Effects of internal potassium and sodium on the anomalous rectification of the starfish egg as examined by internal perfusion.

Hagiwara, Susumu; Yoshii, Mitsunobu

doi:10.1113/jphysiol.1979.sp012849

Cited by 158 publications

(136 citation statements)

References 12 publications

(15 reference statements)

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“…This current, IIR, was readily blocked by 1 mM Cs' (not illustrated), and its amplitude (consequently, conductance) was augmented by an increase in external concentration of K+ (b (2)). These features of IIR were identical to those of the typical inward (anomalous) rectifier current in marine egg cells (Hagiwara & Yoshii, 1979). IIR was not affected by a high concentration (0.1 mM) of CPZ.…”

Section: Drugssupporting

confidence: 59%

Differential inhibition of a transient K+ current by chlorpromazine and 4‐aminopyridine in neurones of the rat dorsal root ganglia

Ogata

Tatebayashi

1993

British J Pharmacology

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1 K+ currents were recorded from neurones of the newborn rat cultured dorsal root ganglia, by a whole cell variation of the patch-clamp technique. 2 Chlorpromazine (CPZ), a neuroleptic, reversibly reduced the amplitude of the transient K+ current (referred to as 'IT' hereafter) with a dissociation constant (Kd) of 4.5 j4M. The inhibition of the delayed rectifier K+ current (IDR) was much less potent (Kd, 120 l4M). CPZ (100 tM) had no effect on the inward rectifier K+ current.3 The blocking action of CPZ on IT was about seven times more potent than that of 4-aminopyridine (4-AP) which had a Kd of 31 gM. The inhibition of IT followed one-to-one binding stoichiometry with both drugs. 4 The decay time course of IT was not affected by CPZ, whereas 4-AP markedly accelerated the decay phase of IT.5 The steady-state inactivation curve of IT was shifted in the negative direction (about 5 mV) by CPZ, whereas the curve was shifted in the positive direction (about 13 mV) by 4-AP. 6 The recovery from inactivation as measured by a conventional double pulse protocol was described by two exponential components in the control solution. CPZ markedly reduced the first component and slowed down the recovery from inactivation. In contrast, in the presence of 4-AP, the peak amplitude of IT was rather increased by a preceding IT possibly through voltage-dependent unbinding of 4-AP molecules.7 These results indicate that CPZ has a preferential blocking action on IT and the mechanism underlying this block is markedly different from the mechanism underlying the blocking action of 4-AP.

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Section: Drugssupporting

confidence: 59%

Differential inhibition of a transient K+ current by chlorpromazine and 4‐aminopyridine in neurones of the rat dorsal root ganglia

Ogata

Tatebayashi

1993

British J Pharmacology

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“…However, this does not imply that the conductance in cat ventricular myocytes depends solely on the K + driving force. In starfish egg cells (Hagiwara and Yoshii, 1979) and frog skeletal muscle (Hestrin, 1981;Leech and Stanfield, 1981), changing [K+]i affected the maximum conductance level as expected, but did not result in a shift of the relationship along the voltage axis such as occurred when [K+],, was altered.…”

Section: Comparison Of Iki With Other Inward-rectifying K § Currentsmentioning

confidence: 78%

“…Inactivation of IKI in isolated ventricular myocytes was viewed as being the result of two INTRODUCTION Since Katz (1949) first discovered the property of anomalous rectification in skeletal muscle, it has been described in several different preparations. This anomalous or inward rectification has been studied extensively in starfish (Hagiwara and Takahashi, 1974;Hagiwara et al, 1976;Hagiwara and Yoshii, 1979) and tunicate (Miyazaki et al, 1974;Ohmori, 1978Ohmori, , 1980Fukusbima, 1982) egg cells as well as skeletal muscle preparations (Adrian et al, 1970;Almers, 1972a, b;Standen and Stanfield, 1979;Hestrin, 1981;Leech and Stanfield, 1981). Inward rectification is associated with the presence of a background K ion conductance that contributes to the maintenance of the resting membrane potential.…”

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confidence: 99%

Characterization of the inward-rectifying potassium current in cat ventricular myocytes.

