Does phospholipid flip-flop affect axon potassium channels?
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Biomedical subjects
Publications and source records attributed to R J Lipicky.
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Diphenylhydantoin, in concentration of 5-50 muM, decreases the early, transient (sodium) currents of voltage-clamped squid giant axons. These effects are dose-dependent and largely reversible. It appears that diphenylhydantoin reduces the number of open, early, transient (sodium) channels.
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In isolated fiber bundles of external intercostal muscle from each of 13 normal volunteers and each of 6 patients with myotonia congenita, some or all of the following were measured: concentrations of Na(+), K(+), and Cl(-), extracellular volume, water content, K(+) efflux, fiber size, fiber cable parameters, and fiber resting potentials. Muscle from patients with myotonia congenita differed significantly (0.001 <P< 0.025) with respect to the following mean values (myotonia congenita vs. normal): the membrane resistance was greater (5729 vs. 2619 omega.cm(2)), the internal resistivity was less (75.0 vs. 123.2 omega.cm), the water content was less (788.2 vs. 808.2 ml/kg wet weight), and the mean resting potential was greater (68 vs. 61 mv).NO SIGNIFICANT DIFFERENCES WERE FOUND WITH RESPECT TO THE FOLLOWING VARIABLES: K(+) content (73.5 vs. 66.7 mEq/kg wet weight) and the calculated intracellular K(+) concentration (215 vs. 191 mEq/liter fiber water), fiber capacitance (5.90 vs. 5.15 muf/cm(2)), Na(+) content (97.7 vs. 94.1 mEq/kg wet weight), Cl(-) content (79.0 vs. 74.7 mEq/kg wet weight), mannitol extracellular volume (45.1 vs. 46.6 cc/100 g wet weight), and K(+) efflux (23.2 vs. 21.5 moles x 10(-12) cm(-2).sec(-1)). These abnormalities of skeletal muscle in human myotonia congenita are like those of skeletal muscle in goats with hereditary myotonia. We tentatively conclude that a decreased Cl(-) permeability accounts for some of the abnormal electrical properties of skeletal muscle in myotonia congenita.
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IN ISOLATED BUNDLES OF EXTERNAL INTERCOSTAL MUSCLE FROM NORMAL GOATS AND GOATS WITH HEREDITARY MYOTONIA THE FOLLOWING WERE DETERMINED: concentrations and unidirectional fluxes of Na(+), K(+), and Cl(-), extracellular volume, water content, fiber geometry, and core-conductor constants. No significant difference between the two groups of preparations was found with respect to distribution of fiber size, intracellular concentrations of Na(+) or Cl(-), fiber water, resting membrane potential, or overshoot of action potential. The intracellular Cl(-) concentration in both groups of preparations was 4 to 7 times that expected if Cl(-) were distributed passively between intracellular and extracellular water. The membrane permeability to K (P(K)) calculated from efflux data was (a) at 38 degrees C, 0.365 x 10(-6) cm sec(-1) for normal and 0.492 x 10(-6) for myotonic muscle, and (b) at 25 degrees C, 0.219 x 10(-6) for normal and 0.199 x 10(-6) for myotonic muscle. From Cl(-) washout curves of normal muscle usually only three exponential functions could be extracted, but in every experiment with myotonic muscle there was an additional, intermediate component. From these data PP(cl) could be calculated; it was 0.413 x 10(-6) cm sec(-1) for myotonic fibers and was 0.815 x 10(-6) cm sec(-1) for normal fibers. The resting membrane resistance of myotonic fibers was 4 to 6 times greater than that of normal fibers.
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