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Figure 5 | Molecular Pain

Figure 5

From: Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable

Figure 5

The M1627K mutation alters rate of open-state inactivation and recovery from inactivation properties of Na v 1.7. A, Time constants for development of fast-inactivation as a function of voltage for WT (filled symbols, n = 6) and M1627K (open symbols, n = 6) Nav1.7 channels are shown. Open-channel inactivation time constants were measured at voltages ranging from -45 to +40 mV by fitting the decay phase of currents elicited with depolarizing pulses with single exponentials. The time constants for development of closed-state inactivation were estimated from single exponential fits to time courses measured at inactivation potentials ranging from -90 to -50 mV for WT (filled triangles, n = 6) and with M1627K (open triangles, n = 6) Nav1.7 channels. B, Recovery from inactivation kinetics are faster for M1627K mutant channels (open circles, n = 7) than for WT Nav1.7 channels (filled squares, n = 7). Time constants were estimated from single exponential fits to time courses measured at recovery potentials ranging from -140 to -60 mV. The recovery from inactivation voltage protocol involved prepulsing the cell to -20 mV for 20 ms to inactivate all of the current, then stepping the membrane potential back to the recovery potential for increasing recovery durations prior to the test pulse to 0 mV. The maximum pulse rate was 0.5 Hz.

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