Origin of delayed outward ionic current in charge movement traces from frog skeletal muscle.
1. Non-linear membrane ionic current was studied in highly stretched cut frog twitch fibres in a double Vaseline-gap voltage clamp chamber, with the internal solution containing 0.1 mM EGTA and the external solution containing Cl- as the major anion. After the Na+ currents was abolished by TTX in the external solution and the K+ currents were suppressed by external TEA+ and Rb+ and internal Cs+, a delayed outward ionic current with a time course similar to that of the delayed rectifier current was observed during depolarization. 2. The delayed outward ionic current was resistant to 1 mM 3,4-diaminopyridine (3,4-DAP) in the external solution and was unaltered when a fraction of the internal Cs+ was replaced by K+ or Na+, suggesting that the current was not carried by cations flowing through the delayed rectifiers. 3. The delayed outward ionic current was greatly reduced by replacing the external Cl- with CH3SO3-,SO4(2-), glutamate or gluconate, indicating strongly that the current was carried by Cl- flowing through anion channels. The current was also suppressed by 1 mM external 9-anthracenecarboxylic acid (9-ACA). 4. The delayed outward ionic current was reduced by blockers of calcium-dependent Cl- channels, such as SITS and frusemide (furosemide), in a dose- and voltage-dependent manner and by increasing intracellular [EGTA] to 20 mM, suggesting that part of the Cl- current in the muscle fibres could be calcium dependent. 5. The total Cl- current could be dissected into calcium-dependent and calcium-independent components. Each component accounted for roughly half of the total Cl- current. The maximum slope conductance of the calcium-dependent Cl- channels was 60.9 +/- 6.0 microS microF-1 (mean +/- S.E.M., n = 4).
Hui
C S
CS
Department of Physiology and Biophysics, Indiana University Medical Center, Indianapolis 46202.
Chen
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D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid / Q000494:pharmacology; D015761:4-Aminopyridine / Q000031:analogs & derivatives / Q000494:pharmacology; D000077770:Amifampridine; D000818:Animals; D000838:Anions / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology; D002586:Cesium / Q000502:physiology; D018118:Chloride Channels / Q000187:drug effects / Q000502:physiology; D004533:Egtazic Acid / Q000494:pharmacology; D005665:Furosemide / Q000494:pharmacology; D005942:Gluconates / Q000494:pharmacology; D018698:Glutamic Acid / Q000494:pharmacology; D007473:Ion Channels / Q000032:analysis / Q000502:physiology*; D018482:Muscle, Skeletal / Q000737:chemistry / Q000502:physiology*; D011896:Rana temporaria / Q000502:physiology*; D012413:Rubidium / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors
D000838:Anions; D018118:Chloride Channels; D005942:Gluconates; D007473:Ion Channels; D002586:Cesium; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D018698:Glutamic Acid; D013779:Tetrodotoxin; D004533:Egtazic Acid; D005665:Furosemide; D015761:4-Aminopyridine; D012413:Rubidium; D013755:Tetradecanoylphorbol Acetate; C030691:gluconic acid; D000077770:Amifampridine; D002118:Calcium