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Figure 5 | Molecular Pain

Figure 5

From: Sea-anemone toxin ATX-II elicits A-fiber-dependent pain and enhances resurgent and persistent sodium currents in large sensory neurons

Figure 5

ATX-II induces resurgent currents in Nav1.7 and Nav1.6 expressing cells when β4-peptide is present in the pipette solution. (a) Voltage protocol (top panel) and representative current recordings with the β4-peptide added to the pipette solution (lower panel): left: stable HEK cell line expressing Nav1.7; right: Nav1.6 transfected N1E115 cells. An overlay of recordings under control conditions and ATX-II (5 nM) exposure at −20 mV (for Nav1.7) and −10 mV (for Nav1.6) is shown. (b) Peak current within the first 10 ms after repolarization of control (black symbols) and ATX-II exposed cells (pink symbols, left: Nav1.7, n = 15,17; right: Nav1.6, n = 11,11 for control and ATX-II, respectively). Resurgent currents are enhanced by the presence of ATX-II, when the β4-peptide is present in the pipette solution. (c) Mean persistent currents at the end of the repolarizing pulse are affected in Nav1.6 (right) and in Nav1.7 (left) by addition of extracellular ATX-II to the bath solution (pink symbols). (d) The increase of resurgent current is not due to a persistent current component, as subtraction of the persistent current from peak current reveals a clear corrected resurgent current component in both Nav1.7 (left) and Nav1.6 (right) expressing cells. * p < 0.05, independent-sample T-test for Nav1.7, paired-sample T-test for Nav1.6.

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