S G Waxman

Summary

Affiliation: Yale University
Country: USA

Publications

  1. ncbi request reprint Upregulation of persistent and ramp sodium current in dorsal horn neurons after spinal cord injury
    Angelika Lampert
    Department of Neurology, Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Exp Brain Res 174:660-6. 2006
  2. doi request reprint Interview: Pathways to discovery: making the translational leap
    Stephen G Waxman
    Neurorehabilitation Research, Yale University School of Medicine and Veterans Affairs Medical Center, CT, USA
    Pain Manag 2:117-8. 2012
  3. pmc Expression of Nav1.7 in DRG neurons extends from peripheral terminals in the skin to central preterminal branches and terminals in the dorsal horn
    Joel A Black
    Department of Neurology and Paralyzed Veterans of America Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 8:82. 2012
  4. pmc NaV1.7: stress-induced changes in immunoreactivity within magnocellular neurosecretory neurons of the supraoptic nucleus
    Joel A Black
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 9:39. 2013
  5. doi request reprint Painful Na-channelopathies: an expanding universe
    Stephen G Waxman
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Trends Mol Med 19:406-9. 2013
  6. ncbi request reprint Functional profiles of SCN9A variants in dorsal root ganglion neurons and superior cervical ganglion neurons correlate with autonomic symptoms in small fibre neuropathy
    Chongyang Han
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain 135:2613-28. 2012
  7. doi request reprint Membrane properties and electrogenesis in the distal axons of small dorsal root ganglion neurons in vitro
    Dmytro V Vasylyev
    1Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut, USA
    J Neurophysiol 108:729-40. 2012
  8. pmc Sodium channels, the electrogenisome and the electrogenistat: lessons and questions from the clinic
    Stephen G Waxman
    Department of Neurology and Centre for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    J Physiol 590:2601-12. 2012
  9. doi request reprint Small nerve fibres, small hands and small feet: a new syndrome of pain, dysautonomia and acromesomelia in a kindred with a novel NaV1.7 mutation
    Janneke G J Hoeijmakers
    Neuroscience and Regeneration Research Centre, VA Connecticut Healthcare System, 950 Campbell Avenue, Building 34, West Haven, CT 06516, USA
    Brain 135:345-58. 2012
  10. pmc Nav1.7 is the predominant sodium channel in rodent olfactory sensory neurons
    Hye Sook Ahn
    Department of Neurology, Yale University School of Medicine, New Haven, 06520, USA
    Mol Pain 7:32. 2011

Collaborators

Detail Information

Publications141 found, 100 shown here

  1. ncbi request reprint Upregulation of persistent and ramp sodium current in dorsal horn neurons after spinal cord injury
    Angelika Lampert
    Department of Neurology, Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Exp Brain Res 174:660-6. 2006
    ..The increased persistent sodium current and ramp current, which are consistent with upregulation of Nav1.3 within dorsal horn neurons, suggest a basis for the hyperresponsiveness of these neurons following SCI...
  2. doi request reprint Interview: Pathways to discovery: making the translational leap
    Stephen G Waxman
    Neurorehabilitation Research, Yale University School of Medicine and Veterans Affairs Medical Center, CT, USA
    Pain Manag 2:117-8. 2012
    ....
  3. pmc Expression of Nav1.7 in DRG neurons extends from peripheral terminals in the skin to central preterminal branches and terminals in the dorsal horn
    Joel A Black
    Department of Neurology and Paralyzed Veterans of America Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 8:82. 2012
    ..7 in rat dorsal root ganglia neurons, from peripheral terminals in the skin to central terminals in the spinal cord dorsal horn...
  4. pmc NaV1.7: stress-induced changes in immunoreactivity within magnocellular neurosecretory neurons of the supraoptic nucleus
    Joel A Black
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 9:39. 2013
    ..The two sodium channels previously studied within the rat hypothalamic supraoptic nucleus, NaV1.2 and NaV1.6, display up-regulated expression in response to osmotic stress...
  5. doi request reprint Painful Na-channelopathies: an expanding universe
    Stephen G Waxman
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Trends Mol Med 19:406-9. 2013
    ..7, can cause painful Na-channelopathies. Moreover, recent studies combining atomic level structural models and pharmacogenomics suggest that the goal of genomically guided pain therapy may not be unrealistic...
  6. ncbi request reprint Functional profiles of SCN9A variants in dorsal root ganglion neurons and superior cervical ganglion neurons correlate with autonomic symptoms in small fibre neuropathy
    Chongyang Han
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain 135:2613-28. 2012
    ....
  7. doi request reprint Membrane properties and electrogenesis in the distal axons of small dorsal root ganglion neurons in vitro
    Dmytro V Vasylyev
    1Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut, USA
    J Neurophysiol 108:729-40. 2012
    ..These results provide direct evidence for the presence of TTX-S and TTX-R Na(+) channels that are functionally available at resting potential and contribute to electrogenesis in small-diameter afferent axons...
