Xie YF, Yang J, Ratté S, Prescott SA. (2024). Similar excitability through different sodium channels and implications for the analgesic efficacy of selective drugs. eLife. 12 [PubMed]

See more from authors: Xie YF · Yang J · Ratté S · Prescott SA

References and models cited by this paper

Abrahamsen B et al. (2008). The cell and molecular basis of mechanical, cold, and inflammatory pain. Science (New York, N.Y.). 321 [PubMed]

Agarwal N, Offermanns S, Kuner R. (2004). Conditional gene deletion in primary nociceptive neurons of trigeminal ganglia and dorsal root ganglia. Genesis (New York, N.Y. : 2000). 38 [PubMed]

Akin EJ et al. (2019). Building sensory axons: Delivery and distribution of NaV1.7 channels and effects of inflammatory mediators. Science advances. 5 [PubMed]

Alexandrou AJ et al. (2016). Subtype-Selective Small Molecule Inhibitors Reveal a Fundamental Role for Nav1.7 in Nociceptor Electrogenesis, Axonal Conduction and Presynaptic Release. PloS one. 11 [PubMed]

Alles SRA, Smith PA. (2021). Peripheral Voltage-Gated Cation Channels in Neuropathic Pain and Their Potential as Therapeutic Targets. Frontiers in pain research (Lausanne, Switzerland). 2 [PubMed]

Alsaloum M, Higerd GP, Effraim PR, Waxman SG. (2020). Status of peripheral sodium channel blockers for non-addictive pain treatment. Nature reviews. Neurology. 16 [PubMed]

Amir R, Michaelis M, Devor M. (1999). Membrane potential oscillations in dorsal root ganglion neurons: role in normal electrogenesis and neuropathic pain. The Journal of neuroscience : the official journal of the Society for Neuroscience. 19 [PubMed]

Bankar G et al. (2018). Selective NaV1.7 Antagonists with Long Residence Time Show Improved Efficacy against Inflammatory and Neuropathic Pain. Cell reports. 24 [PubMed]

Baron R, Dickenson AH. (2014). Neuropathic pain: precise sensory profiling improves treatment and calls for back-translation. Pain. 155 [PubMed]

Bean BP. (2007). The action potential in mammalian central neurons. Nature reviews. Neuroscience. 8 [PubMed]

Bennett DL, Clark AJ, Huang J, Waxman SG, Dib-Hajj SD. (2019). The Role of Voltage-Gated Sodium Channels in Pain Signaling. Physiological reviews. 99 [PubMed]

Berta T et al. (2008). Transcriptional and functional profiles of voltage-gated Na(+) channels in injured and non-injured DRG neurons in the SNI model of neuropathic pain. Molecular and cellular neurosciences. 37 [PubMed]

Black JA, Liu S, Tanaka M, Cummins TR, Waxman SG. (2004). Changes in the expression of tetrodotoxin-sensitive sodium channels within dorsal root ganglia neurons in inflammatory pain. Pain. 108 [PubMed]

Blair NT, Bean BP. (2002). Roles of tetrodotoxin (TTX)-sensitive Na+ current, TTX-resistant Na+ current, and Ca2+ current in the action potentials of nociceptive sensory neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience. 22 [PubMed]

Bonin RP, Bories C, De Koninck Y. (2014). A simplified up-down method (SUDO) for measuring mechanical nociception in rodents using von Frey filaments. Molecular pain. 10 [PubMed]

Caffrey JM, Eng DL, Black JA, Waxman SG, Kocsis JD. (1992). Three types of sodium channels in adult rat dorsal root ganglion neurons. Brain research. 592 [PubMed]

Campbell JN, Raja SN, Meyer RA, Mackinnon SE. (1988). Myelinated afferents signal the hyperalgesia associated with nerve injury. Pain. 32 [PubMed]

Cohen SP, Vase L, Hooten WM. (2021). Chronic pain: an update on burden, best practices, and new advances. Lancet (London, England). 397 [PubMed]

Cox JJ et al. (2006). An SCN9A channelopathy causes congenital inability to experience pain. Nature. 444 [PubMed]

Davidson S et al. (2014). Human sensory neurons: Membrane properties and sensitization by inflammatory mediators. Pain. 155 [PubMed]

Dehen H, Willer JC, Prier S, Boureau F, Cambier J. (1978). Congenital insensitivity to pain and the "morphine-like" analgesic system. Pain. 5 [PubMed]

Dib-Hajj SD, Yang Y, Black JA, Waxman SG. (2013). The Na(V)1.7 sodium channel: from molecule to man. Nature reviews. Neuroscience. 14 [PubMed]

