Veratridine modifies the gating of human voltage-gated sodium channel Nav1.7

Authors: Xiao-yu Zhang1, Rui-yun Bi2, Peng Zhang1, Ye-hua Gan1
1 Central Laboratory, Peking University School and Hospital of Stomatology, Beijing, China
2 The Third Dental Center, Peking University School and Hospital of Stomatology, Beijing 100081, China
Correspondence to: Ye-hua Gan:,
DOI: 10.1038/s41401-018-0065-z
Received: 8 November 2017
Accepted: 5 June 2018
Advance online: 27 June 2018


Veratridine is a lipid-soluble neurotoxin derived from plants in the family Liliaceae. It has been broadly investigated for its action as a sodium channel agonist. However, the effects of veratridine on subtypes of sodium channels, especially Nav1.7, remain to be studied. Here, we investigated the effects of veratridine on human Nav1.7 ectopically expressed in HEK293A cells and recorded Nav1.7 currents from the cells using whole-cell patch clamp technique. We found that veratridine exerted a dose-dependent inhibitory effect on the peak current of Nav1.7, with the half-maximal inhibition concentration (IC50) of 18.39 µM. Meanwhile, veratridine also elicited tail current (linearly) and sustained current [half-maximal concentration (EC50): 9.53 µM], also in a dose-dependent manner. Veratridine (75 µM) shifted the half-maximal activation voltage of the Nav1.7 activation curve in the hyperpolarized direction, from −21.64 ± 0.75 mV to −28.14 ± 0.66 mV, and shifted the half-inactivation voltage of the steady-state inactivation curve from −59.39 ± 0.39 mV to −73.78 ± 0.5 mV. An increased frequency of stimulation decreased the peak and tail currents of Nav1.7 for each pulse along with pulse number, and increased the accumulated tail current at the end of train stimulation. These findings reveal the different modulatory effects of veratridine on the Nav1.7 peak current and tail current.
Keywords: veratridine; Nav1.7; channel activation; channel inactivation; electrophysiology; HEK293 cells

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