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Genomes and Genes | J A BlackSummaryAffiliation: Yale University Country: USA Publications
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Publications
Sodium channels contribute to microglia/macrophage activation and function in EAE and MSMatthew 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....- Sodium channels and microglial functionJoel 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... 
Correlation of Nav1.8 and Nav1.9 sodium channel expression with neuropathic pain in human subjects with lingual nerve neuromasEmma V Bird
Academic Unit of Oral and Maxillofacial Medicine and Surgery, School of Clinical Dentistry, University of Sheffield, Claremont Crescent, Sheffield S10 2TA, UK
Mol Pain 9:52. 2013....- Nav1.9 expression in magnocellular neurosecretory cells of supraoptic nucleusJ 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. .. - NaV1.7: stress-induced changes in immunoreactivity within magnocellular neurosecretory neurons of the supraoptic nucleusJoel 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... - Nav1.5 sodium channels in macrophages in multiple sclerosis lesionsJoel 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... - Expression of Nav1.7 in DRG neurons extends from peripheral terminals in the skin to central preterminal branches and terminals in the dorsal hornJoel 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... - Nav1.7 is the predominant sodium channel in rodent olfactory sensory neuronsHye 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)... - Sodium-calcium exchanger and multiple sodium channel isoforms in intra-epidermal nerve terminalsAnna 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... - Sodium channel expression within chronic multiple sclerosis plaquesJoel 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... - Long-term protection of central axons with phenytoin in monophasic and chronic-relapsing EAEJoel 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... - 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 ratsJoel 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.... - Remyelination of dorsal column axons by endogenous Schwann cells restores the normal pattern of Nav1.6 and Kv1.2 at nodes of RanvierJoel 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... - Phenytoin protects central axons in experimental autoimmune encephalomyelitisJoel 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... - Changes in the expression of tetrodotoxin-sensitive sodium channels within dorsal root ganglia neurons in inflammatory painJoel 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.... - Sodium channel activity modulates multiple functions in microgliaJoel 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... - Sodium channel Na(v)1.6 is expressed along nonmyelinated axons and it contributes to conductionJoel 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... - Molecular identities of two tetrodotoxin-resistant sodium channels in corneal axonsJoel 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... - Axotomy does not up-regulate expression of sodium channel Na(v)1.8 in Purkinje cellsJ 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... - Multiple sodium channel isoforms and mitogen-activated protein kinases are present in painful human neuromasJoel 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... - Type III sodium channel mRNA is expressed in embryonic but not adult spinal sensory neurons, and is reexpressed following axotomyS 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... - Voltage-gated sodium channels and the molecular pathogenesis of pain: a reviewS 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... - 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... - NaN, a novel voltage-gated Na channel, is expressed preferentially in peripheral sensory neurons and down-regulated after axotomyS 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.... - Two tetrodotoxin-resistant sodium channels in human dorsal root ganglion neuronsS 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... - Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchangerMatthew 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... - Expression of Nav1.8 sodium channels perturbs the firing patterns of cerebellar Purkinje cellsM 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... - Glial cells have heart: rH1 Na+ channel mRNA and protein in spinal cord astrocytesJ A Black
Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA
Glia 23:200-8. 1998.... - Exacerbation of experimental autoimmune encephalomyelitis after withdrawal of phenytoin and carbamazepineJoel 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... - Upregulation of sodium channel Nav1.3 and functional involvement in neuronal hyperexcitability associated with central neuropathic pain after spinal cord injuryBryan 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... - Co-localization of sodium channel Nav1.6 and the sodium-calcium exchanger at sites of axonal injury in the spinal cord in EAEMatthew 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... - GDNF and NGF reverse changes in repriming of TTX-sensitive Na(+) currents following axotomy of dorsal root ganglion neuronsAndreas 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... - Spinal sensory neurons express multiple sodium channel alpha-subunit mRNAsJ 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... - Direct interaction with contactin targets voltage-gated sodium channel Na(v)1.9/NaN to the cell membraneC 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... - Macromolecular structure of axonal membrane in the optic nerve of the jimpy mouseJ A Black
