increased membrane capacitance, longer latencies at rheobase, and a greater tendency to fire repetitively in response to direct stimulation. DPH (10 or 50 micrograms/ml in the bath solution) decreased latencies at rheobase and repetitive firing in fibers from untreated chicks. In DPH-free solution fibers from dystrophic chicks treated chronically with DPH were still abnormal with respect to latencies at rheobase and ease of repetitive firing. The data support the hypothesis that abnormalities of membrane electrical properties are major features of dystrophic chicken muscles and furthermore, show that DPH suppresses, but does not abolish, these abnormalities.
D000818:Animals; D002645:Chickens / Q000502:physiology*; D003864:Depression, Chemical; D004558:Electric Stimulation; D008564:Membrane Potentials / Q000187:drug effects*; D009132:Muscles / Q000503:physiopathology*; D009137:Muscular Dystrophy, Animal / Q000188:drug therapy / Q000235:genetics / Q000503:physiopathology*; D010672:Phenytoin / Q000494:pharmacology* / Q000627:therapeutic use
D010672:Phenytoin