Theodore R Cummins

Summary

Affiliation: Indiana University
Country: USA

Publications

  1. pmc Setting up for the block: the mechanism underlying lidocaine's use-dependent inhibition of sodium channels
    Theodore R Cummins
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, 950 W Walnut St, R2 Room 468, Indianapolis, IN 46202, USA
    J Physiol 582:11. 2007
  2. pmc A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity
    Patrick L Sheets
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, 950 West Walnut St, R2 468, Indianapolis, IN 46202, USA
    J Physiol 581:1019-31. 2007
  3. pmc Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents
    Brian W Jarecki
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, 950 Walnut Street, Indianapolis, Indiana 46202, USA
    J Clin Invest 120:369-78. 2010
  4. pmc An atypical role for collapsin response mediator protein 2 (CRMP-2) in neurotransmitter release via interaction with presynaptic voltage-gated calcium channels
    Joel M Brittain
    Paul and Carole Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA
    J Biol Chem 284:31375-90. 2009
  5. pmc Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navbeta4 peptide-mediated resurgent sodium currents
    Jonathan W Theile
    Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    J Physiol 589:597-608. 2011
  6. pmc Delayed calcium dysregulation in neurons requires both the NMDA receptor and the reverse Na+/Ca2+ exchanger
    Matthew K Brittain
    Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    Neurobiol Dis 46:109-17. 2012
  7. pmc Lidocaine reduces the transition to slow inactivation in Na(v)1.7 voltage-gated sodium channels
    Patrick L Sheets
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA
    Br J Pharmacol 164:719-30. 2011
  8. pmc Alternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T
    Brian W Jarecki
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA
    Channels (Austin) 3:259-67. 2009
  9. pmc Ifenprodil, a NR2B-selective antagonist of NMDA receptor, inhibits reverse Na+/Ca2+ exchanger in neurons
    Matthew K Brittain
    Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    Neuropharmacology 63:974-82. 2012
  10. pmc The human Nav1.5 F1486 deletion associated with long QT syndrome leads to impaired sodium channel inactivation and reduced lidocaine sensitivity
    Weihua Song
    Riley Heart Research Center, Department of Pediatrics Herman B Wells Center for Pediatric Research and Department of Pharmacology and Toxicology, Indiana University School of Medicine, 1044 W Walnut Street, R4 W302D, Indianapolis, IN 46202, USA
    J Physiol 590:5123-39. 2012

Collaborators

Detail Information

Publications62

  1. pmc Setting up for the block: the mechanism underlying lidocaine's use-dependent inhibition of sodium channels
    Theodore R Cummins
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, 950 W Walnut St, R2 Room 468, Indianapolis, IN 46202, USA
    J Physiol 582:11. 2007
  2. pmc A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity
    Patrick L Sheets
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, 950 West Walnut St, R2 468, Indianapolis, IN 46202, USA
    J Physiol 581:1019-31. 2007
    ..7 and suggests that the response of individuals with hereditary erythromelalgia to lidocaine treatment may be determined, at least in part, by their specific genotype...
  3. pmc Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents
    Brian W Jarecki
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, 950 Walnut Street, Indianapolis, Indiana 46202, USA
    J Clin Invest 120:369-78. 2010
    ..Our results indicate that resurgent currents are associated with multiple channelopathies and are likely to be important contributors to neuronal and muscle disorders of excitability...
  4. pmc An atypical role for collapsin response mediator protein 2 (CRMP-2) in neurotransmitter release via interaction with presynaptic voltage-gated calcium channels
    Joel M Brittain
    Paul and Carole Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA
    J Biol Chem 284:31375-90. 2009
    ..Toxin block of Ca(2+) entry via CaV2.2 abolished this stimulated release. Thus, the CRMP-2-Ca(2+) channel interaction represents a novel mechanism for modulation of Ca(2+) influx into nerve terminals and, hence, of synaptic strength...
  5. pmc Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navbeta4 peptide-mediated resurgent sodium currents
    Jonathan W Theile
    Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    J Physiol 589:597-608. 2011
    ..This knowledge provides us with a better understanding of the mechanism of I(NaR) generation and may lead to the development of specialized treatment for pain disorders associated with I(NaR)...
  6. pmc Delayed calcium dysregulation in neurons requires both the NMDA receptor and the reverse Na+/Ca2+ exchanger
    Matthew K Brittain
    Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    Neurobiol Dis 46:109-17. 2012
    ..Overall, our data suggest that both NMDAR and NCXrev are essential for DCD in glutamate-exposed neurons and inhibition of individual mechanism is not sufficient to prevent calcium dysregulation...
