Scorpion toxin BmK I directly activates Nav1.8 in primary sensory neurons to induce neuronal hyperexcitability in rats

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Abstract

© 2015, The Author(s). Voltage-gated sodium channels (VGSCs) in primary sensory neurons play a key role in transmitting pain signals to the central nervous system. BmK I, a site-3 sodium channel-specific toxin from scorpion Buthus martensi Karsch, induces pain behaviors in rats. However, the subtypes of VGSCs targeted by BmK I were not entirely clear. We therefore investigated the effects of BmK I on the current amplitude, gating and kinetic properties of Na v 1.8, which is associated with neuronal hyperexcitability in DRG neurons. It was found that BmK I dose-dependently increased Na v 1.8 current in small-sized ( < 25 μm) acutely dissociated DRG neurons, which correlated with its inhibition on both fast and slow inactivation. Moreover, voltage-dependent activation and steady-state inactivation curves of Na v 1.8 were shifted in a hyperpolarized direction. Thus, BmK I reduced the threshold of neuronal excitability and increased action potential firing in DRG neurons. In conclusion, our data clearly demonstrated that BmK I modulated Na v 1.8 remarkably, suggesting BmK I as a valuable probe for studying Na v 1.8. And Nav1.8 is an important target related to BmK I-evoked pain.

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Ye, P., Jiao, Y., Li, Z., Hua, L., Fu, J., Jiang, F., … Ji, Y. (2015). Scorpion toxin BmK I directly activates Nav1.8 in primary sensory neurons to induce neuronal hyperexcitability in rats. Protein and Cell, 6(6), 443–452. https://doi.org/10.1007/s13238-015-0154-4

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