The cytokine TNFα increases the proportion of DRG neurones expressing the TRPV1 receptor via the TNFR1 receptor and ERK activation

[1]  R. Myers,et al.  TNF-α and Phosphorylation of ERK in DRG and Spinal Cord: Insights Into Mechanisms of Sciatica , 2006 .

[2]  Robert W. Gereau,et al.  Acute p38-Mediated Modulation of Tetrodotoxin-Resistant Sodium Channels in Mouse Sensory Neurons by Tumor Necrosis Factor-α , 2006, The Journal of Neuroscience.

[3]  S. Hunt,et al.  The differential contribution of tumour necrosis factor to thermal and mechanical hyperalgesia during chronic inflammation , 2005, Arthritis research & therapy.

[4]  M. Vasko,et al.  Tumor necrosis factor a and interleukin-1b stimulate the expression of cyclooxygenase II but do not alter prostaglandin E2 receptor mRNA levels in cultured dorsal root ganglia cells , 2004 .

[5]  Yanzhang Li,et al.  Cell-Specific Expression and Lipopolysaccharide-Induced Regulation of Tumor Necrosis Factor α (TNFα) and TNF Receptors in Rat Dorsal Root Ganglion , 2004, The Journal of Neuroscience.

[6]  R. Schicho,et al.  Increased expression of TRPV1 receptor in dorsal root ganglia by acid insult of the rat gastric mucosa , 2004, The European journal of neuroscience.

[7]  L. Sorkin,et al.  Spinal nerve ligation induces transient upregulation of tumor necrosis factor receptors 1 and 2 in injured and adjacent uninjured dorsal root ganglia in the rat , 2003, Neuroscience Letters.

[8]  Zhihong Zhao,et al.  State‐dependent phosphorylation of ε‐isozyme of protein kinase C in adult rat dorsal root ganglia after inflammation and nerve injury , 2003, Journal of neurochemistry.

[9]  J. Levine,et al.  Tumor necrosis factor receptor type‐1 in sensory neurons contributes to induction of chronic enhancement of inflammatory hyperalgesia in rat , 2003, The European journal of neuroscience.

[10]  L. Sorkin,et al.  Tumor Necrosis Factor-α Induces Mechanical Allodynia after Spinal Nerve Ligation by Activation of p38 MAPK in Primary Sensory Neurons , 2003, The Journal of Neuroscience.

[11]  Masaki Tanaka,et al.  Local inflammation increases vanilloid receptor 1 expression within distinct subgroups of DRG neurons , 2003, Brain Research.

[12]  C. Svensson,et al.  Selective increase of tumour necrosis factor‐alpha in injured and spared myelinated primary afferents after chronic constrictive injury of rat sciatic nerve , 2003, The European journal of neuroscience.

[13]  L. Klesse,et al.  Activation of Ras is necessary and sufficient for upregulation of vanilloid receptor type 1 in sensory neurons by neurotrophic factors , 2003, Molecular and Cellular Neuroscience.

[14]  C. Woolf,et al.  p38 MAPK Activation by NGF in Primary Sensory Neurons after Inflammation Increases TRPV1 Levels and Maintains Heat Hyperalgesia , 2002, Neuron.

[15]  Yi Dai,et al.  VR1, but not P2X3, increases in the spared L4 DRG in rats with L5 spinal nerve ligation , 2002, PAIN.

[16]  S. Mohand-Said,et al.  Neurodegenerative and Neuroprotective Effects of Tumor Necrosis Factor (TNF) in Retinal Ischemia: Opposite Roles of TNF Receptor 1 and TNF Receptor 2 , 2002, The Journal of Neuroscience.

[17]  R. Myers,et al.  Anterograde TNFα transport from rat dorsal root ganglion to spinal cord and injured sciatic nerve , 2002, Neuroscience Letters.

[18]  S. M. McFarlane,et al.  TNF-α receptors simultaneously activate Ca2+ mobilisation and stress kinases in cultured sensory neurones , 2002, Neuropharmacology.

[19]  C. Geis,et al.  Anterograde Transport of Tumor Necrosis Factor-α in the Intact and Injured Rat Sciatic Nerve , 2002, The Journal of Neuroscience.

[20]  J. Ting,et al.  TNFα promotes proliferation of oligodendrocyte progenitors and remyelination , 2001, Nature Neuroscience.

[21]  C. Sommer,et al.  Anti-TNF-neutralizing antibodies reduce pain-related behavior in two different mouse models of painful mononeuropathy , 2001, Brain Research.

[22]  C. Sommer,et al.  Combined epineurial therapy with neutralizing antibodies to tumor necrosis factor-alpha and interleukin-1 receptor has an additive effect in reducing neuropathic pain in mice , 2001, Neuroscience Letters.

[23]  R. Coggeshall,et al.  Peripheral capsaicin receptors increase in the inflamed rat hindpaw: a possible mechanism for peripheral sensitization , 2001, Neuroscience Letters.