  7. pmc Lidocaine reduces the transition to slow inactivation in Na(v)1.7 voltage-gated sodium channels
    Patrick L Sheets
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA
    Br J Pharmacol 164:719-30. 2011
    ..The aim of this study was to determine how lidocaine interacts with multiple inactivated conformations of Na(v)1.7 channels...
  8. pmc Alternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T
    Brian W Jarecki
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA
    Channels (Austin) 3:259-67. 2009
    ....
  9. pmc Ifenprodil, a NR2B-selective antagonist of NMDA receptor, inhibits reverse Na+/Ca2+ exchanger in neurons
    Matthew K Brittain
    Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    Neuropharmacology 63:974-82. 2012
    ..Overall our data suggest that both NR2A- and NR2B-NMDARs are involved in DCD in "older" neurons, and it is necessary to inhibit both NMDARs and NCX(rev) to prevent glutamate-induced DCD...
  10. pmc The human Nav1.5 F1486 deletion associated with long QT syndrome leads to impaired sodium channel inactivation and reduced lidocaine sensitivity
    Weihua Song
    Riley Heart Research Center, Department of Pediatrics Herman B Wells Center for Pediatric Research and Department of Pharmacology and Toxicology, Indiana University School of Medicine, 1044 W Walnut Street, R4 W302D, Indianapolis, IN 46202, USA
    J Physiol 590:5123-39. 2012
    ..5 mutations can have complex functional consequences and highlight the importance of identifying the specific molecular defect when evaluating potential treatments for individuals with prolonged QT intervals...
  11. pmc Calcium/calmodulin-dependent protein kinase II (CaMKII) inhibition induces neurotoxicity via dysregulation of glutamate/calcium signaling and hyperexcitability
    Nicole M Ashpole
    Stark Neuroscience Research Institute, Indiana University of School of Medicine, Indianapolis, Indiana 46202, USA
    J Biol Chem 287:8495-506. 2012
    ....
  12. pmc The tarantula toxins ProTx-II and huwentoxin-IV differentially interact with human Nav1.7 voltage sensors to inhibit channel activation and inactivation
    Yucheng Xiao
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    Mol Pharmacol 78:1124-34. 2010
    ....
  13. pmc Ca2+/calmodulin-dependent protein kinase II (CaMKII) regulates cardiac sodium channel NaV1.5 gating by multiple phosphorylation sites
    Nicole M Ashpole
    Indiana University School of Medicine, Indianapolis, Indiana 46202, USA
    J Biol Chem 287:19856-69. 2012
    ..5 at multiple sites (including Thr-594 and Ser-516) appears to be required to evoke loss-of-function changes in gating that could contribute to acquired Brugada syndrome-like effects in heart failure...
  14. doi request reprint Voltage-clamp and current-clamp recordings from mammalian DRG neurons
    Theodore R Cummins
    Department of Pharmacology and Toxicology, Stark Neurosciences Institute, Indiana University School of Medicine, Indianapolis, IN, USA
    Nat Protoc 4:1103-12. 2009
    ..These electrophysiological studies help to elucidate the role of specific channels in setting threshold and suprathreshold responses of neurons, under normal and pathological conditions...
  15. pmc Common molecular determinants of tarantula huwentoxin-IV inhibition of Na+ channel voltage sensors in domains II and IV
    Yucheng Xiao
    Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA
    J Biol Chem 286:27301-10. 2011
    ..Increasing our understanding of the molecular determinants of toxin interactions with voltage-gated sodium channels may permit development of enhanced isoform-specific voltage-gating modifiers...
  16. pmc Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation
    Brian W Jarecki
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    J Physiol 586:4137-53. 2008
    ..7 in a residue-specific manner and (2) disruption of the fast-inactivated state by PEPD mutations can be more moderate than previously indicated, which has important implications for the pathophysiology of PEPD...
  17. pmc Protein kinase C enhances human sodium channel hNav1.7 resurgent currents via a serine residue in the domain III-IV linker
    Zhi Yong Tan
    Department of Pharmacology and Toxicology and Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA Electronic address
    FEBS Lett 588:3964-9. 2014
    ..Our results suggest that PKC can increase sodium resurgent currents through phosphorylation of a conserved Serine residue located in the domain III-IV linker of sodium channels. ..