Djouhri L et al. (2003). Sensory and electrophysiological properties of guinea-pig sensory neurones expressing Nav 1.7 (PN1) Na+ channel alpha subunit protein. The Journal of physiology. 546 [PubMed]

Drion G, Massotte L, Sepulchre R, Seutin V. (2011). How modeling can reconcile apparently discrepant experimental results: the case of pacemaking in dopaminergic neurons. PLoS computational biology. 7 [PubMed]

Drion G, O'Leary T, Marder E. (2015). Ion channel degeneracy enables robust and tunable neuronal firing rates. Proceedings of the National Academy of Sciences of the United States of America. 112 [PubMed]

Dustrude ET, Wilson SM, Ju W, Xiao Y, Khanna R. (2013). CRMP2 protein SUMOylation modulates NaV1.7 channel trafficking. The Journal of biological chemistry. 288 [PubMed]

Eagles DA, Chow CY, King GF. (2022). Fifteen years of NaV 1.7 channels as an analgesic target: Why has excellent in vitro pharmacology not translated into in vivo analgesic efficacy? British journal of pharmacology. 179 [PubMed]

Edelman GM, Gally JA. (2001). Degeneracy and complexity in biological systems. Proceedings of the National Academy of Sciences of the United States of America. 98 [PubMed]

Emery EC, Luiz AP, Wood JN. (2016). Nav1.7 and other voltage-gated sodium channels as drug targets for pain relief. Expert opinion on therapeutic targets. 20 [PubMed]

Fertleman CR et al. (2006). SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes. Neuron. 52 [PubMed]

Finnerup NB et al. (2015). Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis. The Lancet. Neurology. 14 [PubMed]

Goaillard JM, Marder E. (2021). Ion Channel Degeneracy, Variability, and Covariation in Neuron and Circuit Resilience. Annual review of neuroscience. 44 [PubMed]

Gold MS, Gebhart GF. (2010). Nociceptor sensitization in pain pathogenesis. Nature medicine. 16 [PubMed]

Gould HJ, England JD, Liu ZP, Levinson SR. (1998). Rapid sodium channel augmentation in response to inflammation induced by complete Freund's adjuvant. Brain research. 802 [PubMed]

Grashow R, Brookings T, Marder E. (2010). Compensation for variable intrinsic neuronal excitability by circuit-synaptic interactions. The Journal of neuroscience : the official journal of the Society for Neuroscience. 30 [PubMed]

Grubinska B et al. (2019). Rat NaV1.7 loss-of-function genetic model: Deficient nociceptive and neuropathic pain behavior with retained olfactory function and intra-epidermal nerve fibers. Molecular pain. 15 [PubMed]

Haroutounian S et al. (2014). Primary afferent input critical for maintaining spontaneous pain in peripheral neuropathy. Pain. 155 [PubMed]

Hay M, Thomas DW, Craighead JL, Economides C, Rosenthal J. (2014). Clinical development success rates for investigational drugs. Nature biotechnology. 32 [PubMed]

Jarvis MF et al. (2007). A-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat. Proceedings of the National Academy of Sciences of the United States of America. 104 [PubMed]

Kingwell K. (2019). Nav1.7 withholds its pain potential. Nature reviews. Drug discovery. [PubMed]

Kitano Y, Shinozuka T. (2022). Inhibition of NaV1.7: the possibility of ideal analgesics. RSC medicinal chemistry. 13 [PubMed]

Knox AT, Glauser T, Tenney J, Lytton WW, Holland K. (2018). Modeling pathogenesis and treatment response in childhood absence epilepsy. Epilepsia. 59 [PubMed]

Koltzenburg M, Lundberg LER, Torebjörk EH. (1992). Dynamic and static components of mechanical hyperalgesia in human hairy skin. Pain. 51 [PubMed]

Kushnarev M, Pirvulescu IP, Candido KD, Knezevic NN. (2020). Neuropathic pain: preclinical and early clinical progress with voltage-gated sodium channel blockers. Expert opinion on investigational drugs. 29 [PubMed]

Lee KY, Prescott SA. (2015). Chloride dysregulation and inhibitory receptor blockade yield equivalent disinhibition of spinal neurons yet are differentially reversed by carbonic anhydrase blockade. Pain. 156 [PubMed]

Liang L, Fan L, Tao B, Yaster M, Tao YX. (2013). Protein kinase B/Akt is required for complete Freund's adjuvant-induced upregulation of Nav1.7 and Nav1.8 in primary sensory neurons. The journal of pain. 14 [PubMed]

Liu CN et al. (2000). Tactile allodynia in the absence of C-fiber activation: altered firing properties of DRG neurons following spinal nerve injury. Pain. 85 [PubMed]

