Figure 5. Deletion of BACE1 causes modification of sodium channel function in hippocampal neurons. A, Sample sodium current from acutely dissociated hippocampal neurons from postnatal day 21–30 mice. Peak Na+ current was elicited by the step depolarization between −60 and +20 mV in an increment of 10 mV. Calibration: 5 ms, 500 pA. B, Normalized peak Na+ current density (in picoamperes/picofarad) versus voltage in acutely dissociated hippocampal neurons. BACE1−/− neurons yielded significant greater Na+ current density (181 ± 13 pA/pF; n = 8) compared with that of wild-type neurons (136 ± 21 pA/pF; n = 10). *p < 0.05. C, The activation curve of sodium channel recorded from acutely dissociated hippocampal neurons. The activation curve was fitted by the Boltzmann equation: G/Gmax = 1/(1 + exp((V1/2 − V)/k)). V1/2 is the voltage of half-maximal Na+ conductance, and k is a slope factor. D, Sample sodium current traces elicited by prepulse potential between −120 and 0 mV, followed by the depolarization command potential at 0 mV. Calibration: 5 ms, 500 pA. E, Steady-state inactivation curve of sodium channel. Peak Na+ current (I) at such prepulse potential was normalized to the maximum peak current (Imax) and fitted by the following Boltzmann equation: I/Imax = 1/(1+exp((V − V1/2)/k)). V1/2 is the voltage of half-maximal availability, and k is the slope. Note that inactivation curve obtained from BACE1-null neurons displays a shift in the depolarization direction compared with that of wild-type controls (V1/2: BACE1-null, −60 ± 1 mV, vs wild-type, −69 ± 1 mV). *p < 0.05. Error bars indicate SEM.