  8. pmc Sodium channels, the electrogenisome and the electrogenistat: lessons and questions from the clinic
    Stephen G Waxman
    Department of Neurology and Centre for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    J Physiol 590:2601-12. 2012
    ....
  9. doi request reprint Small nerve fibres, small hands and small feet: a new syndrome of pain, dysautonomia and acromesomelia in a kindred with a novel NaV1.7 mutation
    Janneke G J Hoeijmakers
    Neuroscience and Regeneration Research Centre, VA Connecticut Healthcare System, 950 Campbell Avenue, Building 34, West Haven, CT 06516, USA
    Brain 135:345-58. 2012
    ....
  10. pmc Nav1.7 is the predominant sodium channel in rodent olfactory sensory neurons
    Hye Sook Ahn
    Department of Neurology, Yale University School of Medicine, New Haven, 06520, USA
    Mol Pain 7:32. 2011
    ..These findings led us to hypothesize that Nav1.7 is the main sodium channel in the peripheral olfactory sensory neurons (OSN, also known as olfactory receptor neurons)...
  11. pmc Sodium-calcium exchanger and multiple sodium channel isoforms in intra-epidermal nerve terminals
    Anna Karin Persson
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 6:84. 2010
    ..In this study, we examined the expression and distribution of Na+/Ca2+ exchanger (NCX) and voltage-gated sodium channel isoforms in intra-epidermal free nerve terminals...
  12. pmc Temperature dependence of erythromelalgia mutation L858F in sodium channel Nav1.7
    Chongyang Han
    Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China
    Mol Pain 3:3. 2007
    ..It has recently been shown that several disease-causing erythromelalgia mutations alter channel-gating behavior in a manner that increases DRG neuron excitability...
  13. pmc Inactivation properties of sodium channel Nav1.8 maintain action potential amplitude in small DRG neurons in the context of depolarization
    T Patrick Harty
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 3:12. 2007
    ..8...
  14. pmc Mutation I136V alters electrophysiological properties of the Na(v)1.7 channel in a family with onset of erythromelalgia in the second decade
    Xiaoyang Cheng
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Mol Pain 4:1. 2008
    ..7 mutations reported to date, which have been localized in the voltage sensor S4, the linker joining segments S4 and S5 or pore-lining segments S5 and S6 in DI, II and III...
  15. pmc Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable
    Sulayman D Dib-Hajj
    Deptartment of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 4:37. 2008
    ..Carbamazepine has been effective in relieving symptoms, while other drugs including other anti-epileptics are less effective...
  16. pmc Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na V 1.7 produce distinct pain disorders
    Xiaoyang Cheng
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT, USA
    Mol Pain 6:24. 2010
    ....
  17. pmc Effects of ranolazine on wild-type and mutant hNav1.7 channels and on DRG neuron excitability
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 6:35. 2010
    ..7 and on DRG neuron excitability have not been investigated. We used voltage- and current-clamp recordings to evaluate the hypothesis that ranolazine may be effective in regulating Nav1.7-induced DRG neuron hyperexcitability...
  18. pmc Sodium channel expression in the ventral posterolateral nucleus of the thalamus after peripheral nerve injury
    Peng Zhao
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 2:27. 2006
    ..3 sodium channel increases the excitability of VPL neurons injury, contributing to neuropathic pain...
  19. doi request reprint Mechanisms of disease: sodium channels and neuroprotection in multiple sclerosis-current status
    Stephen G Waxman
    Department of Neurology, LCI 707, Yale Medical School, PO Box 20818, New Haven, CT 06520 8018, USA
    Nat Clin Pract Neurol 4:159-69. 2008
    ..This article reviews the development of the concept of sodium channel blockers as neuroprotectants in MS, the path from laboratory to clinic, and the current status of research in this area...
  20. ncbi request reprint Fire and phantoms after spinal cord injury: Na+ channels and central pain
    Stephen G Waxman
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Trends Neurosci 29:207-15. 2006
    ....
  21. ncbi request reprint Patterned electrical activity modulates sodium channel expression in sensory neurons
    Joshua P Klein
    Department of Neurology and PVA EPVA Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci Res 74:192-8. 2003
    ..These results show that a change in neuronal activity can alter the expression of sodium channel genes in a subtype-specific manner, via a mechanism independent of NGF withdrawal...
  22. ncbi request reprint Gifts from the molecular revolution: protection and repair of the injured spinal cord
    Stephen G Waxman
    Department of Neurology, Center for Neuroscience and Regeneration Research, LCI 707, Yale School of Medicine, 15 York Street, New Haven, CT 06520 8018, USA
    J Spinal Cord Med 27:304-10. 2004
    ..Although much work remains to be done, we are coming much closer to our goals in each of these areas, and the overall objective--of protecting and repairing the injured spinal cord--appears achievable...
