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Fig. 3 | The Journal of Headache and Pain

Fig. 3

From: Contribution of tetrodotoxin-resistant persistent Na+ currents to the excitability of C-type dural afferent neurons in rats

Fig. 3

Voltage-inactivation relationships of TTX-R Na+ channels in dural afferent neurons. A. Schematic illustration of voltage step pulses for the steady-state fast inactivation of TTX-R Na+ channels. Conditioning prepulses (500 ms duration; -120 mV to -10 mV in 10 mV increments) were immediately followed by test pulses (100 ms duration; up to -10 mV). B. a, Typical traces of TTX-R INa elicited by step pulses shown in A obtained from small- (left) and medium-sized (right) DiI-positive neurons. b, Voltage-inactivation relationships of TTX-R Na+ channels in small- (open circles) and medium-sized (closed circles) DiI-positive neurons. The points and error bars represent the mean and SEM from 32 small- and 44 medium-sized DiI-positive neurons. The continuous lines represent the best fits using a Boltzmann function. C. a, Scatter plot of the half-maximal voltage for inactivation (V50, inactivation) against membrane capacitance (Cm) (n = 76). The linear trend line represents the best fit using a least-squares fit (r = 0.64). b, The mean values of the V50, inactivation in small- (S) and medium-sized (M) DiI-positive neurons. The columns and error bars represent the mean and SEM from 32 small- and 44 medium-sized DiI-positive neurons. **; p < 0.01 (unpaired t-test). D. Scatter plot of the half-maximal voltage for inactivation (V50, inactivation) against the density of TTX-R INaP (n = 76). The linear trend line represents the best fit using a least-squares fit (r = 0.86). E. Time-dependent changes in V50, inactivation immediately after making a membrane rupture in small- (open circles) and medium-sized (closed circles) DiI-positive neurons. The points and error bars represent the mean and SEM from six small- and eight medium-sized DiI-positive neurons. F. a, Typical traces of TTX-R INa elicited by voltage step pulses in small- (left) and medium-sized (right) DiI-positive neurons. TTX-R INa were elicited by test pulses (100 ms duration; up to -10 mV) immediately after conditioning prepulses (10–500 ms duration; -120 mV to -10 mV in 10-mV increments). b, Changes in V50, inactivation with various durations (10–500 ms) of depolarizing prepulses. The points and error bars represent the mean and SEM from six small- and eight medium-sized DiI-positive neurons. **; p < 0.01, n.s; not significant (unpaired t-test). G. Schematic illustration of voltage step protocols for the slow inactivation of TTX-R Na+ channels. The conditioning prepulses (5 s duration, -100 mV to -10 mV, 10 mV increments) were followed by the test pulses (100 ms duration, up to -10 mV) with an interval of 100 ms at a potential of -80 mV. H. a, Typical traces of TTX-R INa elicited by voltage step pulses in small- (left) and medium-sized (right) DiI-positive neurons. b, Voltage-slow inactivation relationships of TTX-R Na+ channels in small- (open circles) and medium-sized (closed circles) DiI-positive neurons. The points and error bars represent the mean and SEM from 32 small- and 44 medium-sized DiI-positive neurons. The continuous lines represent the best fits using a Boltzmann function. I. Scatter plots of the half-maximal voltage for inactivation (V50, inactivation) against membrane capacitance (Cm) (a, n = 76) and the density of TTX-R INaP (b, n = 76). The linear trend lines represent the best fits using a least-squares fit (a, r = 0.69; b, r = 0.81)

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