J A Black

Summary

Affiliation: Yale University
Country: USA

Publications

  1. 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
  2. doi request reprint Sodium channels and microglial function
    Joel A Black
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06511, USA
    Exp Neurol 234:302-15. 2012
  3. 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
  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 Nav1.5 sodium channels in macrophages in multiple sclerosis lesions
    Joel A Black
    Department of Neurology and Paralyzed Veterans of America Center for Neuroscience and Regeneration Research, Yale University School of Medicine, USA
    Mult Scler 19:532-42. 2013
  6. 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. 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
  8. 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
  9. ncbi request reprint Sodium channel Na(v)1.6 is expressed along nonmyelinated axons and it contributes to conduction
    Joel A Black
    Department of Neurology and Paralyzed Veterans of America Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain Res Mol Brain Res 105:19-28. 2002
  10. doi request reprint Phenytoin protects central axons in experimental autoimmune encephalomyelitis
    Joel A Black
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, CT 06510, United States
    J Neurol Sci 274:57-63. 2008

Collaborators

Detail Information

Publications63

  1. 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
    ....
  2. doi request reprint Sodium channels and microglial function
    Joel A Black
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06511, USA
    Exp Neurol 234:302-15. 2012
    ..These studies also provide strong evidence that Nav1.6 is the predominant sodium channel isoform expressed in microglia and that its activity contributes to the response of microglia to multiple activating signals...
  3. 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. ..
  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 Nav1.5 sodium channels in macrophages in multiple sclerosis lesions
    Joel A Black
    Department of Neurology and Paralyzed Veterans of America Center for Neuroscience and Regeneration Research, Yale University School of Medicine, USA
    Mult Scler 19:532-42. 2013
    ..5 is present in the limiting membrane of maturing endosomes where it plays a prominent role in the accumulation of protons. However, a contribution of the Nav1.5 channel to macrophage-mediated events in vivo has not been demonstrated...
  6. 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...
  7. 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)...
  8. 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...
  9. ncbi request reprint Sodium channel Na(v)1.6 is expressed along nonmyelinated axons and it contributes to conduction
    Joel A Black
    Department of Neurology and Paralyzed Veterans of America Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain Res Mol Brain Res 105:19-28. 2002
    ..These observations indicate that Na(v)1.6 functions not only in saltatory conduction in myelinated axons but also in continuous conduction in nonmyelinated axons...
  10. doi request reprint Phenytoin protects central axons in experimental autoimmune encephalomyelitis
    Joel A Black
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, CT 06510, United States
    J Neurol Sci 274:57-63. 2008
    ..Our results also, however, indicate that we need to learn more about the long-term effects of sodium-channel blockers, and of their withdrawal, in neuroinflammatory disorders...
  11. doi request reprint Multiple sodium channel isoforms and mitogen-activated protein kinases are present in painful human neuromas
    Joel A Black
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, USA
    Ann Neurol 64:644-53. 2008
    ..We also examined the expression of two mitogen-activated protein (MAP) kinases, activated p38 and extracellular signal-regulated kinases 1 and 2 (ERK1/2), which are known to contribute to chronic pain, within these human neuromas...
  12. ncbi request reprint Tetrodotoxin-resistant sodium channels Na(v)1.8/SNS and Na(v)1.9/NaN in afferent neurons innervating urinary bladder in control and spinal cord injured rats
    Joel A Black
    Department of Neurology and PVA EPVA Neuroscience Research Center, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain Res 963:132-8. 2003
    ....
  13. ncbi request reprint Changes in the expression of tetrodotoxin-sensitive sodium channels within dorsal root ganglia neurons in inflammatory pain
    Joel A Black
