The apamin-sensitive potassium current in frog skeletal muscle: its dependence on the extracellular calcium and sensitivity to calcium channel blockers

Traoré, Flavien; Cognard, Christian; Potreau, Daniel; Raymond, Guy

doi:10.1007/bf00580676

Cited by 15 publications

(8 citation statements)

References 28 publications

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“…A similar incomplete block has been observed with apamin in rat sympathetic ganglion cells (See Fig. 3 of Kawai & Watanabe, 1986) in frog skeletal muscle (Traore et al 1986) and in cultured rat skeletal muscle (Blatz & Magleby, 1986). Blatz & Magleby (1986) found that in the presence of apamin, voltage-insensitive, calcium-sensitive channels had a conductance (4 pS) less than 25% of that observed in the absence of apamin.…”

Section: Discussionmentioning

confidence: 66%

“…Currents analogous to IAHP have been observed in mammalian neurones both central (Seagar, Granier & Couraud, 1984;Zhang & Krnjevic, 1986) and peripheral (Kawai & Watanabe, 1986), in skeletal (Romey & Lazdunski, 1984;Traore, Cognard, Potreau & Raymond, 1986) and smooth (Gater, Haylett & Jenkinson, 1985) muscle cells and in hepatocytes (Cook & Haylett, 1985). In this paper, the physiological and pharmacological properties of IAHP are described, strategies for studying the current in isolation are presented and the contribution of IAHP to the electrical activity of B neurones is illustrated.…”

Section: Introductionmentioning

confidence: 99%

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Pharmacological and physiological properties of the after‐hyperpolarization current of bullfrog ganglion neurones.

Goh

Pennefather

1987

The Journal of Physiology

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SUMMARY1. The slowly decaying, calcium-dependent after-hyperpolarization (a.h.p.) that follows action potentials in bullfrog ganglion B cells has previously been shown to be generated by a potassium current called IAHP. We have recorded IAHP using a switched, single-electrode hybrid clamp where current-clamp mode was changed to voltage-clamp mode immediately after repolarization of a spike or the last spike of a train.2. Reduction of extracellular calcium reduced the decay time Of IAHP following a single spike. At all levels of extracellular calcium tested (0 5-4 mM), the decay time of IAHP was longer following a train of action potentials than following a single action potential. Thus, the time course of IAHP evoked by action potentials is a function of the calcium load induced by the action potentials. Conversely, agents that reduce the amount of IAHP activated without affecting its rate of decay, probably do not affect calcium influx.3. Muscarine (2 or 10 #/M) inhibits IAHP following an action potential by at most 30 % and has no effect on decay rate Of IAHP. These results suggest that muscarine has little or no effect on either calcium influx or sequestration. Decay of the a.h.p. is accelerated by muscarine but this effect is due to an increased leak conductance.4. Charybdotoxin (CTX) between 4 and 20 nm, prolongs action potential duration in a manner consistent with blockade of the voltage-and calcium-dependent potassium current (Ic) involved in spike repolarization in these cells. This action is consistent with its reported action on analogous channels in other systems. However, CTX also reduces IAHP. Thus, in bullfrog ganglion neurones, two distinct calciumdependent potassium currents exhibit a comparable sensitivity to CTX. This cannot .be due to a decreased influx of calcium because the decay rate Of IAHP following an action potential is unchanged. The action of CTX was observed with both crude and purified preparations of CTX.

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Section: Discussionmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 99%

Pharmacological and physiological properties of the after‐hyperpolarization current of bullfrog ganglion neurones.

Goh

Pennefather

1987

The Journal of Physiology

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“…Vincent & Lazdunski. 1982;Traore, Cognard, Poitreau & Raymond. 1986) was unable to modify RVD in rat thymocytes.…”

Section: Discussionmentioning

confidence: 99%

“…1986(Garay et at. , 1988 Burgess, Claret & Jenkinson, 1981;Hugues et al 1982;Traore et al 1986). EIPA increased red cell K+ leak at concentrations higher than 5 x 10-5 mol l-l. n.m., not measured.…”

Section: The Effect Of Anisotonicity and Ion Substitutionmentioning

confidence: 95%

Cell volume regulation in rat thymocytes.