  18. pmc Gating-pore currents demonstrate selective and specific modulation of individual sodium channel voltage-sensors by biological toxins
    Yucheng Xiao
    Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, Indiana Y X, T R C Department of Biochemistry, School of Medicine and Biomedical Sciences, State University of New York, Buffalo, New York K B
    Mol Pharmacol 86:159-67. 2014
    ..We propose this approach could be adapted to identify the molecular mechanisms of action for gating modifiers of various voltage-gated ion channels. ..
  19. pmc Tetrodotoxin-resistant sodium channels in sensory neurons generate slow resurgent currents that are enhanced by inflammatory mediators
    Zhi Yong Tan
    Department of Pharmacology and Toxicology and Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana 46202, and
    J Neurosci 34:7190-7. 2014
    ....
  20. pmc The roles of sodium channels in nociception: Implications for mechanisms of pain
    Theodore R Cummins
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, United States
    Pain 131:243-57. 2007
    ..In this review we will examine what is known about the roles of voltage-gated sodium channels in nociception...
  21. pmc Inhibition of Navβ4 peptide-mediated resurgent sodium currents in Nav1.7 channels by carbamazepine, riluzole, and anandamide
    Jonathan W Theile
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    Mol Pharmacol 80:724-34. 2011
    ....
  22. pmc In silico docking and electrophysiological characterization of lacosamide binding sites on collapsin response mediator protein-2 identifies a pocket important in modulating sodium channel slow inactivation
    Yuying Wang
    Department of Pharmacology and Toxicology, Paul and Carole Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA
    J Biol Chem 285:25296-307. 2010
    ..Collectively, these results identify key CRMP-2 residues that can coordinate LCM binding thus making it more effective on its primary clinical target...
  23. pmc Upregulation of the sodium channel NaVβ4 subunit and its contributions to mechanical hypersensitivity and neuronal hyperexcitability in a rat model of radicular pain induced by local dorsal root ganglion inflammation
    Wenrui Xie
    aPain Research Center, Department of Anesthesiology, University of Cincinnati College of Medicine, Cincinnati, OH, USA bDepartment of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA
    Pain 157:879-91. 2016
    ..NaVβ4 may represent a more specific target for pain conditions that depend on myelinated neurons expressing NaV1.6...
  24. doi request reprint FHF2 isoforms differentially regulate Nav1.6-mediated resurgent sodium currents in dorsal root ganglion neurons
    Cindy Barbosa
    Department of Pharmacology and Toxicology, Indiana University, Indianapolis, IN, USA
    Pflugers Arch . 2016
    ..As such, these findings suggest that FHF2A and FHF2B regulate resurgent current in sensory neurons and may contribute to hyperexcitability associated with some pain pathologies...
  25. pmc Tarantula huwentoxin-IV inhibits neuronal sodium channels by binding to receptor site 4 and trapping the domain ii voltage sensor in the closed configuration
    Yucheng Xiao
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA
    J Biol Chem 283:27300-13. 2008
    ..In contrast to scorpion beta-toxins that trap the IIS4 voltage sensor in an outward configuration, we propose that HWTX-IV traps the voltage sensor of domain II in the inward, closed configuration...
  26. doi request reprint Differential block of sensory neuronal voltage-gated sodium channels by lacosamide [(2R)-2-(acetylamino)-N-benzyl-3-methoxypropanamide], lidocaine, and carbamazepine
    Patrick L Sheets
    Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA
    J Pharmacol Exp Ther 326:89-99. 2008
    ..This suggests that lacosamide should be more effective than carbamazepine and lidocaine at selectively blocking the electrical activity of neurons that are chronically depolarized compared with those at more normal resting potentials...
  27. pmc Further insights into the antinociceptive potential of a peptide disrupting the N-type calcium channel-CRMP-2 signaling complex
    Sarah M Wilson
    Paul and Carole Stark Neurosciences Research Institute, Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA
    Channels (Austin) 5:449-56. 2011
    ..2 binding and dramatically increased efficacy in an animal model of migraine. Taken together, TAT-CBD3 potentially represents a novel class of therapeutics targeting channel regulation as opposed to the channel itself...
  28. pmc Aberrant epilepsy-associated mutant Nav1.6 sodium channel activity can be targeted with cannabidiol
    Reesha R Patel
    1 Program in Medical Neuroscience, Neuroscience Research Building, 320 West 15th St, Indianapolis, IN, 46202, USA 2 Paul and Carole Stark Neurosciences Research Institute, 320 West 15th St, Indianapolis, IN, 46202, USA
    Brain 139:2164-81. 2016
    ....