    Department of Neurology and Paralyzes Veterans of America, Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale University School of Medicine, New Haven CT 06510, USA
    Pain 108:237-47. 2004
    ....
  14. ncbi request reprint Remyelination of dorsal column axons by endogenous Schwann cells restores the normal pattern of Nav1.6 and Kv1.2 at nodes of Ranvier
    Joel A Black
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, 2 Rehabilitation Research Center, VA Connecticut Healthcare System, West Haven, CT 06518, USA
    Brain 129:1319-29. 2006
    ..6 the predominant subtype of sodium channel present at such nodes at all stages of their development...
  15. doi request reprint Sodium channel activity modulates multiple functions in microglia
    Joel A Black
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, Connecticut 06518, USA
    Glia 57:1072-81. 2009
    ..6) indicate that Nav1.6 plays a role in microglial migration. The results demonstrate that the activity of sodium channels contributes to effector roles of activated microglia...
  16. ncbi request reprint Molecular identities of two tetrodotoxin-resistant sodium channels in corneal axons
    Joel A Black
    Department of Neurology and Paralyzed Veterans of America Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale University School of Medicine, New Haven, CT 06510, USA
    Exp Eye Res 75:193-9. 2002
    ..These observations suggest that both TTX-R sodium channels Na(v)1.8 and Na(v)1.9 contribute to the electrogenesis of non-myelinated axons of the cornea...
  17. 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...
  18. ncbi request reprint Long-term protection of central axons with phenytoin in monophasic and chronic-relapsing EAE
    Joel A Black
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT, USA
    Brain 129:3196-208. 2006
    ..These observations demonstrate that phenytoin provides long-term protection of CNS axons and improves clinical status in both monophasic and chronic-relapsing models of neuroinflammation...
  19. ncbi request reprint Sodium channel expression within chronic multiple sclerosis plaques
    Joel A Black
    Department of Neurology and Paralyzed Veterans of America United Spinal Association Neuroscience Research Center, Yale University School of Medicine, New Haven, CT, USA
    J Neuropathol Exp Neurol 66:828-37. 2007
    ..6 and NCX in acute lesions but independent of coexpression of these 2 molecules in chronic lesions...
  20. 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...
  21. 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...
  22. 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
    ....
  23. 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...
  24. 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...
  25. 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...
  26. 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
    ....
  27. 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...
  28. 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...
  29. 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...
  30. 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...
  31. 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...
  32. 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...
  33. ncbi request reprint Macromolecular structure of axonal membrane in the optic nerve of the jimpy mouse
    J A Black
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510
    J Neuropathol Exp Neurol 47:588-98. 1988
    ....
  34. 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...
  35. doi request reprint Phosphorylation of sodium channel Na(v)1.8 by p38 mitogen-activated protein kinase increases current density in dorsal root ganglion neurons
    Andy Hudmon
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 28:3190-201. 2008
    ..Our study suggests a mechanism by which activated p38 contributes to inflammatory, and possibly neuropathic, pain through a p38-mediated increase of Na(v)1.8 current density...
  36. 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...
  37. 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...
  38. 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...
  39. 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...
  40. doi request reprint Astrocytes within multiple sclerosis lesions upregulate sodium channel Nav1.5
    Joel A Black
    Neuroscience Research Centre Bldg 34, VA Connecticut Healthcare System 127A, 950 Campbell Avenue, West Haven, CT 06516, USA
    Brain 133:835-46. 2010
    ..Our observations suggest that the upregulated expression of Nav1.5 in astrocytes may provide a compensatory mechanism, which supports sodium/potassium pump-dependent ionic homoeostasis in areas of central nervous system injury...
