Inactivation of delayed outward current in molluscan neurone somata.

Aldrich, Richard W.; Getting, Peter A.; Thompson, Stuart H.

doi:10.1113/jphysiol.1979.sp012828

Cited by 189 publications

(154 citation statements)

References 41 publications

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“…In addition, as seen for mShab1 (Fig. 6A), IK in vivo also undergoes cumulative inactivation (Aldrich et al, 1979). Z, and mShab, however, do not seem to match in all measured properties; the major difference is the midpoint of the prepulse inactivation curve (Table 1).…”

Section: Discussionmentioning

confidence: 99%

“…mShabl, in contrast, only recovered to about 25% of its original amplitude in response to the second pulse, which is less than the amplitude of the current at the end of the preceding pulse. This is most likely due to cumulative inactivation (Aldrich et al, 1979), which causes mShab1 to recover more slowly thanflhab. Indeed, at a holding potential of -90 mV, the recovery from inactivation was almost 10 times faster forfShab than for mShab1 (Fig.…”

Section: Resultsmentioning

confidence: 99%

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A mouse brain homolog of the Drosophila Shab K+ channel with conserved delayed-rectifier properties

et al. 1991

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We have cloned and expressed a mouse brain K+ channel that is the homolog of the Drosophila Shab K+ channel. Mouse and Drosophila Shab K+ channels (mShab and fShab, respectively) represent an instance of K+ channels and structurally related species that are both functionally and structurally conserved; most kinetic, voltage-sensitive, and pharmacological properties are similar for the 2 channels. The greatest functional difference between the currents is recovery from inactivation, which is several times slower for mShab than for fShab currents. In addition to conserved structure, the mShab polypeptide has an unusually long nonconserved region at the carboxyl end of the protein. Truncation of 293 residues from the carboxyl end produced no noticeable change in voltage-sensitive, kinetic, or pharmacological properties. Thus, the measured functional properties of mShab are determined by the remaining 564 residues, most of which are conserved. The mShab and fShab channels are naturally occurring structural variants having substitutions in conserved portions that appear relatively neutral with respect to all measured properties except for, possibly, the rate of recovery from inactivation. The mShab current closely resembles a native delayed-rectifier-type potassium current, IK, in hippocampal neurons.

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Section: Discussionmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

A mouse brain homolog of the Drosophila Shab K+ channel with conserved delayed-rectifier properties

et al. 1991

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“…This is consistent with reports Saito, 1959: Smith andZucker, 1980) that high external TEA almost completely blocks outward membrane currents. There is, however, data (Thompson, 1977;Aldrich et al, 1979;Connor, 1979) that suggest that in some molluscan neurons external TEA may block the delayed outward K + current with greater efficiency. The effects of internal TEA on different components of the K § current have also been studied .…”

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confidence: 99%

Effects of tetraethylammonium on potassium currents in a molluscan neurons.

Hermann¹,

Gorman²

1981

The Journal of General Physiology

186

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The effects of tetraethylammonium (TEA) on the delayed K + current and on the Ca2+-activated K + current of the Aplysia pacemaker neurons R-15 and L-6 were studied. The delayed outward K + current was measured in Ca2+-free ASW containing tetrodotoxin (TTX), using brief depolarizing clamp pulses. External TEA blocks the delayed K + current reversibly in a dosedependent manner. The experimental results are well fitted with a MichaelisMenten expression, assuming a one-to-one reaction between TEA and a receptor site, with an apparent dissociation constant of 6.0 raM. The block depends on membrane voltage and is reduced at positive membrane potentials. The Ca 2+-activated K + current was measured in Ca2+-free artificial seawater (ASW) containing TTX, using internal Ca 2+ ion injection to directly activate the K + conductance. External TEA and a number of other quaternary ammonium ions block the Ca2+-activated K + current reversibly in a dose-dependent manner. TEA is the most effective blocker, with an apparent dissociation constant, for a one-to-one reaction with a receptor site, of 0.4 raM. The block decreases with depolarization. The Caa+-activated K + current was also measured after intracellular iontophoretic TEA injection. Internal TEA blocks the Ca2+-activated K + current (but the block is only apparent at positive membrane potentials), is increased by depolarization, and is irreversible. The effects of external and internal TEA can be seen in measurements of the total outward K + current at different membrane potentials in normal ASW.The quaternary ammonium ion, tetraethylammonium (TEA), blocks voltagedependent potassium channels in nerve and muscle cells (Hagiwara

