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Na v 1. 9 voltage-gated sodium channel is preferentially expressed in peripheral nociceptive neurons. Recent progresses have proved its role in pain sensation, but our understanding of Na v 1.9, in general, has lagged behind because of limitations in heterologous expression in mammal cells. In this work, functional expression of human Na v 1.9 (hNa v 1.9) was achieved by fusing GFP to the C-terminal of hNa v 1.9 in ND7/23 cells, which has been proved to be a reliable method to the electrophysiological and pharmacological studies of hNa v 1.9. By using the hNa v 1.9 expression system, we investigated the electrophysiological properties of four mutations of hNa v 1.9 (K419N, A582T, A842P, and F1689L), whose electrophysiological functions have not been determined yet. The four mutations significantly caused positive shift of the steady-state fast inactivation and therefore increased hNa v 1.9 activity, consistent with the phenotype of painful peripheral neuropathy. Meanwhile, the effects of inflammatory mediators on hNa v 1.9 were also investigated. Impressively, histamine was found for the first time to enhance hNa v 1.9 activity, indicating its vital role in hNa v 1.9 modulating inflammatory pain. Taken together, our research provided a useful platform for hNa v 1.9 studies and new insight into mechanism of hNa v 1.9 linking to pain.

Electrophysiological and Pharmacological Analyses of Nav1.9 Voltage-Gated Sodium Channel by Establishing a Heterologous Expression System