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REGULATION OF SKELETAL-MUSCLE CHLORIDE CHANNEL IN NORMAL AND MYOTONIC GOAT - A PHARMACOLOGICAL STUDY
No full textCHLORIDE CHANNEL REGULATION IN SKELETAL MUSCLE OF NORMAL AND MIOTONIC GOATS
No full textExternal intercostal muscle biopsies from normal and congenitally myotonic goats were studied in vitro at 30°C using a two-microelectrode square-pulse cable analysis assisted by computer. The resting chloride conductance (G(cl)) was estimated from the difference between the mean membrane conductance in chloride-containing and chloride-free bathing media. The protein kinase C (PKC) activator, 4-β-phorbol-12,13-dibutyrate, (0.1-2.0 μM) blocks a maximum of 76% of G(cl) in normal goat fibers and induces myotonic hyperexcitability similar to that of congenitally myotonic goat fibers. The G(cl) block was partially antagonized by pretreatment with the PKC inhibitor, staurosporine (10 μM). The 'inactive' 4-α-phorbol-12,13,didecanoate had no effect at 50μM, whereas the 'active' 4-β isomer blocked 41% G(cl) at 1 μM. The nearly absent G(cl) of congenitally myotonic goat fibers was not restored by treatment with high concentrations of the PKC inhibitors staurosporine, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7), or tetrahydropapaveralone (THP). Also, forskolin and cholera toxin, which may increase cyclic adenosine monophosphate (cAMP) levels, or the R(+) clofibric acid enantiomers and taurine, which increase G(cl) in normal fibers, were also unable to restore G(cl) in myotonic goat fibers. The data suggest that PKC may be a chloride channel regulator in normal goat skeletal muscle fibers, however the molecular defect of congenitally myotonic fibers does not appear to be due to excessive activity of PKC
EFFECTS OF DENERVATION AND COLCHICINE TREATMENT ON THE CHLORIDE CONDUCTANCE OF RAT SKELETAL MUSCLE FIBERS.
No full textThe influence of tetrodotoxin-inactive nerve on electrical parameters of rat skeletal muscle
No full textPHARMACOLOGICAL BLOCK OF NERVE CONDUCTION AFFECTS ELECTRICAL PROPERTIES OF MUSCLE MEMBRANES
No full textELECTRICAL PROPERTIES OF RAT EXTENSOR DIGITORUM LONGUS MUSCLE AFTER CHRONIC APPLICATION OF EMETINE TO THE MOTOR NERVE.
No full textMuscle weakness is a side effect of the chronic administration of emetine [(-)emetine] in the treatment of amoebiasis. The precise nature of the weakness is still controversial. In this study we were interested in whether or not emetine can alter the electrical behavior of muscle fibers when applied to the nerve at some distance from the muscle. To test this idea, silastic cuffs containing 0.1 to 0.2% emetine were placed on the peroneal nerve of adult rats and the electrical properties of the extensor digitorum longus (EDL) muscle fibers were monitored in vitro at 4 to 40 days after application of the cuff. Action potential generation was affected by emetine treatment: the rheobasic current was significantly lowered (from a control value of 78 to 40 nA), and a small increase in current in the treated fibers produced seven or more action potentials. In the emetine-treated fibers, mean chloride conductance G(Cl) decreased from a control value of 3737 to 2453 ?S/cm2 while mean potassium conductance G(K) showed an insignificant increase from 304 to 408 ?S/cm2. We conclude that emetine interferes with specific materials involved in the maintenance of the high resting G(CI) of mammalian skeletal muscle fibers
Modulation of rat skeletal muscle chloride channels by activators and inhibitors of protein kinase C.
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