Liu X, Eschenfelder S, Blenk KH, Jänig W, Häbler H. (2000). Spontaneous activity of axotomized afferent neurons after L5 spinal nerve injury in rats. Pain. 84 [PubMed]

M Flake N, Lancaster E, Weinreich D, Gold MS. (2004). Absence of an association between axotomy-induced changes in sodium currents and excitability in DRG neurons from the adult rat. Pain. 109 [PubMed]

MacDonald DI et al. (2021). A central mechanism of analgesia in mice and humans lacking the sodium channel NaV1.7. Neuron. 109 [PubMed]

Malin SA, Davis BM, Molliver DC. (2007). Production of dissociated sensory neuron cultures and considerations for their use in studying neuronal function and plasticity. Nature protocols. 2 [PubMed]

Mao J. (2012). Current challenges in translational pain research. Trends in pharmacological sciences. 33 [PubMed]

Marder E, Goaillard JM. (2006). Variability, compensation and homeostasis in neuron and network function. Nature reviews. Neuroscience. 7 [PubMed]

McCormack K et al. (2013). Voltage sensor interaction site for selective small molecule inhibitors of voltage-gated sodium channels. Proceedings of the National Academy of Sciences of the United States of America. 110 [PubMed]

McDermott LA et al. (2019). Defining the Functional Role of NaV1.7 in Human Nociception. Neuron. 101 [PubMed]

Medlock L et al. (2022). Multiscale computer model of the spinal dorsal horn reveals changes in network processing associated with chronic pain The Journal of neuroscience : the official journal of the Society for Neuroscience. 42 [PubMed]

Minett MS et al. (2014). Pain without nociceptors? Nav1.7-independent pain mechanisms. Cell reports. 6 [PubMed]

Minett MS et al. (2012). Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons. Nature communications. 3 [PubMed]

Minett MS et al. (2015). Endogenous opioids contribute to insensitivity to pain in humans and mice lacking sodium channel Nav1.7. Nature communications. 6 [PubMed]

Mishra P, Narayanan R. (2022). Conjunctive changes in multiple ion channels mediate activity-dependent intrinsic plasticity in hippocampal granule cells. iScience. 25 [PubMed]

Mogil JS. (2009). Animal models of pain: progress and challenges. Nature reviews. Neuroscience. 10 [PubMed]

Moreno AM et al. (2021). Long-lasting analgesia via targeted in situ repression of NaV1.7 in mice. Science translational medicine. 13 [PubMed]

Mulcahy JV et al. (2019). Challenges and Opportunities for Therapeutics Targeting the Voltage-Gated Sodium Channel Isoform NaV1.7. Journal of medicinal chemistry. 62 [PubMed]

Nassar MA, Levato A, Stirling LC, Wood JN. (2005). Neuropathic pain develops normally in mice lacking both Na(v)1.7 and Na(v)1.8. Molecular pain. 1 [PubMed]

Nassar MA et al. (2004). Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain. Proceedings of the National Academy of Sciences of the United States of America. 101 [PubMed]

O'Leary T, Williams AH, Franci A, Marder E. (2014). Cell types, network homeostasis, and pathological compensation from a biologically plausible ion channel expression model. Neuron. 82 [PubMed]

Osteen JD et al. (2016). Selective spider toxins reveal a role for the Nav1.1 channel in mechanical pain. Nature. 534 [PubMed]

Payne CE et al. (2015). A novel selective and orally bioavailable Nav 1.8 channel blocker, PF-01247324, attenuates nociception and sensory neuron excitability. British journal of pharmacology. 172 [PubMed]

Prescott SA, De Koninck Y, Sejnowski TJ. (2008). Biophysical basis for three distinct dynamical mechanisms of action potential initiation. PLoS computational biology. 4 [PubMed]

Prescott SA, Sejnowski TJ, De Koninck Y. (2006). Reduction of anion reversal potential subverts the inhibitory control of firing rate in spinal lamina I neurons: towards a biophysical basis for neuropathic pain. Molecular pain. 2 [PubMed]

Prinz AA, Bucher D, Marder E. (2004). Similar network activity from disparate circuit parameters. Nature neuroscience. 7 [PubMed]

Puopolo M, Raviola E, Bean BP. (2007). Roles of subthreshold calcium current and sodium current in spontaneous firing of mouse midbrain dopamine neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience. 27 [PubMed]

Ratté S, Prescott SA. (2016). Afferent hyperexcitability in neuropathic pain and the inconvenient truth about its degeneracy. Current opinion in neurobiology. 36 [PubMed]

Renganathan M, Cummins TR, Waxman SG. (2001). Contribution of Na(v)1.8 sodium channels to action potential electrogenesis in DRG neurons. Journal of neurophysiology. 86 [PubMed]

