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	Figure 2. Direct recording of the Ca2+ current by injection of EGTA. Oocytes activated by thapsigargin were clamped at −60 mV and superfused with Mg70 medium. (A) The ramp-voltage shown in the inset of Fig. 1 was applied regularly at intervals of 40 s. CaCl2 10 mM in NR was applied as indicated (solid bars) to induce Ca2+ entry. Large outward ICl(Ca) traces responding to ramp voltage were truncated. 4 nmol EGTA was injected at time indicated (arrow). The Ca2+ current was blocked by 0.1 mM La+3 (hollow bar) at the end of recording to measure the leak current. Pairs of current traces (a to g) were subtracted to cancel leakage and plotted against membrane potential in B and C respectively. (B) I-V relation of Ca2+ influx-induced current obtained before (b-a) and 1 min after (d-c) injection of EGTA. (C) I-V relation of Ca2+ influx-induced current obtained at ∼4 (e-g) and 9 min (f-g) after the injection of EGTA .
	Figure 3. Direct recording of Ca2+ current by injection of MeBAPTA. Similar procedures were followed as described in legend of Fig. 2, except 4 nmol MeBAPTA was injected at time indicated (A, arrow). Ca2+ influx-induced currents b, d, e, and f  were obtained at time as indicated in A . They were leak-subtracted and plotted versus membrane voltage in B and C.
	Figure 4. Transient ISOC induced by membrane hyperpolarization. (A) Oocytes had been activated by thapsigargin and injected with EGTA. (a) The membrane voltage was stepped from the holding potential −60 mV to +60 mV for 100 ms, followed by hyperpolarizing steps in increments of −20 mV to −120 mV final. (b) Current was recorded in Ca70 medium containing (in mM) 70 CaCl2, 10 HEPES, pH 7.2. (c) Leak current was acquired after addition of 1 mM LaCl3 into Ca70 medium. (d) La3+-sensitive calcium current was obtained as the difference between (b and c). (B) The current in A d was expanded to show the initial current decay. (C) I-V relation of transient (+) and sustained current components (×) as marked under the current traces in A d.
	Figure 5. Dependence of oocyte ISOC on extracellular concentration of Ca2+. Ca2+ entry in oocytes was activated by thapsigargin. The oocyte was then injected with MeBAPTA and superfused with Mg70 medium while clamping at −60 mV. (A) The Ca2+ current was elicited by perfusion of Ringers containing various concentrations of CaCl2. Applications of CaCl2 are indicated with solid bars with concentrations in mM. (B) Relative peak current as a function of extracellular [CaCl2], normalized to the value at 100 mM CaCl2. The symbols and error bars represent means ±SE (n = 6). The smooth curve is the best fit of the equation I/Imax = 1/(1 + Km/ [CaCl2]) where I is the current amplitude, Imax the saturating value of I at infinite [CaCl2], and Km is the Michaelis-Menten activation constant.
	Figure 6. Selectivity of ISOC for Ca2+ over K+ and Na+. (A) Oocytes activated by thapsigargin and pre-loaded with MeBAPTA were clamped at −60 mV and perfused with Mg70 medium. Introduction of Ca2+-containing solutions into bath was indicated as solid bars in the figure. The Ca2+ current was induced subsequently by solutions containing (in mM): 30 CaCl2, 55 XCl, and 10 HEPES, pH 7.2, where X = Na, NMDG, or K, and then by a Cl−-free solution containing (in mM): 30 Ca(CH3SO3)2, 55 KCH3SO3, and 10 HEPES, pH 7.2. (B) I-V relations were acquired in the above solutions using the same ramp-voltage protocol as in the inset of Fig. 1. Leak current was obtained after adding 30 μM La3+ to the above corresponding solutions to block the Ca2+ current.
