Effect of temperature on the anomalous rectification of the membrane of the egg of the starfish, Mediaster aequalis.

Hagiwara, Susumu; Yoshii, Mitsunobu

doi:10.1113/jphysiol.1980.sp013451

Cited by 18 publications

(12 citation statements)

References 19 publications

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“…The high E values of r--j and r-are similar to those reported for gating processes, while the low E value of Fca is similar to that reported for the permeability of ionic channels (Frankenhaeuser & Moore, 1963;Almers 1972 a, b;Hladky & Haydon, 1972;Schauf, 1973;Ohmori, 1978;Almers, 1980;Hagiwara & Yoshii, 1980;Kniffki et al 1981;Leech & Stanfield, 1981). According to the diffusional hypothesis for the decay of ICa' 7-' should be proportional to the peak amplitude of ICa and, therefore, the E values for r-1 and PCa should be similar.…”

Section: Temperature Effectssupporting

confidence: 86%

Calcium‐channel gating in frog skeletal muscle membrane: effect of temperature.

Cota¹,

Siri²,

Stefani³

1983

The Journal of Physiology

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SUMMARY1. Voltage-clamp experiments using the three micro-electrode method were performed to study the temperature dependence of the calcium current ICa in intact twitch skeletal muscle fibres of the frog. Contraction was blocked by recording in hypertonic sucrose solutions.2. For depolarizations smaller than 0 mV the decay of the transient, slow, inward current, recorded in the presence of external tetraethylammonium (TEA+) and by replacing Cl-for CH3SO3-, followed a complex time course. For larger depolarizations, after the initial inward current, there was a prominent, slow, outward current which showed two phases: after reaching a peak (time to peak 1-0 sec, peak amplitude 20-50 #sA/cm2 at 20 mV) it slowly declined to a steady level in about 2-3 see at 23 'C.3. The inward current was greatly reduced or abolished by the adding of2 mM-Cd2+ or by replacing external Ca2+ with Mg2+. The amplitude and time course of slow, outward currents were not obviously modified by replacing Ca2+ with Mg2+, having the two described phases. However, in the presence of Cd2+ the first transient phase of the outward current was not detected and only outward currents slowly increasing to a steady level were observed.4. Reliable ICa records were obtained by further blocking K+ outward currents by incubating the muscles in a K+-free TEA+-and Cs+-containing solution prior to experiments. Tubular space clamp was improved by recording ICa from small fibres with 20-30 jsm radius.5. The decay phase of ICa under a maintained depolarization in incubated muscles was fitted by a single exponential. The corresponding rate constant determined between 12 and 24 OC strongly depended on temperature, as expected for a gating process. The values for the activation energy and the corresponding Q10 (calculated for a 10-20 0C transition) were respectively: 17-5 + 1'0 kcal/mole and 2-9 + 0-2 at 0 mV, and 18-0 + 1-5 kcal/mole and 3 0 + 0-3 at -20 mV.6. The activation phase of Ica, analysed following the ma2h Hodgkin-Huxley kinetic model, showed a similar temperature dependence with a Q10 of 3-0 + 0 3. The

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Section: Temperature Effectssupporting

confidence: 86%

Calcium‐channel gating in frog skeletal muscle membrane: effect of temperature.

Cota¹,

Siri²,

Stefani³

1983

The Journal of Physiology

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“…The time constant logarithm is roughly linear with the potential. The potential necessary to increase tenfold the time constant is 80 to 100 mV, either in normal or isotonic K. This value is higher that what has been reported on skeletal muscle (Leech & Stanfield, 1981) and the egg of the starfish (Hagiwara & Yoshii, 1980), which reflects a weaker voltage-dependence. In their study, Hagiwara and Yoshii show that the voltage dependence of the time constant is lower when the temperature is increased and their data are consistent with the present results if we extrapolate to the mammalian physiological temperature.…”

Section: Discussionmentioning

confidence: 56%

Activation propetties of the inward-recifying potassium channel on mammalian heart cells

et al. 1987

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The early phase of activation of the inward-rectifying potassium channel is studied on single cells from guinea-pig heart. The current is quasi-instantaneous when it is outward, but activates with time when it is inward. This relaxation is exponential and its time-constant decreases with hyperpolarization. The I/V curve reflects a strong inward rectification and has a negative slope conductance on depolarization. Similar results were recorded in the absence of sodium, calcium, chloride ions and in isotonic potassium. Cesium slows down the phase of activation, and eventually appears to block the channels by suppression of the activation. Barium, conversely, does not affect the activation, but promotes an 'inactivation' of this current, which blocks it. These results are independent on the cells' dissociation method. They suggest that this current is the inward rectifier, called IK1 on heart. Its activation curve suggests that the inward and outward currents are flowing through the same channels. The inward rectifier is time- and voltage-dependent on heart as on other tissues. The effects of cesium and barium are also similar. The importance of its negative slope conductance is discussed.

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“…The mean Qowas 1v66+ 011 (n = 5). This value compares with values of 165-169 found by Almers (1971), who assumed a Q10 for sarcoplasmic resistivity in his calculation, and with a value of P@62 found by Hagiwara & Yoshii (1980) for inward rectification in starfish egg at temperatures greater than 10°C. We found no evidence in frog muscle for a higher Q10 for current amplitude at low temperatures, such as occurs in starfish egg below 10°C (Hagiwara &z Yoshii, 1980).…”

Section: A Leech and P R Stanfieldmentioning

confidence: 49%