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Inherited pain: sodium channel Nav1.7 A1632T mutation causes erythromelalgia due to a shift of fast inactivation.

Eberhardt M, Nakajima J, Klinger AB, Neacsu C, Hühne K, O'Reilly AO, Kist AM, Lampe AK, Fischer K, Gibson J, Nau C, Winterpacht A, Lampert A.

J Biol Chem. 2014 Jan 24;289(4):1971-80. doi: 10.1074/jbc.M113.502211.


Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navbeta4 peptide-mediated resurgent sodium currents.

Theile JW, Jarecki BW, Piekarz AD, Cummins TR.

J Physiol. 2011 Feb 1;589(Pt 3):597-608. doi: 10.1113/jphysiol.2010.200915.


Sea-anemone toxin ATX-II elicits A-fiber-dependent pain and enhances resurgent and persistent sodium currents in large sensory neurons.

Klinger AB, Eberhardt M, Link AS, Namer B, Kutsche LK, Schuy ET, Sittl R, Hoffmann T, Alzheimer C, Huth T, Carr RW, Lampert A.

Mol Pain. 2012 Sep 15;8:69. doi: 10.1186/1744-8069-8-69.


Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents.

Jarecki BW, Piekarz AD, Jackson JO 2nd, Cummins TR.

J Clin Invest. 2010 Jan;120(1):369-78. doi: 10.1172/JCI40801.


Sodium channel slow inactivation interferes with open channel block.

Hampl M, Eberhardt E, O'Reilly AO, Lampert A.

Sci Rep. 2016 May 13;6:25974. doi: 10.1038/srep25974.


The endocannabinoid anandamide inhibits voltage-gated sodium channels Nav1.2, Nav1.6, Nav1.7, and Nav1.8 in Xenopus oocytes.

Okura D, Horishita T, Ueno S, Yanagihara N, Sudo Y, Uezono Y, Sata T.

Anesth Analg. 2014 Mar;118(3):554-62. doi: 10.1213/ANE.0000000000000070.


Navβ4 regulates fast resurgent sodium currents and excitability in sensory neurons.

Barbosa C, Tan ZY, Wang R, Xie W, Strong JA, Patel RR, Vasko MR, Zhang JM, Cummins TR.

Mol Pain. 2015 Sep 25;11:60. doi: 10.1186/s12990-015-0063-9.


Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na V 1.7 produce distinct pain disorders.

Cheng X, Dib-Hajj SD, Tyrrell L, Wright DA, Fischer TZ, Waxman SG.

Mol Pain. 2010 Apr 29;6:24. doi: 10.1186/1744-8069-6-24.


Aberrant epilepsy-associated mutant Nav1.6 sodium channel activity can be targeted with cannabidiol.

Patel RR, Barbosa C, Brustovetsky T, Brustovetsky N, Cummins TR.

Brain. 2016 Aug;139(Pt 8):2164-81. doi: 10.1093/brain/aww129.


Tetrodotoxin-resistant sodium channels in sensory neurons generate slow resurgent currents that are enhanced by inflammatory mediators.

Tan ZY, Piekarz AD, Priest BT, Knopp KL, Krajewski JL, McDermott JS, Nisenbaum ES, Cummins TR.

J Neurosci. 2014 May 21;34(21):7190-7. doi: 10.1523/JNEUROSCI.5011-13.2014.


Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable.

Dib-Hajj SD, Estacion M, Jarecki BW, Tyrrell L, Fischer TZ, Lawden M, Cummins TR, Waxman SG.

Mol Pain. 2008 Sep 19;4:37. doi: 10.1186/1744-8069-4-37.


Alternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T.

Jarecki BW, Sheets PL, Xiao Y, Jackson JO 2nd, Cummins TR.

Channels (Austin). 2009 Jul-Aug;3(4):259-67.


Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7.

Estacion M, Han C, Choi JS, Hoeijmakers JG, Lauria G, Drenth JP, Gerrits MM, Dib-Hajj SD, Faber CG, Merkies IS, Waxman SG.

Mol Pain. 2011 Dec 2;7:92. doi: 10.1186/1744-8069-7-92.


NaV1.7 gain-of-function mutations as a continuum: A1632E displays physiological changes associated with erythromelalgia and paroxysmal extreme pain disorder mutations and produces symptoms of both disorders.

Estacion M, Dib-Hajj SD, Benke PJ, Te Morsche RH, Eastman EM, Macala LJ, Drenth JP, Waxman SG.

J Neurosci. 2008 Oct 22;28(43):11079-88. doi: 10.1523/JNEUROSCI.3443-08.2008.

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