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Channelopathic Pain: A Growing but Still Small List of Model Disorders

Stephen G. Waxman
2010 Neuron  
The presence of wild-type Na V 1.8 can support firing at very high frequencies within permissive cell backgrounds (Waxman, 2006) , and it is possible that gain-of-function mutations of Na V 1.8 do not  ... 
doi:10.1016/j.neuron.2010.05.029 pmid:20547120 fatcat:j3on7wrn2zawza2fss5kfixfzu

A Question from Emilio: Hypotheses, Hope, and the Legacy of Dominick P. Purpura

Stephen G. Waxman
2016 Einstein Journal of Biology and Medicine  
It is part of the enduring legacy of Dominick Purpura. 4STEPHEN G. WAXMAN A Question from Emilio: Hypotheses, Hope, and the Legacy of Dominick P. Purpura  ...  Waxman, I just read about your research on erythromelalgia and was most interested in it. My daughter has erythromelalgia. She is fifteen and nothing treatment-wise has helped.  ... 
doi:10.23861/ejbm200622519 fatcat:lg4moa636jcztbhnfi6bhwivsu

Ion Channels and Neuronal Dysfunction in Multiple Sclerosis

Stephen G. Waxman
2002 Archives of Neurology  
W hat causes the signs and symptoms of multiple sclerosis (MS)? It is almost axiomatic to regard MS as a demyelinating disorder in which axonal conduction block, caused by loss of myelin, produces clinical deficits. In addition, during the past few years, increased attention has focused on axonal degeneration in MS. The available evidence suggests that demyelination provides a structural correlate for relapsingremitting disease while axonal degeneration, which may be associated with atrophy of
more » ... ed with atrophy of the brain and spinal cord, produces nonremitting deficits.
doi:10.1001/archneur.59.9.1377 pmid:12223023 fatcat:uy5fxp7iebhx5ihhzuyrnc6mcq

Alabama to Beijing… and Back: The Search for a Pain Gene

Stephen G Waxman
2018 Cerebrum  
R. & Waxman, S. G. Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons. J Physiol 579, 1-14, (2007).  ...  That longer story is told in my book, Chasing Men on Fire: The Story of the Search for a Pain Gene. 25 Bio Stephen Waxman, M.D., Ph.D. is the Flaherty Professor of Neurology, Neurobiology, and Pharmacology  ... 
pmid:30746027 pmcid:PMC6353114 fatcat:kjbj6idfsjhyhaivb5mk5lau34

Mechanisms of Disease: sodium channels and neuroprotection in multiple sclerosis—current status

Stephen G Waxman
2008 Nature Clinical Practice Neurology  
Moreover, preliminary experiments suggest that gradual, tapering withdrawal of phenytoin over a 7-day period does not cause worsening of EAE (JA Black and SG Waxman, unpublished observations).  ...  Permission obtained from Nature Publishing Group © Waxman SG (2006) Nat Rev Neurosci 5: 932-942. shown that transcription of genes that encode mitochondrial respiratory chain complexes was impaired in  ... 
doi:10.1038/ncpneuro0735 pmid:18227822 fatcat:bez7puo3wfgydbipm73jffgofy

Channelopathies have many faces

Stephen G. Waxman
2011 Nature  
G.  ...  See Article p.186 ST E P H E N G .  ... 
doi:10.1038/472173a pmid:21490662 fatcat:ph5dtjf44jaufillmda25p5pw4

Axon-glia interactions: Building a smart nerve fiber

Stephen G Waxman
1997 Current Biology  
Genetics & Development which included the following reviews, edited by Margaret Buckingham and Michael Dexter, on Differentiation and gene development: Somite differentiation and the onset of myogenesis G  ... 
doi:10.1016/s0960-9822(06)00203-x pmid:9210363 fatcat:jl6cgdvon5e5jhlshyya3p24gu

The response of NaV1.3 sodium channels to ramp stimuli: multiple components and mechanisms

Mark Estacion, Stephen G. Waxman
2013 Journal of Neurophysiology  
Estacion M, Waxman SG.  ...  Conductance data were normalized by maximum conductance and fit with a Boltzmann equation of the form G ϭ G min ϩ (G max Ϫ G min )/{1 ϩ exp[(V 1/2 Ϫ V m )/k]}, where V 1/2 is the activation midpoint, and  ...  The expression of Na V 1.3 within DRG neurons is increased after axonal injury Dib-Hajj et al. 1999; Waxman et al. 1994) .  ... 
doi:10.1152/jn.00438.2012 pmid:23114218 fatcat:4urzw6wmhrfkzeapxfi2fovogu

Nonlinear effects of hyperpolarizing shifts in activation of mutant Nav1.7 channels on resting membrane potential