  29. ncbi request reprint Voltage-gated sodium channel blockers for the treatment of neuropathic pain
    Theodore R Cummins
    Assistant Professor of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University, School of Medicine, 950 W Walnut St, R2 Room 468, Indianapolis, IN 46202, USA
    Expert Rev Neurother 7:1597-612. 2007
    ....
  30. ncbi request reprint Nav1.6 channels generate resurgent sodium currents in spinal sensory neurons
    Theodore R Cummins
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    FEBS Lett 579:2166-70. 2005
    ..6 produce resurgent currents. These results demonstrate for the first time the intrinsic ability of Na(v)1.6 to produce a resurgent current, and also show that cell background is critical in permitting the generation of these currents...
  31. ncbi request reprint Inhibition of Nav1.7 and Nav1.4 sodium channels by trifluoperazine involves the local anesthetic receptor
    Patrick L Sheets
    Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    J Neurophysiol 96:1848-59. 2006
    ..7 channels with nanomolar concentrations of TFP raises the possibility that TFP, or TFP analogues, might be useful for regional anesthesia and pain management and could be more potent than traditional local anesthetics...
  32. pmc Navβ4 regulates fast resurgent sodium currents and excitability in sensory neurons
    Cindy Barbosa
    Department of Pharmacology and Toxicology, Indiana University, Indianapolis, IN, USA
    Mol Pain 11:60. 2015
    ..Previous studies suggest Navβ4 subunit mediates INaR in central nervous system neurons. The goal of this study was to determine whether Navβ4 regulates INaR in DRG sensory neurons...
  33. pmc Cardiac sodium channel palmitoylation regulates channel availability and myocyte excitability with implications for arrhythmia generation
    Zifan Pei
    Department of Pharmacology and Toxicology, Indiana University School of Medicine, 635 Barnhill Drive, Indianapolis, Indiana 46202, USA
    Nat Commun 7:12035. 2016
    ..5 function and cardiac excitability and this form of post-translational modification is likely an important contributor to acquired and congenital arrhythmias. ..
  34. pmc Human Nav1.6 Channels Generate Larger Resurgent Currents than Human Nav1.1 Channels, but the Navβ4 Peptide Does Not Protect Either Isoform from Use-Dependent Reduction
    Reesha R Patel
    Program in Medical Neuroscience, Indiana University School of Medicine, Indianapolis, Indiana, United States of America Paul and Carole Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana, United States of America
    PLoS ONE 10:e0133485. 2015
    ..Overall, these two channels have distinct biophysical properties that may differentially contribute to regulating neuronal excitability. ..
  35. pmc KB-R7943, an inhibitor of the reverse Na+ /Ca2+ exchanger, blocks N-methyl-D-aspartate receptor and inhibits mitochondrial complex I
    Tatiana Brustovetsky
    Department of Pharmacology and Toxicology Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA
    Br J Pharmacol 162:255-70. 2011
    ..Here, the effects of KB-R7943 on N-methyl-D-aspartate (NMDA) receptors and mitochondrial complex I were tested...
  36. pmc Tlx3 exerts context-dependent transcriptional regulation and promotes neuronal differentiation from embryonic stem cells
    Takako Kondo
    Department of Otolaryngology Head and Neck Surgery, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    Proc Natl Acad Sci U S A 105:5780-5. 2008
    ..The context-dependent function of Tlx3 as a selector gene may be used to establish a novel strategy to conditionally generate excitatory glutamatergic neurons from ES cells to cure various types of neurodegenerative disorders...
  37. pmc Stepwise Differentiation of Retinal Ganglion Cells from Human Pluripotent Stem Cells Enables Analysis of Glaucomatous Neurodegeneration
    Sarah K Ohlemacher
    Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, IN, USA
    Stem Cells 34:1553-62. 2016
    ..Moreover, iPSC-derived RGCs can be utilized for future drug screening approaches to identify targets for the treatment of glaucoma and other optic neuropathies. Stem Cells 2016;34:1553-1562. ..
  38. ncbi request reprint Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy
    Theodore R Cummins
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA
    J Neurosci 24:8232-6. 2004
    ....
  39. pmc Recent developments regarding voltage-gated sodium channel blockers for the treatment of inherited and acquired neuropathic pain syndromes
    Jonathan W Theile
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine Indianapolis, IN, USA
    Front Pharmacol 2:54. 2011
    ....
  40. ncbi request reprint The role of sodium channels in chronic inflammatory and neuropathic pain
    Ron Amir
    Department of Cell and Animal Biology, Institute of Life Sciences, Hebrew University of Jerusalem, Jerusalem, Israel
    J Pain 7:S1-29. 2006
    ..This restricted expression raises the possibility that isoform-specific drugs might be analgesic and lacking the cardiotoxicity and neurotoxicity that limit the use of current sodium-channel blockers...
