Effects of Taurine Depletion on Membrane Electrical Properties of Rat Skeletal Muscle

Abstract

Taurine is abundantly present in mammalian skeletal muscle but its physiological role is not yet completely understood. Findings from our laboratory support the proposed hypothesis of a membrane-stabilizer action exerted by the amino acid in this tissue (Huxtable and Sebring, 1986). Indeed, in vitro application of taurine can markedly reduce membrane excitability of rat skeletal muscle as a result of a specific increase of membrane chloride conductance (GC1) (Conte Camerino et al., 1987). It is well known that a large membrane GC1 ensures the electrical stability of sarcolemma, since an abnormally low GC1 triggers the hyperexcitability characteristic of myotonic muscles (Bryant and Morales-Aguilera, 1971; Rüdel and Lehmann-Horn, 1985). Therefore, our finding has given a rationale for the observed relief of myotonic signs in human patients after taurine administration (Durelli et al., 1983). To better understand the action of taurine on skeletal muscle chloride channels, we have further investigated the ability of the amino acid to reverse or prevent the decrease of GC1 and the myotonic hyperexcitability in different experimental models of myotonia induced pharmacologically in rats (Conte Camerino et al., 1989). The finding that taurine fails to restore GC1 when the channels have been sterically blocked by anthracene-9-carboxylic acid (Bryant and Morales-Aguilera, 1971; Palade and Barchi, 1977), whereas it normalizes GC1 when it is lowered indirectly by 20-25 diazacholesterol which mainly changes the lipid environment of the membrane (Furman and Barchi, 1981), suggests that taurine is not a chloride channel ionophore.