  41. pmc Molecular reconstruction of nodes of Ranvier after remyelination by transplanted olfactory ensheathing cells in the demyelinated spinal cord
    Masanori Sasaki
    Department of Neurology, Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 26:1803-12. 2006
    ....
  42. ncbi request reprint Abnormal sodium channel distribution in optic nerve axons in a model of inflammatory demyelination
    Matthew J Craner
    Department of Neurology LCI 707, Yale University School of Medicine, New Haven, CT 06520 8018, USA
    Brain 126:1552-61. 2003
    ..6 and increased expression of Nav1.2 suggest that electrogenesis in EAE may revert to a stage similar to that observed in immature retinal ganglion cells in which Nav1.2 channels support conduction of action potentials along axons...
  43. 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
    ....
  44. ncbi request reprint Phenytoin protects spinal cord axons and preserves axonal conduction and neurological function in a model of neuroinflammation in vivo
    Albert C Lo
    Department of Neurology and Paralyzed Veterans Association Eastern Paralyzed Veterans Association of America Neuroscience Research Center, Yale University School of Medicine, New Haven, CT 06510, USA
    J Neurophysiol 90:3566-71. 2003
    ....
  45. ncbi request reprint Annexin II/p11 is up-regulated in Purkinje cells in EAE and MS
    Matthew J Craner
    Department of Neurology and PVA EPVA Center for Neuroscience Research, Yale University School of Medicine, 333 Cedar Street, P O Box 208018, New Haven, CT 06520 8018, USA
    Neuroreport 14:555-8. 2003
    ..8 within Purkinje cells perturbs the temporal pattern of impulse generation in these cells, our results extend the evidence for an acquired channelopathy which interferes with cerebellar function in MS...
  46. ncbi request reprint Temporal course of upregulation of Na(v)1.8 in Purkinje neurons parallels the progression of clinical deficit in experimental allergic encephalomyelitis
    Matthew J Craner
    Department of Neurology and PVA EPVA Center for Neuroscience Research, Yale University School of Medicine, New Haven, Connecticut 06520 8018, USA
    J Neuropathol Exp Neurol 62:968-75. 2003
    ..8 expression. These results provide evidence that the expression of sodium channel Na(v)1.8 contributes to the development of clinical deficits in an in vivo model of neuroinflammatory disease...
  47. doi request reprint Voltage-gated sodium channel expression in rat and human epidermal keratinocytes: evidence for a role in pain
    Peng Zhao
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Pain 139:90-105. 2008
    ....
  48. ncbi request reprint Sodium channel expression in hypothalamic osmosensitive neurons in experimental diabetes
    Joshua P Klein
    Department of Neurology and PVA EPVA Center for Neuroscience and Regeneration Research, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA
    Neuroreport 13:1481-4. 2002
    ..In the setting of chronic uncontrolled diabetes, these changes in sodium channel expression in the supraoptic nucleus may be maladaptive, contributing to the development of secondary renal complications...
  49. ncbi request reprint Upregulation and colocalization of p75 and Nav1.8 in Purkinje neurons in experimental autoimmune encephalomyelitis
    Tina G Damarjian
    Department of Neurology, The Center for Neuroscience and Regeneration Research, Yale University School of Medicine, LCI 707, 333 Cedar Street, P O Box 208018, New Haven, CT 06520 8018, USA
    Neurosci Lett 369:186-90. 2004
    ..These findings, together with previous studies demonstrating a modulatory role of NGF on sodium channel expression, suggest that NGF acting via p75 contributes to the upregulation of Na(v)1.8 in Purkinje cells in EAE...
  50. ncbi request reprint Diverse functions and dynamic expression of neuronal sodium channels
    Stephen G Waxman
    Department of Neurology and PVA EPVA Neuroscience Research Center, Yale School of Medicine, New Haven, CT 06510, USA
    Novartis Found Symp 241:34-51; discussion 51-60. 2002
    ..In addition, they may present therapeutic opportunities as selective modulators for various Na+ channel subtypes become available...
  51. doi request reprint ERK1/2 mitogen-activated protein kinase phosphorylates sodium channel Na(v)1.7 and alters its gating properties
    Severine Stamboulian
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 30:1637-47. 2010