  41. ncbi request reprint Modulation of the cardiac sodium channel Nav1.5 by fibroblast growth factor homologous factor 1B
    Chuan Ju Liu
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Biol Chem 278:1029-36. 2003
    ..5 channel with FHF1B. This is the first report showing that interaction with a growth factor can modulate properties of a voltage-gated sodium channel...
  42. 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
    ....
  43. ncbi request reprint Painful research: identification of a small-molecule inhibitor that selectively targets Nav1.8 sodium channels
    Anthony M Rush
    NeuroSolutions Ltd, Coventry CV4 7ZS, UK
    Mol Interv 7:192-5, 180. 2007
    ..This exciting new compound shows efficacy in several animal models of pain and is anticipated to be only the first of many new isoform-specific sodium channel blockers...
  44. ncbi request reprint Pharmacological properties of neuronal TTX-resistant sodium channels and the role of a critical serine pore residue
    Andreas Leffler
    Klinik fur Anasthesiologie, Friedrich Alexander Universität Erlangen Nuremberg, Krankenhausstr 12, 91054 Erlangen, Germany
    Pflugers Arch 451:454-63. 2005
    ....
  45. 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
    ....
  46. ncbi request reprint Molecular interactions of the gating modifier toxin ProTx-II with NaV 1.5: implied existence of a novel toxin binding site coupled to activation
    Jaime J Smith
    Department of Biochemistry, School of Medicine and Biomedical Sciences, State University of New York, Buffalo, New York 14214, USA
    J Biol Chem 282:12687-97. 2007
    ....
  47. 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...
  48. pmc Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons
    Anthony M Rush
    NeuroSolutions Ltd, PO Box 3517, Coventry CV4 7ZS, UK
    J Physiol 579:1-14. 2007
    ....
  49. 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...
  50. 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...
  51. 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...
  52. ncbi request reprint Critical molecular determinants of voltage-gated sodium channel sensitivity to mu-conotoxins GIIIA/B
    Theodore R Cummins
    Department of Neurology and PVA EPVA Neuroscience Research Center, Yale University School of Medicine, New Haven, Connecticut 06516, USA
    Mol Pharmacol 61:1192-201. 2002
    ..Our results should aid the development of toxins that block specific neuronal sodium channel isoforms...
  53. ncbi request reprint Calmodulin binds to the C terminus of sodium channels Nav1.4 and Nav1.6 and differentially modulates their functional properties
    Raimund I Herzog
    Department of Neurology and Paralyzed Veterans of America Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 23:8261-70. 2003
    ..Our data demonstrate that CaM can regulate the properties of VGSCs via calcium-dependent and calcium-independent mechanisms and suggest that modulation of neuronal sodium channels may play a role in calcium-dependent neuronal plasticity...
  54. ncbi request reprint GTP gamma S increases Nav1.8 current in small-diameter dorsal root ganglia neurons
    Carl Y Saab
    Department of Neurology and PVA Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale Medical School, New Haven, CT 06510, USA
    Exp Brain Res 152:415-9. 2003
    ..8 channel modulation by G proteins independent of a PKA/PKC pathway or binding to aluminum...
  55. 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...
  56. 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...
  57. ncbi request reprint Characterization and developmental changes of Na+ currents of petrosal neurons with projections to the carotid body
    Theodore R Cummins
    Department of Neurology, Yale University School of Medicine, New Haven Connecticut 06510, USA
    J Neurophysiol 88:2993-3002. 2002
    ....
  58. ncbi request reprint Molecular determinant of Na(v)1.8 sodium channel resistance to the venom from the scorpion Leiurus quinquestriatus hebraeus
    Carl Y Saab
    Department of Neurology and PVA EPVA Neuroscience Research Center, Yale Medical School, CT New Haven 06510, USA
    Neurosci Lett 331:79-82. 2002
    ..Therefore, we conclude that the tetrapeptide SLEN at the D4S3-S4 linker region is sufficient to make Na(v)1.8 resistant to LQTX...
  59. 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...
  60. 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...
  61. 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...
  62. ncbi request reprint HSV-1 helper virus 5dl1.2 suppresses sodium currents in amplicon-transduced neurons
    Benjamin H White
    Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Neurophysiol 87:2149-57. 2002
    ..We conclude that Na(+) current suppression by the amplicon preparation results from the preferential coinfection of transduced neurons by the 5dl1.2 helper virus...