Rosenberger DC, Blechschmidt V, Timmerman H, Wolff A, Treede RD. (2020). Challenges of neuropathic pain: focus on diabetic neuropathy. Journal of neural transmission (Vienna, Austria : 1996). 127 [PubMed]

Rothenberg ME et al. (2019). Safety, Tolerability, and Pharmacokinetics of GDC-0276, a Novel NaV1.7 Inhibitor, in a First-in-Human, Single- and Multiple-Dose Study in Healthy Volunteers. Clinical drug investigation. 39 [PubMed]

Rush AM, Cummins TR, Waxman SG. (2007). Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons. The Journal of physiology. 579 [PubMed]

Schild JH, Kunze DL. (1997). Experimental and modeling study of Na+ current heterogeneity in rat nodose neurons and its impact on neuronal discharge. Journal of neurophysiology. 78 [PubMed]

Shields SD et al. (2018). Insensitivity to Pain upon Adult-Onset Deletion of Nav1.7 or Its Blockade with Selective Inhibitors. The Journal of neuroscience : the official journal of the Society for Neuroscience. 38 [PubMed]

Strege PR et al. (2017). Sodium channel NaV1.3 is important for enterochromaffin cell excitability and serotonin release. Scientific reports. 7 [PubMed]

Stöber TM, Batulin D, Triesch J, Narayanan R, Jedlicka P. (2023). Degeneracy in epilepsy: multiple routes to hyperexcitable brain circuits and their repair. Communications biology. 6 [PubMed]

Swensen AM, Bean BP. (2005). Robustness of burst firing in dissociated purkinje neurons with acute or long-term reductions in sodium conductance. The Journal of neuroscience : the official journal of the Society for Neuroscience. 25 [PubMed]

Taneja A, Di Iorio VL, Danhof M, Della Pasqua O. (2012). Translation of drug effects from experimental models of neuropathic pain and analgesia to humans. Drug discovery today. 17 [PubMed]

Theile JW, Fuller MD, Chapman ML. (2016). The Selective Nav1.7 Inhibitor, PF-05089771, Interacts Equivalently with Fast and Slow Inactivated Nav1.7 Channels. Molecular pharmacology. 90 [PubMed]

Vetter I et al. (2017). NaV1.7 as a pain target - From gene to pharmacology. Pharmacology & therapeutics. 172 [PubMed]

Vijayaragavan K, O'Leary ME, Chahine M. (2001). Gating properties of Na(v)1.7 and Na(v)1.8 peripheral nerve sodium channels. The Journal of neuroscience : the official journal of the Society for Neuroscience. 21 [PubMed]

Waxman SG, Zamponi GW. (2014). Regulating excitability of peripheral afferents: emerging ion channel targets. Nature neuroscience. 17 [PubMed]

Woolf CJ. (2010). Overcoming obstacles to developing new analgesics. Nature medicine. 16 [PubMed]

Yamane M et al. (2017). A functional coupling between CRMP1 and Nav1.7 for retrograde propagation of Semaphorin3A signaling. Journal of cell science. 130 [PubMed]

Yang J, Prescott SA. (2023). Homeostatic regulation of neuronal function: importance of degeneracy and pleiotropy. Frontiers in cellular neuroscience. 17 [PubMed]

Yang J, Shakil H, Ratté S, Prescott SA. (2022). Minimal requirements for a neuron to co-regulate many properties and the implications for ion channel correlations and robustness eLife. 11 [PubMed]

Yang Y, Mis MA, Estacion M, Dib-Hajj SD, Waxman SG. (2018). NaV1.7 as a Pharmacogenomic Target for Pain: Moving Toward Precision Medicine. Trends in pharmacological sciences. 39 [PubMed]

Yang Y et al. (2004). Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia. Journal of medical genetics. 41 [PubMed]

Yatziv SL, Devor M. (2019). Suppression of neuropathic pain by selective silencing of dorsal root ganglion ectopia using nonblocking concentrations of lidocaine. Pain. 160 [PubMed]

Zhang JM, Donnelly DF, Song XJ, Lamotte RH. (1997). Axotomy increases the excitability of dorsal root ganglion cells with unmyelinated axons. Journal of neurophysiology. 78 [PubMed]

Zhang JM, Song XJ, LaMotte RH. (1999). Enhanced excitability of sensory neurons in rats with cutaneous hyperalgesia produced by chronic compression of the dorsal root ganglion. Journal of neurophysiology. 82 [PubMed]

References and models that cite this paper
This website requires cookies and limited processing of your personal data in order to function. By continuing to browse or otherwise use this site, you are agreeing to this use. See our Privacy policy and how to cite and terms of use.