Fig. 2.
Ipe is carried by Ca2+ and Na+. A–D,Ipe was triggered by NMDA exposure (10 min, 100 μm) or intracellular perfusion of high-calcium solution. A, Responses of Ipeto changes of extracellular ionic composition. Line above current traces indicates period of perfusion of 20 mm NaCl solution, 20 mm KCl solution, or 10 mm CaCl2 solution. Changes ofIpe reached a plateau (indication of complete solution change around cell) within 2 sec. These responses are not from the same cell; because Ipe grows over time, we chose instead to show responses in which theIpe amplitudes (directly before the change to test solution) matched. B, C, Voltage ramps (−90 mV to +90 mV, 600 msec duration) performed 3–6 sec after changing to the indicated solutions. B,Ipe during the voltage ramp in the presence of extracellular control solution (continuous trace) and low-Cl− solution (dotted trace). (Traces essentially overlap.) The reversal potentials ofIpe were 0.8 ± 0.6 mV (control solution) and 0.8 ± 0.7 mV (low-Cl− solution, mean ± SD, n = 5). C,Ipe during the voltage ramp in the presence of extracellular control (a), 10 mmCaCl2 (b), 20 mm KCl (c), and 20 mm NaCl (d) solutions. During the voltage ramps, TTX (5 μm) and Co2+ (200 μm) were applied to block voltage-dependent Na+ and Ca2+ currents. Baseline leak current before NMDA exposure was not subtracted from current traces shown in B and C, because the subtraction made no significant difference in the reversal potential or conductance measured. D, Neither MK-801 (20 μm) nor Co2+ (200 μm) suppressed Ipe. Voltage steps (+10 mV) were applied every 25 sec. Cells examined had anIpe smaller than −1 nA.
