Figure 3: rDc1a promotes opening of BgNav1 channels.

(a) Comparison of the gating properties of BgNav1 before (black), and after (red), addition of 1 μM rDc1a. Shown are the normalized deduced conductance (G)–voltage (filled circles) (G/Gmax) and steady-state inactivation (open circles; I/Imax) relationships. Currents were elicited by 5-mV step depolarizations from a holding voltage of −90 mV or −100 mV, respectively. n=3–5, and error bars represent s.e.m. Descriptive values resulting from Boltzmann fits can be found in the Results section. (b) Recovery from fast inactivation of WT BgNav1 before (black), and after (red), addition of 1 μM rDc1a (red) determined by a double-pulse protocol to −30 mV with a varying time between pulses (0–50 ms). Values are reported in the Results section. Data represents n=4 experiments, and error bars represent the s.e.m. (c) On addition of 1 μM rDc1a to channels depolarized to −60 mV every 5 s (red open circles) or 50 s (green open circles; holding voltage was −100 mV), BgNav1-mediated sodium currents become rapidly visible. Channels completely recover after toxin washout. Inset shows current trace before (black), and after (red), addition of 1 μM rDc1a at −60 mV (5 s pulses). Noticeable is the persistent current that appears at this voltage, even in control experiments. Abscissa scale is 10 ms, ordinate scale is 0.3 μA. (d) Concentration dependence of rDc1a-induced current potentiation determined from shifts in the midpoint of channel activation (V1/2). Line represents a fit of the data with the Hill equation resulting in a half-maximal concentration (EC50) of 65±1 nM and a slope factor of 1.19±0.02; n=5 and error bars represent s.e.m.