Arrázola

Rota

Hannaert

et al. 1993

The Journal of Physiology

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SUMMARY1. DIOA (dihydroindenyl-oxy-alkanoic acid), a potent inhibitor of the K+-Cl-cotransport system, fully blocked regulatory volume decrease (RVD) in swelled rat thymocytes, with an IC50 of 2-2 + 0 5 x 10-5 mol 1-1 (mean + S.D., n = 4). Conversely, RVD was resistant to quinine, quinidine, apamin, cetiedil, amiloride, bumetanide and DIDS (4,4'-diisothiocyanostilbene-2,2'-disulphonate).2. DIOA-sensitive RVD followed mono-exponential kinetics, with th (half-lifetime) of 1-3 min and maximal capacity (Cmax) of about 55 % of the initial cell swelling.Cmax and the initial rate of RVD (V.) were both linear functions of the increase in cell volume.3. RVD was: (i) slightly increased by replacing external Cl-by NO3-, (ii) reversed by replacing external Na+ by K+ (in the presence of external Cl-) and (iii) inhibited by cell K+ depletion. All these phenomena were blocked by DIOA (86 jmol 1-1).4. Increased membrane potassium permeability by valinomycin was unable to accelerate RVD or RVD reversal.5. In the presence of DIOA, thymocytes responded like osmometers (the relative cell volume was a linear function of the reciprocal of the relative osmolality) in a large range of osmolalities.6. The results strongly suggest that RVD in rat thymocytes is mediated by the K+-Cl-co-transport system.

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“…In an attempt to dissect the components of the ∆k K,o promoted by caffeine we used both of these toxins. Apamin binds to several tissues including skeletal muscle with a K D of 15-60 pM [20] and effectively blocks a Ca 2+ -dependent component of the slow outward current on frog skeletal muscle [26]. Apamin (10 nM) did not affect ∆k K,o (data not shown).…”

Section: Resultsmentioning

confidence: 92%

Effect of caffeine on K + efflux in frog skeletal muscle

Venosa

Hoya

1999

Pfl�gers Archiv European Journal of Physiology

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The exposure of frog skeletal muscle to caffeine (3-4 mM) generates an increase of the K+ (42K+) efflux rate coefficient (kK,o) which exhibits the following characteristics. First it is promoted by the rise in cytosolic Ca2+ ([Ca2+]i), because the effect is mimicked by ionomycin (1.25 microM), a Ca2+ ionophore. Second, the inhibition of caffeine-induced Ca2+ release from the sarcoplasmic reticulum (SR) by 40 microM tetracaine significantly reduced the increase in kK,o (DeltakK,o). Third, charybdotoxin (23 nM), a blocker of the large-conductance Ca2+-dependent K+ channels (BKCa channels) reduced DeltakK,o by 22%. Fourth, apamin (10 nM), a blocker of the small-conductance Ca2+-dependent K+ channels (SKCa channels), did not affect DeltakK,o. Fifth, tolbutamide (800 microM), an inhibitor of KATP channels, reduced DeltakK,o by about 23%. Sixth, Ba2+, a blocker of most K+ channels, did not preclude the caffeine-induced DeltakK,o. Seventh, omitting Na+ from the external medium reduced DeltakK,o by about 40%. Eight, amiloride (5 mM) decreased DeltakK,o by 65%. It is concluded that the caffeine-induced rise of [Ca2+]i increases K+ efflux, through the activation of: (1) two channels (BKCa and KATP) and (2) an external Na+-dependent amiloride-sensitive process.

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The apamin-sensitive potassium current in frog skeletal muscle: its dependence on the extracellular calcium and sensitivity to calcium channel blockers

Cited by 15 publications

References 28 publications

Pharmacological and physiological properties of the after‐hyperpolarization current of bullfrog ganglion neurones.

Pharmacological and physiological properties of the after‐hyperpolarization current of bullfrog ganglion neurones.

Cell volume regulation in rat thymocytes.

Effect of caffeine on K + efflux in frog skeletal muscle

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