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“…Earlier studies of the dependence of action potentials of various cells in molluscan ganglion upon Na+ and Ca2+ suggest that some action potentials depended upon Na+ ion movement alone, whereas others depended upon the movement of Ca2+ ions or upon both Na+ and Ca2+ ions (Kerkut & Gardner, 1967). A similar diversity of outward currents has been shown in other molluscan neurone studies (Heyer & Lux, 1976; Thompson, 1977;Aldrich, Getting & Thompson, 1979). Our results suggest that the difference between cells may be quantitative as well as qualitative and that these differences in membrane conductance may lead to quite different cell behaviour.…”

Section: Discussionmentioning

confidence: 70%

Quantitative differences in the currents of bursting and beating molluscan pace‐maker neurones

Gorman

Hermann

1982

The Journal of Physiology

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SUMMARY1. The spontaneous activity and the membrane conductances to Na+, Ca2+ and K+ ions of the bursting pace-maker neurone R-15 and the repetitively discharging (beating) pace-maker neurone L-1 1 in the abdominal ganglion of the marine mollusc, Aplysia californica, were compared.2. The bursting pace-maker R-15 can be converted to a beating pace-maker neurone by the removal of external Ca2+ or by the injection of EGTA intracellularly. Bursting pace-maker activity is not restored by changes in the resting potential.3. Spontaneous action potentials of cell R-15 are reduced, but not abolished, by the addition of tetrodotoxin (TTX) to block Na+ currents or by the removal of external Ca2+ to abolish Ca2+ currents, whereas the spontaneous action potentials of cell L-1 1 are abolished by external TTX, but are unaffected by external Ca2+ removal.4. The membranes of both cells contain Na+ and Ca2+ inward currents. The specific Na+ conductance of both cells is of similar magnitude, whereas the specific Ca2+ conductance is about half the Na+ conductance in R-15 cells and an order of magnitude smaller in L-1 1 cells.5. The delayed K+ conductance of cell L-1 1 is about 1-2 times greater than this conductance in cell R-15. The transient K+ currents of the two cells are about the same magnitude.6. The Ca2+-activated K+ conductance of cell R-15 and cell L-11 was estimated using two methods. The Ca2+-activated K+ conductance of cell R-15 estimated from the difference in the total outward current in normal external solution and the delayed K+ current in Ca2+-free solution (to preclude Ca2+ influx) or after internal EGTA injection (to prevent Ca2+ accumulation) is about 23 times greater than this conductance in cell L-1 1. The Ca2+-activated K+ conductance of cell R-15, estimated from local internal Ca2+ injections in Ca2+-free solution, is about 3 times greater than this conductance in cell L-11.7. The leakage conductance of cell L-11 is about 1.3 times greater than this conductance in cell R-15. This conductance increases by a factor of about 2 in both cells in Ca2+-free external solutions containing 1 mM-EGTA, but is unchanged or is decreased slightly by injection of EGTA internally.* To whom reprint requests should be addressed.A. L. F. GORMAN AND A. HERMANN 8. It is concluded that the Ca2+ conductance and the Ca2+-activated K+ conductance are appreciably greater in the bursting pace-maker neurone R-15 than in the beating pace-maker neurone L-1 1, whereas other voltage-dependent conductances to Na+ and K+ ions as well as the leakage conductance are quite similar. These quantitative differences provide a basis for understanding the different spontaneous activities of the two cells.

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Inactivation of delayed outward current in molluscan neurone somata.

Cited by 189 publications

References 41 publications

A mouse brain homolog of the Drosophila Shab K+ channel with conserved delayed-rectifier properties

A mouse brain homolog of the Drosophila Shab K+ channel with conserved delayed-rectifier properties

Effects of tetraethylammonium on potassium currents in a molluscan neurons.

Quantitative differences in the currents of bursting and beating molluscan pace‐maker neurones

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