    ..7 by pERK1/2, which unlike the modulation of Na(v)1.6 and Na(v)1.8 by pp38, regulates gating properties of this channel but not its current density and contributes to the effects of MAPKs on DRG neuron excitability...
  52. 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...
  53. ncbi request reprint NaN/Nav1.9: a sodium channel with unique properties
    Sulayman Dib-Hajj
    Department of Neurology and PVA EPVA Neuroscience Research Center, Yale University School of Medicine, New Haven, CT 06510, USA
    Trends Neurosci 25:253-9. 2002
    ..Thus, Na(v)1.9 appears to play a key role in nociception and is an attractive target in the search for more effective treatments for pain...
  54. ncbi request reprint Changes of sodium channel expression in experimental painful diabetic neuropathy
    Matthew J Craner
    Department of Neurology, Paralyzed Veterans of America Eastern Paralyzed Veterans Association Center for Neuroscience and Regeneration Research, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA
    Ann Neurol 52:786-92. 2002
    ..3, Na(v)1.6, Na(v)1.8, and Na(v)1.9 in dorsal root ganglion neurons in experimental diabetes and suggest that misexpression of sodium channels contributes to neuropathic pain associated with diabetic neuropathy...
  55. doi request reprint Voltage-gated sodium channels: therapeutic targets for pain
    Sulayman D Dib-Hajj
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06520 8018, USA
    Pain Med 10:1260-9. 2009
    ..To provide an overview of the role of voltage-gated sodium channels in pathophysiology of acquired and inherited pain states, and of recent developments that validate these channels as therapeutic targets for treating chronic pain...
  56. doi request reprint Transfection of rat or mouse neurons by biolistics or electroporation
    Sulayman D Dib-Hajj
    Department of Neurology, School of Medicine, Yale University, New Haven, CT, USA
    Nat Protoc 4:1118-26. 2009
    ..Although we have used sodium channels for the examples that we show here, these methods can also be used to study other types of molecules...
  57. pmc A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons
    Anthony M Rush
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Proc Natl Acad Sci U S A 103:8245-50. 2006
    ..Moreover, these findings show that a single ion channel mutation can produce opposing phenotypes (hyperexcitability or hypoexcitability) in the different cell types in which the channel is expressed...
  58. ncbi request reprint From genes to pain: Na v 1.7 and human pain disorders
    Sulayman D Dib-Hajj
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Trends Neurosci 30:555-63. 2007
    ..The contribution of Na(v)1.7 to acquired and inherited pain states and the absence of motor, cognitive and cardiac deficits in patients lacking this channel make it an attractive target for the treatment of neuropathic pain...
  59. ncbi request reprint CAP-1A is a novel linker that binds clathrin and the voltage-gated sodium channel Na(v)1.8
    Chuanju Liu
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Cell Neurosci 28:636-49. 2005
    ..CAP-1A thus is the first example of an adapter protein that links clathrin and a sodium channel and may regulate Na(v)1.8 channel density at the cell surface...
  60. ncbi request reprint Primary cortical motor neurons undergo apoptosis after axotomizing spinal cord injury
    Bryan C Hains
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Comp Neurol 462:328-41. 2003
    ....
  61. ncbi request reprint The presence and role of the tetrodotoxin-resistant sodium channel Na(v)1.9 (NaN) in nociceptive primary afferent neurons
    Xin Fang
    Department of Physiology, University of Bristol, Medical School, Bristol BS8 1TD, United Kingdom
    J Neurosci 22:7425-33. 2002
    ..The data provide direct evidence that Na(v)1.9 is expressed selectively in (but not in all) C- and A-fiber nociceptive-type units and suggest that Na(v)1.9 contributes to membrane properties that are typical of nociceptive neurons...
  62. ncbi request reprint Selective expression of a persistent tetrodotoxin-resistant Na+ current and NaV1.9 subunit in myenteric sensory neurons
    Francois Rugiero
    Int├ęgration des Informations Sensorielles, Unite Mixte de Recherche 6150, Centre National de la Recherche Scientifique, 13916 Marseille, France
    J Neurosci 23:2715-25. 2003
    ..TTX-R I(Na) may play an important role in regulating subthreshold electrogenesis and boosting synaptic stimuli, thereby conferring distinct integrative properties to myenteric sensory neurons...
  63. ncbi request reprint Retinal involvement in multiple sclerosis
    Stephen G Waxman
    Neurology 69:1562-3. 2007