  23. ncbi request reprint Na+ channel expression along axons in multiple sclerosis and its models
    Stephen G Waxman
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, CT 06510, USA
    Trends Pharmacol Sci 25:584-91. 2004
    ....
  24. ncbi request reprint Sodium channel blockers and axonal protection in neuroinflammatory disease
    Stephen G Waxman
    Department of Neurology and The Center for Neuroscience and Regeneration Research, Yale Medical School, 333 Cedar Street, PO Box 208018, New Haven, CT 06520 8018, USA
    Brain 128:5-6. 2005
  25. ncbi request reprint Erythromelalgia: a hereditary pain syndrome enters the molecular era
    Stephen G Waxman
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Ann Neurol 57:785-8. 2005
    ....
  26. ncbi request reprint Erythermalgia: molecular basis for an inherited pain syndrome
    Stephen G Waxman
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Trends Mol Med 11:555-62. 2005
    ....
  27. ncbi request reprint Ions, energy and axonal injury: towards a molecular neurology of multiple sclerosis
    Stephen G Waxman
    Department of Neurology, LCI 707, Yale Medical School, P O Box 208018, New Haven, CT 06520, USA
    Trends Mol Med 12:192-5. 2006
    ....
  28. ncbi request reprint Axonal conduction and injury in multiple sclerosis: the role of sodium channels
    Stephen G Waxman
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, Connecticut 06510, USA
    Nat Rev Neurosci 7:932-41. 2006
    ..By manipulating the activity of these channels or their expression, it might be possible to develop new therapeutic approaches that will prevent or limit disability in MS...
  29. pmc Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 7:92. 2011
    ..In this paper we describe three patients who house the NaV1.7/I228M variant...
  30. ncbi request reprint Channel, neuronal and clinical function in sodium channelopathies: from genotype to phenotype
    Stephen G Waxman
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Nat Neurosci 10:405-9. 2007
    ..I discuss evidence showing that cell background acts as a filter that can strongly influence the effects of ion channel mutations...
  31. pmc Nav1.9, G-proteins, and nociceptors
    Stephen G Waxman
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    J Physiol 586:917-8. 2008
  32. ncbi request reprint Sodium channels as molecular targets in multiple sclerosis
    Stephen G Waxman
    Department of Neurology and Paralyzed Veterans of America Eastern Paralyzed Veterans Association Center for Neuroscience Research, Yale University School of Medicine, New Haven, CT 06510, USA
    J Rehabil Res Dev 39:233-42. 2002
    ..Identifying the underlying channel may permit the development of therapeutic strategies that will prevent or retard axonal degeneration in MS...
  33. ncbi request reprint Acquired channelopathies in nerve injury and MS
    S G Waxman
    Department of Neurology and the Paralyzed Veterans of America, Yale University School of Medicine, New Haven 06510, USA
    Neurology 56:1621-7. 2001
    ..The acquired channelopathies associated with nerve injury and MS may thus represent prototype disorders that present therapeutic opportunities...
  34. ncbi request reprint The molecular pathophysiology of pain: abnormal expression of sodium channel genes and its contributions to hyperexcitability of primary sensory neurons
    S G Waxman
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Pain . 1999
    ....
  35. pmc The neuron as a dynamic electrogenic machine: modulation of sodium-channel expression as a basis for functional plasticity in neurons
    S G Waxman
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Philos Trans R Soc Lond B Biol Sci 355:199-213. 2000
    ....
  36. ncbi request reprint Sodium channels and their genes: dynamic expression in the normal nervous system, dysregulation in disease states(1)
    S G Waxman
    Department of Neurology and PVA EPVA Neuroscience Research Center, Yale School of Medicine, 333 Cedar Street, 06510, New Haven, CT, USA
    Brain Res 886:5-14. 2000
    ..The dynamic nature of sodium channel gene expression makes it a complex topic for investigation, but it also introduces therapeutic opportunities, since subtype-specific sodium channel modulating drugs may soon be available...
  37. ncbi request reprint Voltage-gated sodium channels and the molecular pathogenesis of pain: a review
    S G Waxman
    Center of Excellence for Functional Restoration in MS and SCI, VA Medical Center, West Haven, CT 06516, USA
    J Rehabil Res Dev 37:517-28. 2000
    ..The multiplicity of sodium channels, and the dynamic nature of their expression, makes them important targets for pharmacologic manipulation in the search for new therapies for pain...
  38. ncbi request reprint The molecular basis for electrogenic computation in the brain: you can't step in the same river twice
    S G Waxman
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Psychiatry 4:222-8. 1999
    ..The molecular plasticity of electrogenic membrane has important functional implications, since it can retune the neuron, changing its input-output relations...
  39. doi request reprint Physiological interactions between Na(v)1.7 and Na(v)1.8 sodium channels: a computer simulation study
    Jin Sung Choi
    College of Pharmacy, Catholic University of Korea, Bucheon, Gyeonggi Do, South Korea
    J Neurophysiol 106:3173-84. 2011
    ..7 following the first AP. These results indicate that changes in the level of expression of Na(v)1.7 and Na(v)1.8 may provide a regulatory mechanism that tunes the excitability of small DRG neurons...
