[1] [1] TREEDE R D. The international association for the study of pain definition of pain: as valid in 2018 as in 1979，but in need of regularly updated footnotes[J]. Pain Reports, 2018, 3(2): e643.

[2] [2] HYLANDS-WHITE N, DUARTE R V, RAPHAEL J H. An over-view of treatment approaches for chronic pain management[J]. Rheumatology International, 2017, 37(1): 29-42.

[3] [3] BENNETT D L, CLARK A J, HUANG J, et al. The role of volt-age-gated sodium channels in pain signaling[J]. Physiological Reviews, 2019, 99(2): 1079-1151.

[4] [4] ZAKRZEWSKA J M, PALMER J, MORISSET V, et al. Safety and e.cacy of a NaV1.7 selective sodium channel blocker in patients with trigeminal neuralgia: a double-blind, placebo-controlled, randomised withdrawal phase 2a trial[J]. The Lancet Neurology, 2017, 16(4): 291-300.

[5] [5] KINGWELL K. NaV1.7 withholds its pain potential[J]. Nature Reviews Drug Discovery, 2019, 18: 321-323.

[6] [6] DIB-HAJJ S D, BLACK J A, WAXMAN S G. NaV1.9: a sodium channel linked to human pain[J]. Nature Reviews Neuroscience, 2015, 16(9): 511-519.

[7] [7] DIB-HAJJ S, BLACK J A, CUMMINS T R, et al. NaN/NaV1.9: a sodium channel with unique properties[J]. Trends in Neurosci-ences, 2002, 25(5): 253-259.

[8] [8] LIN Z, SANTOS S, PADILLA K, et al. Biophysical and pharma-cological characterization of NaV1.9 voltage dependent sodium channels stably expressed in HEK-293 cells[J]. PLoS One, 2016,11(8): e0161450.

[9] [9] LIU C J, DIB-HAJJ S D, BLACK J A, et al. Direct interaction with contactin targets voltage-gated sodium channel NaV1.9/NaN to the cell membrane[J]. The Journal of Biological Chemistry, 2001, 276(49): 46553-46561.

[10] [10] HERZOG R I, CUMMINS T R, WAXMAN S G. Persistent ttx-resistant Na+ current affects resting potential and response to depolarization in simulated spinal sensory neurons[J]. Journal of Neurophysiology, 2001, 86(3): 1351-1364.

[11] [11] PRIEST B T, MURPHY B A, LINDIA J A, et al. Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior[J]. Proceedings of the National Academy of Sciences of the United States of America,2005, 102(26): 9382-9387.

[12] [12] YUYQ, ZHAOF,GUAN SM, et al. Antisense-mediated knock-down of NaV1.8, but not NaV1.9, generates inhibitory effects on complete freund’s adjuvant-induced in.ammatory pain in rat[J]. PLoS One, 2011, 6(5): e19865.

[13] [13] MAINGRET F, COSTE B, PADILLA F, et al. Inflammatory mediators increase NaV1.9 current and excitability in nociceptors through a coincident detection mechanism[J]. The Journal of General Physiology, 2008, 131(3): 211-225.

[14] [14] AMSALEM M, POILBOUT C, FERRACCI G, et al. Membrane cholesterol depletion as a trigger of NaV1.9 channel-mediated in-.ammatory pain[J]. The EMBO Journal, 2018, 37(8): e97349.

[15] [15] LUIZ A P, KOPACH O, SANTANA-VARELA S, et al. The role of NaV1.9 channel in the development of neuropathic orofacial pain associated with trigeminal neuralgia[J]. Molecular Pain, 2015,25(11): 72.

[16] [16] BONNET C, HAO J, OSORIO N, et al. Maladaptive activation of NaV1.9 channels by nitric oxide causes triptan-induced medica-tion overuse headache[J]. Nature Communications, 2019, 10(1): 4253.

[17] [17] LOLIGNIER S, BONNET C, GAUDIOSO C, et al. The NaV1.9 channel is a key determinant of cold pain sensation and cold allo-dynia[J]. Cell Reports, 2015, 11(7): 1067-1078.

[18] [18] QIU F, JIANG Y, ZHANG H, et al. Increased expression of tetrodotoxin-resistant sodium channels NaV1.8 and NaV1.9 within dorsal root ganglia in a rat model of bone cancer pain[J]. Neuro-science Letters, 2012, 512(2): 61-66.

[19] [19] LEIPOLD E, LIEBMANN L, KORENKE G C, et al. A de novo gain-of-function mutation in SCN11A causes loss of pain percep-tion[J]. Nature Genetics, 2013, 45(11): 1399-1404.

[20] [20] ZHANG X Y, WEN J, YANG W, et al. Gain-of-function mutations in SCN11A cause familial episodic pain[J]. American Journal of Human Genetics, 2013, 93(5): 957-966.

[21] [21] HUANG J, HAN C, ESTACION M, et al. Gain-of-function muta-tions in sodium channel NaV1.9 in painful neuropathy[J]. Brain, 2014, 137(6): 1627-1642.

[22] [22] SALVATIERRA J, DIAZ-BUSTAMANTE M, MEIXIONG J, et al. A disease mutation reveals a role for NaV1.9 in acute itch[J]. The Journal of Clinical Investigation, 2018, 128(12): 5434-5447.

[23] [23] ZHOU X, XIAO Z, XU Y, et al. Electrophysiological and phar-macological analyses of NaV1.9 voltage-gated sodium channel by establishing a heterologous expression system[J]. Frontiers in Pharmacology, 2017, 22(8): 852.

[24] [24] ZHOU X, MA T, YANG L, et al. Spider venom-derived peptide induces hyperalgesia in NaV1.7 knockout mice by activating NaV1.9 channels[J]. Nature Communications, 2020, 11(1): 2293.

[25] [25] LIANG J, LIU X, ZHENG J, et al. Effect of amitriptyline on tetrodotoxin-resistant NaV1.9 currents in nociceptive trigeminal neurons[J]. Molecular Pain, 2013, 22(9): 31.

[26] [26] BLACK J A, VASYLYEV D, DIB-HAJJ S D, et al. NaV1.9 expression in magnocellular neurosecretory cells of supraoptic nucleus[J]. Experimental Neurology, 2014, 253: 174-179.

[27] [27] CARINE C, NANCY O, MARCEL C, et al. Activation of neuroki-nin 3 receptor increases NaV1.9 current in enteric neurons[J]. The Journal of Physiology, 2009, 587(7): 1461-1479.