Mark Estacion, Stephen G. Waxman
2017 Journal of Neurophysiology  
Estacion M, Waxman SG. Nonlinear effects of hyperpolarizing shifts in activation of mutant Na v 1.7 channels on resting membrane potential.  ...  G. Waxman. DISCLOSURES No conflicts of interest, financial or otherwise, are declared by the author(s). AUTHOR CONTRIBUTIONS  ...  2007; Rush et al. 2006; Waxman and Dib-Hajj 2005) .  ... 
doi:10.1152/jn.00898.2016 pmid:28148645 pmcid:PMC5380781 fatcat:pqzc2ydd3rb4tf5bb2e7hkybby

Neuroprotection by Sodium Channel Blockade with Phenytoin in an Experimental Model of Glaucoma

Bryan C. Hains, Stephen G. Waxman
2005 Investigative Ophthalmology and Visual Science  
The atlas section was reproduced with permission from Paxinos G, Watson C.  ...  Serum phenytoin levels were within the clinical therapeutic range (10 -20 g/mg).  ... 
doi:10.1167/iovs.05-0618 pmid:16249495 fatcat:6tuo2zjcfbeuxkqzmegdnrdzd4

Inactivation Properties of Sodium Channel Nav1.8 Maintain Action Potential Amplitude in Small DRG Neurons in the Context of Depolarization

T Patrick Harty, Stephen G Waxman
2007 Molecular Pain  
Possible mechanisms include G-protein activation, which has been shown to depolarize inactivation V 1/2 of Na v 1.8 currents by 3-4 mV in DRG neurons [30] , the presence of arachidonic acid, which hyperpolarizes  ... 
doi:10.1186/1744-8069-3-12 pmid:17540018 pmcid:PMC1892009 fatcat:z2jgzgwsp5enhcu72v2amkh434

Familial pain syndromes from mutations of the Nav1.7 sodium channel

Tanya Z. Fischer, Stephen G. Waxman
2009 Annals of the New York Academy of Sciences  
The literature currently suggests that voltage-gated sodium channels play a major role in the pathogenesis of neuropathic pain. Alterations in the expression and targeting of specific sodium channels within injured dorsal root ganglia neurons appear to predispose the neurons to abnormal firing properties, allowing for the development of neuropathic pain. Mutations of one particular sodium channel (Na v 1.7) have been shown to cause inherited neuropathic pain in humans, specifically in
more » ... ically in erythromelalgia and paroxysmal extreme pain disorder. Inherited erythromelalgia is the first human pain syndrome to be understood at a molecular level, having been linked to gain-of-function mutations of Na v 1.7. Conversely, a loss-of-function of the Na v 1.7 channel can produce channelopathy-associated insensitivity to pain. Therefore, the Na v 1.7 channel may provide a unique target for the pharmacotherapy of pain in humans. In this review article we summarize current knowledge regarding several different disease manifestations arising from changes within the Na v 1.7 channel.
doi:10.1111/j.1749-6632.2009.05110.x pmid:20146699 fatcat:yrqvhnoxajherml6zfxqglol3a

Downregulation of Tetrodotoxin-Resistant Sodium Currents and Upregulation of a Rapidly Repriming Tetrodotoxin-Sensitive Sodium Current in Small Spinal Sensory Neurons after Nerve Injury

Theodore R. Cummins, Stephen G. Waxman
1997 Journal of Neuroscience  
., May 15, 1997, 17(10):3503-3514 Cummins and Waxman • Nerve Injury Differentially Alters DRG Na Currents  ...  Cells were not considered for analysis if the initial seal resistance was Ͻ5 G⍀ or if they had high leakage currents (holding current Ͼ1.0 nA at Ϫ80 mV), membrane blebs, or an access resistance Ͼ4 M⍀.  ... 
doi:10.1523/jneurosci.17-10-03503.1997 pmid:9133375 fatcat:n5mpdadlc5cunl2ilqimrlgnme

Physiological interactions between Nav1.7 and Nav1.8 sodium channels: a computer simulation study

Jin-Sung Choi, Stephen G. Waxman
2011 Journal of Neurophysiology  
The peak current of 25 nA was modeled by setting the peak value g Nav1.8 to 0.026 S/cm 2 , which was chosen to match experimental values (Choi et al. 2007; Cummins and Waxman 1997) .  ...  The K DR current was defined as: I KDR ϭ g KDR * n * (V Ϫ E k ), where g KDR is the delayed rectifier potassium conductance and n is a dimensionless activation variable that varies between 0 and 1.  ... 
doi:10.1152/jn.00100.2011 pmid:21940606 fatcat:alo3lpvajvet3k6fmwrfg6srdq

Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders

Joost P.H. Drenth, Stephen G. Waxman
2007 Journal of Clinical Investigation  
Waxman is the recipient of grants from the Department of Veterans Affairs and the Erythromelalgia Association.  ... 
doi:10.1172/jci33297 pmid:18060017 pmcid:PMC2096434 fatcat:2g564ub6w5dmpioebsj4l2tbku
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