  40. pmc Sodium currents of large (Abeta-type) adult cutaneous afferent dorsal root ganglion neurons display rapid recovery from inactivation before and after axotomy
    B Everill
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Neuroscience 106:161-9. 2001
    ..Like small neurons, the majority of large neurons downregulate the tetrodotoxin-resistant current following sciatic nerve section...
  41. ncbi request reprint Nav1.3 sodium channels: rapid repriming and slow closed-state inactivation display quantitative differences after expression in a mammalian cell line and in spinal sensory neurons
    T R Cummins
    Department of Neurology and Paralyzed Veterans of America/Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale Medical School, New Haven, Connecticut 06510, USA
    J Neurosci 21:5952-61. 2001
    ..The relatively rapid recovery from inactivation and the slow closed-state inactivation kinetics of Nav1.3 channels suggest that neurons expressing Nav1.3 may exhibit a reduced threshold and/or a relatively high frequency of firing...
  42. ncbi request reprint Glycosylation alters steady-state inactivation of sodium channel Nav1.9/NaN in dorsal root ganglion neurons and is developmentally regulated
    L Tyrrell
    Department of Neurology and Paralyzed Veterans of America/Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 21:9629-37. 2001
    ..9, making it indistinguishable from that of adult DRG neurons. Our data show that extensive glycosylation of rat Na(v)1.9 is developmentally regulated and changes a critical property of this channel in native neurons...
  43. ncbi request reprint Sodium channels contribute to microglia/macrophage activation and function in EAE and MS
    Matthew J Craner
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, Connecticut 06520 8018, USA
    Glia 49:220-9. 2005
    ....
  44. ncbi request reprint Contactin regulates the current density and axonal expression of tetrodotoxin-resistant but not tetrodotoxin-sensitive sodium channels in DRG neurons
    Anthony M Rush
    Department of Neurology, Yale School of Medicine, LCI 707, 333 Cedar St, New Haven, CT 06510, USA
    Eur J Neurosci 22:39-49. 2005
    ....
  45. ncbi request reprint Axotomy does not up-regulate expression of sodium channel Na(v)1.8 in Purkinje cells
    J A Black
    Department of Neurology and PVA EPVA Center for Neuroscience Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain Res Mol Brain Res 101:126-31. 2002
    ..6 were clearly present, demonstrating that sodium channel transcripts and protein were present in experimental cerebella. These results demonstrate that axotomy does not trigger the expression of Na(v)1.8 in Purkinje cells...
  46. ncbi request reprint Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons
    S D Dib-Hajj
    Department of Neurology, Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain 128:1847-54. 2005
    ..Erythromelalgia is the first inherited pain disorder in which it is possible to link a mutation with an abnormality in ion channel function and with altered firing of pain signalling neurons...
  47. ncbi request reprint Persistent TTX-resistant Na+ current affects resting potential and response to depolarization in simulated spinal sensory neurons
    R I Herzog
    Department of Neurology, Paralyzed Veterans of America/Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale School of Medicine, New Haven, CT 06510, USA
    J Neurophysiol 86:1351-64. 2001
    ....
  48. pmc Differential role of two Ca(2+)-permeable non-NMDA glutamate channels in rat retinal ganglion cells: kainate-induced cytoplasmic and nuclear Ca2+ signals
    T Leinders-Zufall
    Department of Neurology, Yale University School of Medicine, West Haven, Connecticut
    J Neurophysiol 72:2503-16. 1994
    ..However, in the type 2 neurons kainate no longer induced large Ca2+ signals in the cytoplasm and nucleus, despite normal influx of Ca2+.(ABSTRACT TRUNCATED AT 400 WORDS)..
  49. pmc Type III sodium channel mRNA is expressed in embryonic but not adult spinal sensory neurons, and is reexpressed following axotomy
    S G Waxman
    Department of Neurology, Yale University School of Medicine, New Haven 06510
    J Neurophysiol 72:466-70. 1994
    ..Different channel characteristics, as well as an altered spatial distribution of sodium channels, may contribute to the electrophysiological changes that are observed in axotomized neurons...
  50. ncbi request reprint 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
    M Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 28:11079-88. 2008
    ..These observations indicate that IEM and PEPD mutants are part of a physiological continuum that can produce a continuum of clinical phenotypes...
  51. ncbi request reprint Two tetrodotoxin-resistant sodium channels in human dorsal root ganglion neurons
    S D Dib-Hajj
    Department of Neurology LCI 707, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA
    FEBS Lett 462:117-20. 1999
    ..Thus SNS and NaN channels appear to produce different currents in human DRG neurons...
  52. pmc Can robots patch-clamp as well as humans? Characterization of a novel sodium channel mutation
    M Estacion
    Department of Neurology, Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    J Physiol 588:1915-27. 2010
    ....
