Table 1.
Expression of sodium currents in HEK293 cells transfected with the Nav1.6 sodium channel α subunit alone or cotransfected with the β1 subunit.
Figure 1.
Sodium currents recorded from HEK-Nav1.6 and HEK-Nav1.6β1 cells.
(A) Representative sodium current traces recorded from HEK-Nav1.6 and HEK-Nav1.6β1 cells following 40-ms depolarizations from −120 mV to −15 mV. (B) Sodium currents recorded from a HEK-Nav1.6β1 cell before and after exposure to 0.5 µM TTX. Dashed lines indicate zero current.
Table 2.
Effects of coexpression with the β1 subunit on the kinetics of sodium current activation and inactivation and amplitudes of persistent currents in HEK293 cells expressing Nav1.6 sodium channels.
Figure 2.
Voltage-dependent activation of Nav1.6 and Nav1.6β1 sodium channels expressed in HEK293 cells.
(A) Representative current traces recorded from a HEK-Nav1.6 cell using the indicated pulse protocol (left) and the plot of peak sodium current in these traces as a function of test potential (right). (B) Representative current traces recorded from a HEK-Nav1.6β1 cell using the pulse protocol shown in Panel A and the plot of peak sodium current in these traces as a function of test potential. (C) Conductance – voltage plots for the activation of Nav1.6 and Nav1.6β1 channels. Peak sodium currents such as those in Panels A and B were transformed to conductances (G) using the equation G = I/(Vt–Vrev), where I is the peak current, Vrev is the reversal potential, and Vt is the voltage of the test potential; conductances were then normalized to the maximum conductance (Gmax) for that cell. Values are means of 64 (Nav1.6) or 65 (Nav1.6β1) separate experiments with different cells; bars show SE values larger than the data point symbols. Curves were fitted to the mean values using the Boltzmann equation.
Table 3.
Effects of coexpression with the β1 subunit on the voltage dependence of activation and steady-state inactivation of Nav1.6 sodium channels expressed in HEK293 cells.a
Figure 3.
Voltage-dependent steady-state fast inactivation of Nav1.6 and Nav1.6β1 sodium channels expressed in HEK293 cells.
Amplitudes of peak transient currents obtained using the indicated pulse protocol are plotted as a function of prepulse potential. Values are means of 63 (Nav1.6) or 66 (Nav1.6β1) separate experiments with different cells; bars show SE values larger than the data point symbols. Curves were fitted to the mean values using the Boltzmann equation.
Figure 4.
Effect of repeated depolarization on the stability of sodium currents recorded from HEK293 cells expressing Nav1.6 and Nav1.6β1 sodium channels.
Sodium currents were recorded during a 40-ms step depolarization from −120 mV to −15 mV following 0–100 conditioning prepulses (5-ms pulses from −120 mV to 10 mV at 20 Hz). Currents for each cell were normalized to the amplitude of the peak current obtained prior to repeated depolarization. Values are means of the indicated number of separate experiments with different cells; bars show SE values larger than the data point symbols.
Table 4.
Comparison of the voltage dependence of activation and steady-state fast inactivation of rat, human and mouse Nav1.6 sodium channels expressed in human embryonic kidney-derived cell lines in the absence of auxiliary β subunits.