Department of Neurology, Yale University School of Medicine, New Haven, CT 06510
J Neuropathol Exp Neurol 47:588-98. 1988.... - Differential modulation of sodium channel Na(v)1.6 by two members of the fibroblast growth factor homologous factor 2 subfamilyAnthony 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... - Contactin associates with sodium channel Nav1.3 in native tissues and increases channel density at the cell surfaceBhaval 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... - Neuroprotection of axons with phenytoin in experimental allergic encephalomyelitisAlbert 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... - Primary motor neurons fail to up-regulate voltage-gated sodium channel Na(v)1.3/brain type III following axotomy resulting from spinal cord injuryBryan 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... - Phosphorylation of sodium channel Na(v)1.8 by p38 mitogen-activated protein kinase increases current density in dorsal root ganglion neuronsAndy 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... - Apoptosis of vasopressinergic hypothalamic neurons in chronic diabetes mellitusJoshua 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... - Molecular reconstruction of nodes of Ranvier after remyelination by transplanted olfactory ensheathing cells in the demyelinated spinal cordMasanori 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.... - Abnormal sodium channel distribution in optic nerve axons in a model of inflammatory demyelinationMatthew 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... - Astrocytes within multiple sclerosis lesions upregulate sodium channel Nav1.5Joel 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... - Na+ channel expression along axons in multiple sclerosis and its modelsStephen 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.... - Phenytoin protects spinal cord axons and preserves axonal conduction and neurological function in a model of neuroinflammation in vivoAlbert 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.... - ERK1/2 mitogen-activated protein kinase phosphorylates sodium channel Na(v)1.7 and alters its gating propertiesSeverine 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... - Diverse functions and dynamic expression of neuronal sodium channelsStephen 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... - Annexin II/p11 is up-regulated in Purkinje cells in EAE and MSMatthew 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... - Sodium channel expression in hypothalamic osmosensitive neurons in experimental diabetesJoshua 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... - Upregulation and colocalization of p75 and Nav1.8 in Purkinje neurons in experimental autoimmune encephalomyelitisTina 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... - Voltage-gated sodium channel expression in rat and human epidermal keratinocytes: evidence for a role in painPeng 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.... - Temporal course of upregulation of Na(v)1.8 in Purkinje neurons parallels the progression of clinical deficit in experimental allergic encephalomyelitisMatthew 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... - From genes to pain: Na v 1.7 and human pain disordersSulayman 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... - A single sodium channel mutation produces hyper- or hypoexcitability in different types of neuronsAnthony 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... - Preferential expression of IGF-I in small DRG neurons and down-regulation following injuryMatthew 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... - Voltage-gated sodium channels: therapeutic targets for painSulayman 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... - Transfection of rat or mouse neurons by biolistics or electroporationSulayman 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... - NaN/Nav1.9: a sodium channel with unique propertiesSulayman 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... - Changes of sodium channel expression in experimental painful diabetic neuropathyMatthew 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... - Tapered withdrawal of phenytoin removes protective effect in EAE without inflammatory rebound and mortalityS Liu
Department of Neurology and Center for Neuroscience Research, Yale University School of Medicine, New Haven, CT 06510, United States Rehabilitation Research Center, VA Connecticut Healthcare System, West Haven, CT 06516, United States
J Neurol Sci 341:8-12. 2014..These observations support sodium channel blockers as a potential therapeutic agent in the treatment of MS, but indicate caution if treatment is ceased. .. - CAP-1A is a novel linker that binds clathrin and the voltage-gated sodium channel Na(v)1.8Chuanju 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... - Primary cortical motor neurons undergo apoptosis after axotomizing spinal cord injuryBryan C Hains
Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
J Comp Neurol 462:328-41. 2003.... - The presence and role of the tetrodotoxin-resistant sodium channel Na(v)1.9 (NaN) in nociceptive primary afferent neuronsXin 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... - Selective expression of a persistent tetrodotoxin-resistant Na+ current and NaV1.9 subunit in myenteric sensory neuronsFrancois Rugiero
Intégration 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... - Retinal involvement in multiple sclerosisStephen G Waxman
Neurology 69:1562-3. 2007