  53. pmc Differential effects of NGF and BDNF on axotomy-induced changes in GABA(A)-receptor-mediated conductance and sodium currents in cutaneous afferent neurons
    A A Oyelese
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurophysiol 78:31-42. 1997
    ..These findings indicate a differential regulation of GABA(A) receptor and sodium channel properties in axotomized rat cutaneous afferent neurons by specific neurotrophic factors...
  54. ncbi request reprint Contribution of Na(v)1.8 sodium channels to action potential electrogenesis in DRG neurons
    M Renganathan
    Department of Neurology and Paralyzed Veterans of America Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale University School of Medicine, New Haven 06510, USA
    J Neurophysiol 86:629-40. 2001
    ..8 (+/+) neurons, and, in the absence of Na(v)1.8, is attenuated with even modest depolarization. These observations indicate that Na(v)1.8 contributes substantially to action potential electrogenesis in C-type DRG neurons...
  55. ncbi request reprint Altered sodium channel expression in second-order spinal sensory neurons contributes to pain after peripheral nerve injury
    Bryan C Hains
    Department of Neurology and the Paralyzed Veterans of America Eastern Paralyzed Veterans Association Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 24:4832-9. 2004
    ..3 sodium channel and central mechanisms that contribute to neuropathic pain after peripheral nerve injury...
  56. ncbi request reprint Upregulation of sodium channel Nav1.3 and functional involvement in neuronal hyperexcitability associated with central neuropathic pain after spinal cord injury
    Bryan C Hains
    Department of Neurology and Paralyzed Veterans of America Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 23:8881-92. 2003
    ..3 expression and neuronal hyperexcitability associated with central neuropathic pain...
  57. ncbi request reprint Inherited erythermalgia: limb pain from an S4 charge-neutral Na channelopathy
    Jin Sung Choi
    Department of Neurology, Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Neurology 67:1563-7. 2006
    ..7 sodium channel, which is preferentially expressed in nociceptors. Thus far, Na(v)1.7 mutations within intracellular linker parts of the channel have been physiologically characterized...
  58. ncbi request reprint Glial cells have heart: rH1 Na+ channel mRNA and protein in spinal cord astrocytes
    J A Black
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA
    Glia 23:200-8. 1998
    ....
  59. pmc NaN, a novel voltage-gated Na channel, is expressed preferentially in peripheral sensory neurons and down-regulated after axotomy
    S D Dib-Hajj
    Department of Neurology, LCI 707, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA
    Proc Natl Acad Sci U S A 95:8963-8. 1998
    ....
  60. pmc Slow sodium conductances of dorsal root ganglion neurons: intraneuronal homogeneity and interneuronal heterogeneity
    M A Rizzo
    Department of Neurology, Yale University School of Medicine, New Haven 06510
    J Neurophysiol 72:2796-815. 1994
    ..abstract truncated at 400 words)..
  61. pmc Mechanisms of enhancement of neurite regeneration in vitro following a conditioning sciatic nerve lesion
    K L Lankford
    Department of Neurology, Yale University School of Medicine, Veterans Affairs Medical Center, West Haven, Connecticut 06515, USA
    J Comp Neurol 391:11-29. 1998
    ..A secondary effect of conditioning lesions on neurite outgrowth rates was dependent on the local environment of the axons prior to culturing...
  62. doi request reprint Nav1.9 expression in magnocellular neurosecretory cells of supraoptic nucleus
    J A Black
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA Rehabilitation Research Center, VA Connecticut Healthcare System, West Haven, CT 06516, USA Electronic address
    Exp Neurol 253:174-9. 2014
    ..These results suggest that Nav1.9 may contribute to the firing pattern of MSC of the SON, and that careful assessment of hypothalamic function be performed as NaV1.9 blocking agents are studied as potential pain therapies. ..
  63. ncbi request reprint Nuclear and cytoplasmic Ca2+ signals in developing rat dorsal root ganglion neurons studied in excised tissue
    D A Utzschneider
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510
    Brain Res 635:231-7. 1994
    ....
  64. ncbi request reprint Beta1 adducin gene expression in DRG is developmentally regulated and is upregulated by glial-derived neurotrophic factor and nerve growth factor
    F Ghassemi
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain Res Mol Brain Res 90:118-24. 2001
    ..The level of expression of beta1 adducin in adult rat DRG and trigeminal ganglia may be maintained by the action of neurotrophic factors that are produced in innervated targets like skin and muscle...
  65. pmc Transplanted olfactory ensheathing cells remyelinate and enhance axonal conduction in the demyelinated dorsal columns of the rat spinal cord
    T Imaizumi
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 18:6176-85. 1998
    ..These data support the conclusion that transplantation of neonatal OECs results in quantitatively extensive and functional remyelination of demyelinated dorsal column axons...
