The effects of taurine on pharmacologically induced myotonia.

Abstract

Taurine reduces the excitability of striated muscle fibers by increasing the membrane conductance to chloride ions (GCl). This action was tested on rats made myotonic by drugs that block GCl by different mechanisms. Experiments were made "in vivo" using electromyographic (EMG) recordings and "in vitro" with intracellular microelectrode recordings from extensor digitorum longus muscle fibers. Taurine did not antagonize the myotonic discharges produced in vivo by anthracene-9-carboxylic acid, nor did it restore GCl lowered in vitro by this agent. However, when myotonia was chronically induced by 20,25 diazacholesterol, taurine given chronically in vivo or acutely in vitro antagonized the EMG myotonia as well as the reduced GCl and increased excitability of single fibers. We conclude that taurine acts directly on chloride channels to modify their kinetics. Our findings suggest that further clinical studies on the use of taurine in muscle disease involving abnormal excitability or chloride channel function will be useful.