Development of ICaduring bFGF treatment. A, Representative current traces of ICa from control neurons (middle) and from bFGF-treated neurons (bottom) at 4 DIV. ICa was evoked by voltage pulses to 0 mV from a holding potential of −100 mV (as indicated at top). B,Current–voltage relationship of ICa in control (n = 5, open circles), bFGF-treated (10 ng/ml) (n = 6, solid squares), and bFGF + cycloheximide-treated (0.1 μm) (n = 3, solid triangles) neurons at 4 DIV. Currents were evoked by step depolarization over the range of −60 to +60 mV from a holding potential of −100 mV. The peak amplitude ofICa was measured and plotted against test potential. Note that bFGF treatment significantly increased high-voltage-activated ICa, whereas low-voltage-activated ICa remained unchanged. Asterisks indicate significant differences from the control group; *p < 0.05 (Student’st test). C, Development ofICa density in the absence (open bars) and presence (hatched bars) of bFGF at indicated concentrations (in ng/ml). Cell membrane capacitance was measured, and the ICa density at 0 mV test potential was calculated. The ICa density increased with the length of culture period (0.5 to 4 DIV). bFGF significantly enhanced the developmental increase of theICa density. CHX (0.1 μm) blocked the enhancement of theICa density by bFGF treatment. Thenumber of neurons examined is given inparentheses. Asterisk indicates significant difference from the control group (C); *p < 0.05 (Duncan’s multiple-range test).