  66. ncbi request reprint Fibroblast growth factor homologous factor 2B: association with Nav1.6 and selective colocalization at nodes of Ranvier of dorsal root axons
    Ellen K Wittmack
    Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 24:6765-75. 2004
    ..The preferential expression of FHF2B in sensory neurons may provide a basis for physiological differences in sodium currents that have been reported at the nodes of Ranvier in sensory versus motor axons...
  67. ncbi request reprint Sodium channel blockade with phenytoin protects spinal cord axons, enhances axonal conduction, and improves functional motor recovery after contusion SCI
    Bryan C Hains
    Department of Neurology and PVA EPVA Neuroscience Research Center, Yale University School of Medicine, New Haven, CT 06510, USA
    Exp Neurol 188:365-77. 2004
    ..Based on these results, we conclude that phenytoin provides neuroprotection and improves functional outcome after experimental SCI, and that it merits further examination as a potential treatment strategy in human SCI...
  68. ncbi request reprint Exacerbation of experimental autoimmune encephalomyelitis after withdrawal of phenytoin and carbamazepine
    Joel A Black
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, CT 06520, USA
    Ann Neurol 62:21-33. 2007
    ..Several clinical studies of sodium channel blockers are under way in patients with multiple sclerosis. Here we asked whether a protective effect would persist after withdrawal of a sodium channel blocker...
  69. ncbi request reprint Fibroblast growth factor homologous factor 1B binds to the C terminus of the tetrodotoxin-resistant sodium channel rNav1.9a (NaN)
    - Liu Cj
    Department of Neurology and Paralyzed Veterans of America Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Biol Chem 276:18925-33. 2001
    ..9a channel directly or by recruiting other proteins to the channel complex. Alternatively, it is possible that rNa(v)1.9a may help deliver this factor to the cell membrane, where it exerts its function...
  70. ncbi request reprint alpha-SNS produces the slow TTX-resistant sodium current in large cutaneous afferent DRG neurons
    M Renganathan
    Department of Neurology and Paralyzed Veterans Association Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale Medical School, New Haven CT 06510, USA
    J Neurophysiol 84:710-8. 2000
    ..These results show that the slow TTX-R Na(+) current in large cutaneous afferent DRG is produced by the SNS sodium channel...
  71. ncbi request reprint Expression of Nav1.8 sodium channels perturbs the firing patterns of cerebellar Purkinje cells
    M Renganathan
    Department of Neurology LCI 707and PVA EPVA Neuroscience Research Center, Yale Medical School, P O Box 208018, New Haven, CT 06510, USA
    Brain Res 959:235-42. 2003
    ..These results provide support for the hypothesis that the expression of Na(v)1.8 channels within Purkinje cells, which occurs in MS, may perturb their function...
  72. ncbi request reprint Na(v)1.5 underlies the 'third TTX-R sodium current' in rat small DRG neurons
    M Renganathan
    Department of Neurology, Yale Medical School, New Haven, CT 06510, USA
    Brain Res Mol Brain Res 106:70-82. 2002
    ..5 in DRG during development. Taken together, these results demonstrate that Na(v)1.5 is expressed in a developmentally regulated manner in DRG neurons and suggest that Na(v)1.5 Na(+) channel produces the third TTX-R current...
  73. ncbi request reprint Astrocyte Na+ channels are required for maintenance of Na+/K(+)-ATPase activity
    H Sontheimer
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510
    J Neurosci 14:2464-75. 1994
    ....
  74. ncbi request reprint Electrogenic pump (Na+/K(+)-ATPase) activity in rat optic nerve
    T R Gordon
    Department of Neurology, Yale University School of Medicine, West Haven, CT 06516
    Neuroscience 37:829-37. 1990
    ..abstract truncated at 250 words)..
  75. ncbi request reprint Direct interaction with contactin targets voltage-gated sodium channel Na(v)1.9/NaN to the cell membrane
    C J Liu
    Department of Neurology and Paralyzed Veterans of America/Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Biol Chem 276:46553-61. 2001
    ..9/NaN alone. Thus contactin binds directly to Na(v)1.9/NaN and participates in the surface localization of this channel along nonmyelinated axons...
  76. pmc Distinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons
    Raimund I Herzog
    Department of Neurology and PVA EPVA Neuroscience Research Center, Yale Medical School, New Haven, CT 06510, USA
    J Physiol 551:741-50. 2003
    ..7 currents. Our results indicate that the firing properties of DRG neurons can be tuned by regulating expression of different sodium channel isoforms that have distinct repriming and closed-state inactivation kinetics...
  77. ncbi request reprint Differential modulation of sodium channel Na(v)1.6 by two members of the fibroblast growth factor homologous factor 2 subfamily
    Anthony M Rush
    Department of Neurology, Yale School of Medicine, New Haven, CT 06510, USA
    Eur J Neurosci 23:2551-62. 2006
    ..6 and are differentially distributed in DRG neurons and their axons. This suggests that FHF2A and FHF2B may selectively alter firing behaviour of specific neuronal compartments via differential modulation of Na(v)1.6...