	Figure 7. Conductances for Sr2+ and Ba2+ in the ISOC pathway. (A) Oocytes activated by thapsigargin and preloaded with MeBAPTA were clamped at −60 mV and perfused with Mg70 medium. Current was induced by perfusing oocytes succesively with Ca70, Sr70, and Ba70, containing (in mM): 70 MCl2, 10 HEPES-Na, pH 7.2, where M = Ca, Sr, and Ba, respectively. (B and C) Sr2+ and Ba2+ currents were recorded applying a pulse-voltage protocol similar to that shown in Fig. 4, A a. Sr2+ current traces (B a) and Ba2+ current traces (C a) were elicited with voltage steps respectively to +40, 0, −40, −80, and −120 mV and have been corrected for leak currents measured after adding 3 μM La3+ to block Sr2+ and Ba2+ currents. I-V relations of initial transient current (+) and sustained current (×) were plotted respectively for Sr2+ (B b) and Ba2+ currents (C b).
	Figure 8. Inhibition of oocyte ISOC by metal ions. Oocytes treated with thapsigargin to induce Ca2+ influx and injected with MeBAPTA were held at −60 mV, superfused with Mg70 medium and repetitively challenged with 10 mM CaCl2 in NR (solid bars) alone (first bar and subsequent unlabeled bars) or in combination with various metal ions at the indicated concentrations.
	Figure 9. Inhibitory effect of niflumic acid on ISOC. Oocytes treated with thapsigargin and injected with MeBAPTA were held at −60 mV. (A) ISOC was repetitively elicited by 10 mM CaCl2 in NR (solid bars). Bath application of niflumic acid 0.5 mM was indicated with a hollow bar. (B) I-V relations of the leak-subtracted current before (a) and during (b) the application of niflumic acid. These were measured at times indicated in A, in which for simplicity the ramp responses are not shown.
	Figure 10. Activation of ISOC by InsP3. (A) The oocyte was superfused with Ca2+-free Ringer (dotted line) at the beginning, then with Mg70 medium (thin solid line) 7 min later. Ca2+ influx was elicited by 10 mM CaCl2 in NR (thick bars). The ramp-voltage command was applied periodically to obtain the I-V relation. InsP3 32 pmol (first arrow) was injected to induce Ca2+ release and influx. EGTA 8 nmol (second arrow) was then injected to block ICl(Ca). (B) I-V relation of the immediate and later Ca2+ currents (a-c and b-c) after subtraction of the leak current (c) obtained after adding La3+ 0.1 mM (A, hollow bar). (C) Time course of ISOC activation by injection of 120 pmol InsP3 (arrows). The oocyte was preinjected with MeBAPTA and recorded in Ca70 medium. Vertical current traces were evoked by the standard ramp-voltage command.
	Figure 11. Activation of ISOC by ionomycin. (A) Oocyte was clamped at −60 mV and perfused with Ca2+-free Ringer (dotted line) or Mg70 medium (thin solid line). Ca2+ influx activity was tested by switching bath to CaCl2 10 mM in NR (thick bar). Ionomycin 10 μM in Ca2+-free Ringer supplemented with 1 mM EGTA (hollow bar) was superfused to induce Ca2+ release. EGTA 8 nmol was injected at the time indicated (arrow). (B). I-V relation of the Ca2+ current (a-b) after ICl(Ca) was abolished by EGTA. The leak current (b) was obtained in Mg70 medium. (C) The time course of ISOC activation by ionomycin. This oocyte was preloaded with MeBAPTA and recorded in Ca70 medium. Vertical current traces were elicited by the ramp-voltage command.
	Figure 12. Time course of oocyte ISOC activation by EGTA. Oocytes were injected with ∼4 nmol EGTA. ISOC was measured in 70 mM CaCl2 at −60 mV. ISOC was continuously recorded for the first 20 min after the injection of EGTA (n = 5). Each subsequent solid symbol represents ISOC measured from a single oocyte and calibrated by the left-hand ordinate axis, whereas each open symbol gives the corresponding input resistance referred to the right-hand axis. Squares, circles, and triangles indicate oocytes obtained from three animals.
	Figure 13. Inhibition of ISOC by activation of protein kinase C. Oocytes were treated with ionomycin and injected with EGTA. Ca2+ current was induced by switching bath perfusion from Mg70 medium to Ca70 medium repetitively as indicated by the solid bars. Bath application of PMA 1 μM (hollow bar) inhibited the Ca2+ current. (B) An albino oocyte was activated by thapsigargin. The oocyte was injected with EGTA and calphostin C 40 min before recording started. The inhibitory effect of PMA was almost completely abolished.

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