The Journal of Neuroscience, July 26, 2006, ():
Sodium Channel 
2 Subunits Regulate Tetrodotoxin-Sensitive Sodium Channels in Small Dorsal Root Ganglion Neurons and Modulate the Response to Pain
J. Neurosci. Lopez-Santiago et al.
26: 7984
Supplemental data
Files in this Data Supplement:
- supplemental material
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Alternative method to analyze INa inactivation:
We performed an alternate calculation of INa inactivation, yielding similar results to these shown in Fig. 3. The same example of INas obtained from one typical small-fast β2+/+ neuron in response to a test pulse to 0 mV are shown in the insets to Fig. 3A and Fig. S1A. For this alternative analysis we took advantage of the differences in the voltage-dependent of inactivation of TTX-S channels compared to TTX-R channels. As observed in the current traces shown in Fig. S1A, TTX-S INa (fast) is inactivated at more negative voltages than TTX-R INa (slow). Thus, we performed INa amplitude measurements at two different time points. First, we measured the TTX-S inactivation curve at the time of maximum INa (Fig. S1A, line 1). The TTX-R inactivation curve was then measured at the peak of the INa evoked following a -50 mV prepulse (Fig. S1A, line 2). Each data set was normalized and fit with a single Boltzmann equations of the form
INa = 1 / 1 + exp((Vm-V½)/k)
where V½ is the potential at which half of the INa was inactivated, and k is the slope factor. The means of individual curves are shown in Fig. S1B for small-fast neurons. The corresponding V½ and k for TTX-S INa are -56.5 ± 3.1 and -10.1 ± 1.3 mV for β2+/+, respectively, -52.2 ± 3.9 and -10.3 ± 1.5 mV for β2-/-, respectively, For TTX-R INa, these values are -29.5 ± 2.4 and -5.0 mV for β2+/+, respectively, and -25.2 ± 1.5 and -5.2 ± 1.9 mV for β2-/-, respectively. These values are statistically indistinguishable from those reported in Fig. 3 using a double Boltzmann fit of on the total INa.