  78. ncbi request reprint Neuroprotection of axons with phenytoin in experimental allergic encephalomyelitis
    Albert C Lo
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Neuroreport 13:1909-12. 2002
    ..These results demonstrate that it is possible to achieve substantial protection of white matter axons in EAE, a model neuroinflammatory/demyelination disease, with a sodium channel blocking agent...
  79. ncbi request reprint Dysregulation of sodium channel expression in cortical neurons in a rodent model of absence epilepsy
    Joshua P Klein
    Department of Neurology, Yale University School of Medicine, New Haven, and Rehabilitation Research Center, VA Connecticut Healthcare System, West Haven, CT, USA
    Brain Res 1000:102-9. 2004
    ..This region of cortex approximately matches the electrophysiologically determined region of seizure onset. Changes in the expression of Nav1.1 and Nav1.6 parallel age-dependent increases in seizure frequency and duration...
  80. ncbi request reprint Modulation of thalamic nociceptive processing after spinal cord injury through remote activation of thalamic microglia by cysteine cysteine chemokine ligand 21
    Peng Zhao
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 27:8893-902. 2007
    ..These data identify a novel pathway by which SCI triggers upregulation of the neuroimmune modulator CCL21 in the thalamus, which induces microglial activation in association with pain phenomena...
  81. ncbi request reprint Preferential expression of IGF-I in small DRG neurons and down-regulation following injury
    Matthew J Craner
    Department of Neurology LCI 707 and PVA EPVA Center for Neuroscience and Regeneration Research, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA
    Neuroreport 13:1649-52. 2002
    ..The loss of IGF-I support to a population of predominantly nociceptive neurons may contribute to neuropathic pain observed in these models...
  82. ncbi request reprint GDNF and NGF reverse changes in repriming of TTX-sensitive Na(+) currents following axotomy of dorsal root ganglion neurons
    Andreas Leffler
    Department of Neurology and Paralyzed Veterans of America Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale Medical School, New Haven 06510, CT, USA
    J Neurophysiol 88:650-8. 2002
    ..3 mRNA, with GDNF plus NGF producing the largest effect. Our data indicate that both GDNF and NGF can partially reverse an important effect of axotomy on the electrogenic properties of sensory neurons and that their effect is additive...
  83. ncbi request reprint PGE2 increases the tetrodotoxin-resistant Nav1.9 sodium current in mouse DRG neurons via G-proteins
    Anthony M Rush
    Department of Neurology, Yale University School of Medicine, LCI 707, 333 Cedar St, New Haven, CT 06510, USA
    Brain Res 1023:264-71. 2004
    ..Our data indicate that Na(v)1.9 current can be increased during inflammation via a G-protein dependent mechanism and suggest that this could contribute to the regulation of electrogenesis in dorsal root ganglia (DRG) neurons...
  84. ncbi request reprint Apoptosis of vasopressinergic hypothalamic neurons in chronic diabetes mellitus
    Joshua P Klein
    Department of Neurology and PVA EPVA Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Neurobiol Dis 15:221-8. 2004
    ..Although upregulation of vasopressin production in response to acute hyperosmolality is adaptive, prolonged overstimulation of vasopressin-producing neurons in chronic diabetes results in neurodegeneration and apoptosis...
  85. pmc Electrophysiological properties of two axonal sodium channels, Nav1.2 and Nav1.6, expressed in mouse spinal sensory neurones
    Anthony M Rush
    Department of Neurology, Center for Neuroscience and Regeneration Research, Yale School of Medicine, LCI 707, 333 Cedar Street, New Haven, CT 06510, USA
    J Physiol 564:803-15. 2005
    ..6 and the Na(+)/Ca(2+) exchanger are colocalized, while selective expression of Na(v)1.2 may support action potential electrogenesis, at least at lower frequencies, while producing a smaller persistent current...
  86. pmc Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger
    Matthew J Craner
    Department of Neurology and Paralyzed Veterans of America Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale School of Medicine, New Haven, CT 06510, USA
    Proc Natl Acad Sci U S A 101:8168-73. 2004
    ..6 and Na+/Ca2+ exchanger is associated with axonal degeneration in MS...
  87. ncbi request reprint Changes in electrophysiological properties and sodium channel Nav1.3 expression in thalamic neurons after spinal cord injury
    Bryan C Hains
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain 128:2359-71. 2005
    ....
  88. pmc Delayed depolarization and slow sodium currents in cutaneous afferents
    O Honmou
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510
    J Neurophysiol 71:1627-37. 1994
    ..Rather, they had a combination of kinetically separable fast and slow currents or a singular relatively slow Na+ current.(ABSTRACT TRUNCATED AT 400 WORDS)..