Harvey

Eick

1988

The Journal of General Physiology

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Whole-cell membrane currents were measured in isolated cat ventricular myocytes using a suction-electrode voltage-clamp technique. An inward-rectifying current was identified that exhibited a time-dependent activation. The peak current appeared to have a linear voltage dependence at membrane potentials negative to the reversal potential. Inward current was sensitive to K channel blockers. In addition, varying the extracellular K § concentration caused changes in the reversal potential and slope conductance expected for a K § current. The voltage dependence of the chord conductance exhibited a sigmoidal relationship, increasing at more negative membrane potentials. Increasing the extraceUular K § concentration increased the maximal level of conductance and caused a shift in the relationship that was directly proportional to the change in reversal potential. Activation of the current followed a monoexponential time course, and the time constant of activation exhibited a monoexponential dependence on membrane potential. Increasing the extracellular K + concentration caused a shift of this relationship that was directly proportional to the change in reversal potential. Inactivation of inward current became evident at more negative potentials, resulting in a negative slope region of the steady state current-voltage relationship between --140 and --180 mV. Steady state inactivation exhibited a sigmoidal voltage dependence, and recovery from inactivation followed a monoexponential time course. Removing extracellular Na + caused a decrease in the slope of the steady state current-voltage relationship at potentials negative to --140 mV, as well as a decrease of the conductance of inward current. It was concluded that this current was IK~, the inward-rectifying K + current found in multicellular cardiac preparations. The K + and voltage sensitivity of IK1 activation resembled that found for the inward-rectifying K + currents in frog skeletal muscle and various egg cell preparations. Inactivation

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“…This anomalous rectifier requires the presence of internal Na+ for gating and has an EC50 for Na+ of 35 mm (Hagiwara & Yoshii, 1978). Furthermore Li+ can act as a less efficient substitute for Na+ to permit channel gating (Hagiwara & Yoshii, 1978).…”

Section: Single-channel Recordingsmentioning

confidence: 99%

A large, sustained Na(+)‐ and voltage‐dependent K+ current in spinal neurons of the frog embryo.

Dale

1993

The Journal of Physiology

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SUMMARY1. Neurons from the Xenopus embryo spinal cord were dissociated and conventional patch clamp techniques were used to record the whole-cell currents in the presence of tetrodotoxin (TTX).2. The outward currents of the acutely isolated spinal neurons were rapidly reduced to about half their control value by substitution of extracellular Na+ with N-methyl-D-glucamine, lysine or choline.3. The use of Li+ as a Na+ substitute partially reduced the outward currents. 4. The reversal potential of the Na+-sensitive current was close to the K+ equilibrium potential and could be altered by changing extracellular K+. The Na+-sensitive current was therefore a K+ current.5. The Na+-sensitive K+ current was voltage dependent and activated in a sustained manner and appeared very similar to the delayed rectifier present in these neurons.6. While the Na+-sensitive current increased with voltage as might be expected for an outward current, at very positive potentials it progressively decreased in amplitude. The voltage range over which this decrease was present moved closer to zero as the levels of intracellular Na+ were increased. The tail currents evoked by positive test potentials did not correspondingly decrease in amplitude, suggesting that channel block was rapidly relieved by stepping back to the holding potential.7. Intracellular perfusion of the patch pipette with solutions containing varying amounts of Na+ (0-20 mM) showed that the K+ currents could be increased in a dosedependent manner by raising intracellular Na+. The current had an EC50 for Na+ of 7-3 mm and a Hill coefficient of 4-6.8. Single channel recordings from isolated inside-out patches revealed a channel that gated more frequently when the bathing levels of Na+ were elevated from 3 to 12 or 50 mM. Xenopus spinal cord neurons therefore possess a current that is not only voltage dependent but is also sensitive to internal Na+.9. Xenopus spinal neurons possess a transient Na+ current (blocked by the inclusion of TTX) and a leak channel permeable to Na+. The inward leakage of Na+ appeared to provide the Na+ necessary for the gating of the Na+-dependent channel.10. Blocking the Na+-K+ exchange pumps by removing extracellular K+, reduced MS 1325 the effect of removal of external Na+, suggesting that the Na+-K+ exchange pumps could be important in controlling the submembrane Na+. 11. A working model that depends on the actions of the Na+-K+ exchange pumps, inward leakage and diffusion from the pipette has been put forward to predict how the submembrane levels of Na+ vary with voltage, membrane permeability to Na+, Na+ in the pipette and extracellular Na+.12. The Na+-dependent current itself has been provisionally modelled by a kinetic scheme that assumes binding of Na+ to the closed channel, voltage-dependent opening and a fast voltage-dependent blockage of the open channel by Na+.13. The model for the Na+-dependent current predicts that this current could be modulated by the accumulation of Na+ resulting from the neural activity during swimming in the embryo.

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Effects of internal potassium and sodium on the anomalous rectification of the starfish egg as examined by internal perfusion.

Cited by 158 publications

References 12 publications

Differential inhibition of a transient K+ current by chlorpromazine and 4‐aminopyridine in neurones of the rat dorsal root ganglia

Differential inhibition of a transient K+ current by chlorpromazine and 4‐aminopyridine in neurones of the rat dorsal root ganglia

Characterization of the inward-rectifying potassium current in cat ventricular myocytes.

A large, sustained Na(+)‐ and voltage‐dependent K+ current in spinal neurons of the frog embryo.

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