  89. ncbi request reprint The pentapeptide QYNAD does not block voltage-gated sodium channels
    T R Cummins
    Department of Neurology, PVA EPVA Neuroscience Research Center, Yale University School of Medicine, New Haven, VA Medical Center, West Haven, CT, USA
    Neurology 60:224-9. 2003
    ..6, the major sodium channel at nodes of Ranvier, and Na(v)1.2, which is expressed in axons with abnormal myelin...
  90. pmc Restoration of normal conduction properties in demyelinated spinal cord axons in the adult rat by transplantation of exogenous Schwann cells
    O Honmou
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06516, USA
    J Neurosci 16:3199-208. 1996
    ..These results demonstrate the functional repair of demyelinated axons in the adult CNS by transplantation of cultured myelin-forming cells from the peripheral nervous system in combination with astrocytes...
  91. ncbi request reprint Spinal sensory neurons express multiple sodium channel alpha-subunit mRNAs
    J A Black
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain Res Mol Brain Res 43:117-31. 1996
    ..These results demonstrate that adult DRG neurons express multiple sodium channel mRNAs in vitro and in situ and suggest a molecular basis for the biophysical heterogeneity of sodium currents observed in these cells...
  92. ncbi request reprint Co-localization of sodium channel Nav1.6 and the sodium-calcium exchanger at sites of axonal injury in the spinal cord in EAE
    Matthew J Craner
    Department of Neurology, PVA EPVA Center for Neuroscience Research, Yale School of Medicine, New Haven, CT 06510, USA
    Brain 127:294-303. 2004
    ..3% of beta-APP positive axons co-express Na(v)1.6 and NCX, compared with 4.4 +/- 1.0% in beta-APP negative axons. Our results indicate that co-expression of Na(v)1.6 and NCX is associated with axonal injury in the spinal cord in EAE...
  93. ncbi request reprint Neuroprotection by sodium channel blockade with phenytoin in an experimental model of glaucoma
    Bryan C Hains
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Invest Ophthalmol Vis Sci 46:4164-9. 2005
    ..This study tested the hypothesis that sodium channel blockade with phenytoin would result in neuroprotection of retinal ganglion cells (RGCs) and optic nerve axons in an experimental model of glaucoma...
  94. ncbi request reprint Contactin associates with sodium channel Nav1.3 in native tissues and increases channel density at the cell surface
    Bhaval S Shah
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 24:7387-99. 2004
    ..We propose that the upregulation of contactin and its colocalization with Na(v)1.3 in axotomized DRG neurons may contribute to the hyper-excitablity of the injured neurons...
  95. ncbi request reprint Size matters: Erythromelalgia mutation S241T in Nav1.7 alters channel gating
    Angelika Lampert
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Biol Chem 281:36029-35. 2006
    ..We conclude that the linker between S4 and S5 in domain I of Nav1.7 modulates gating of this channel, and that a larger side chain at position 241 interferes with its gating mechanisms...
  96. ncbi request reprint Voltage-gated sodium channel Nav1.6 is modulated by p38 mitogen-activated protein kinase
    Ellen K Wittmack
    Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 25:6621-30. 2005
    ..6 current density. This is the first demonstration of MAPK phosphorylation and modulation of a voltage-gated sodium channel, and this modulation may represent an additional role for MAPK in regulating the neuronal response to injury...
  97. doi request reprint Familial pain syndromes from mutations of the NaV1.7 sodium channel
    Tanya Z Fischer
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA
    Ann N Y Acad Sci 1184:196-207. 2010
    ..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...
  98. doi request reprint A sodium channel gene SCN9A polymorphism that increases nociceptor excitability
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven CT
    Ann Neurol 66:862-6. 2009
    ..Our results suggest that polymorphisms in the Na(V)1.7 channel may influence susceptibility to pain...
  99. ncbi request reprint Primary motor neurons fail to up-regulate voltage-gated sodium channel Na(v)1.3/brain type III following axotomy resulting from spinal cord injury
    Bryan C Hains
    Department of Neurology and Paralyzed Veterans of America Eastern Paralyzed Veterans Association Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci Res 70:546-52. 2002
    ..3 in ipsilateral DRG neurons after sciatic nerve transection. These results do not preclude a role for voltage-gated sodium channels in post-SCI epilepsy but suggest that up-regulated expression of Na(v)1.3 channel is not involved...
  100. ncbi request reprint Early- and late-onset inherited erythromelalgia: genotype-phenotype correlation
    Chongyang Han
    Department of Neurology, LCI 707, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520 8018, USA
    Brain 132:1711-22. 2009
    ....
  101. ncbi request reprint Coding sequence, genomic organization, and conserved chromosomal localization of the mouse gene Scn11a encoding the sodium channel NaN
    S D Dib-Hajj
    LCI 707, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Genomics 59:309-18. 1999
    ..The human gene, SCN11A, was mapped to the conserved linkage group on chromosome 3p21-p24, close to human SCN5A and SCN10A. The colocalization of the three sodium channel genes supports a common lineage of the TTX-R sodium channels...