[24]  J. Levine,et al.  Nociceptor Sensitization by Extracellular Signal-Regulated Kinases , 2001, The Journal of Neuroscience.

[25]  M. Karin,et al.  Signal transduction by tumor necrosis factor and its relatives. , 2001, Trends in cell biology.

[26]  A. Straube,et al.  TNF-alpha expression in painful and nonpainful neuropathies , 2001, Neurology.

[27]  J. Szelényi.  Cytokines and the central nervous system , 2001, Brain Research Bulletin.

[28]  R. Myers,et al.  Axonal transport of TNF-α in painful neuropathy: distribution of ligand tracer and TNF receptors , 2001, Journal of Neuroimmunology.

[29]  C. Sommer,et al.  Thalidomide treatment in chronic constrictive neuropathy decreases endoneurial tumor necrosis factor-α, increases interleukin-10 and has long-term effects on spinal cord dorsal horn met-enkephalin , 2000, PAIN.

[30]  A. Reeve,et al.  Intrathecally administered endotoxin or cytokines produce allodynia, hyperalgesia and changes in spinal cord neuronal responses to nociceptive stimuli in the rat , 2000, European journal of pain.

[31]  M. Kress,et al.  Involvement of the Proinflammatory Cytokines Tumor Necrosis Factor-α, IL-1β, and IL-6 But Not IL-8 in the Development of Heat Hyperalgesia: Effects on Heat-Evoked Calcitonin Gene-Related Peptide Release from Rat Skin , 2000, The Journal of Neuroscience.

[32]  J. Naismith,et al.  TNFα and the TNF receptor superfamily: Structure‐function relationship(s) , 2000, Microscopy research and technique.

[33]  L. Sorkin,et al.  Epineurial application of TNF elicits an acute mechanical hyperalgesia in the awake rat , 2000, Journal of the peripheral nervous system : JPNS.

[34]  S. Bingham,et al.  Vanilloid receptor-1 is essential for inflammatory thermal hyperalgesia , 2000, Nature.

[35]  T. J. Nickola,et al.  Brain-derived TNFα mediates neuropathic pain , 1999, Brain Research.

[36]  J. Levine,et al.  A Novel Nociceptor Signaling Pathway Revealed in Protein Kinase C ε Mutant Mice , 1999, Neuron.

[37]  D. Storm,et al.  Circadian Regulation of cAMP Response Element-mediated Gene Expression in the Suprachiasmatic Nuclei* , 1999, The Journal of Biological Chemistry.

[38]  D. Storm,et al.  Making New Connections Role of ERK/MAP Kinase Signaling in Neuronal Plasticity , 1999, Neuron.

[39]  Scott T. Wong,et al.  Cross Talk between ERK and PKA Is Required for Ca2+ Stimulation of CREB-Dependent Transcription and ERK Nuclear Translocation , 1998, Neuron.

[40]  C. Sommer,et al.  Hyperalgesia in Experimental Neuropathy Is Dependent on the TNF Receptor 1 , 1998, Experimental Neurology.

[41]  D. Julius,et al.  The capsaicin receptor: a heat-activated ion channel in the pain pathway , 1997, Nature.

[42]  R Wagner,et al.  Tumour necrosis factor-α induces ectopic activity in nociceptive primary afferent fibres , 1997, Neuroscience.

[43]  J. Lopshire,et al.  Tumor Necrosis Factor Enhances the Capsaicin Sensitivity of Rat Sensory Neurons , 1997, The Journal of Neuroscience.

[44]  D. Rappolee,et al.  Basement Membrane and Repair of Injury to Peripheral Nerve: Defining a Potential Role for Macrophages, Matrix Metalloproteinases, and Tissue Inhibitor of Metalloproteinases-1 , 1996, The Journal of experimental medicine.

[45]  W. Lesslauer,et al.  Tumor Necrosis Factor Receptors (Tnfr) in Mouse Fibroblasts Deficient in Tnfr1 or Tnfr2 are Signaling Competent and Activate the Mitogen-activated Protein Kinase Pathway with Differential Kinetics* , 1996, The Journal of Biological Chemistry.

[46]  R. Myers,et al.  Schwann cells produce tumor necrosis factor alpha: expression in injured and non-injured nerves , 1996, Neuroscience.

[47]  M. T. Brewer,et al.  Mechanisms of tumor necrosis factor-α (TNF-α) hyperalgesia , 1995, Brain Research.

[48]  M. Yokoyama,et al.  Cytokines in the central nervous system: regulatory roles in neuronal function, cell death and repair. , 1995, Neuroimmunomodulation.

[49]  N. Rothwell,et al.  Cytokines and the nervous system I: expression and recognition , 1995, Trends in Neurosciences.

[50]  D. Goeddel,et al.  Decreased sensitivity to tumour-necrosis factor but normal T-cell development in TNF receptor-2-deficient mice , 1994, Nature.

[51]  S. Maier,et al.  Characterization of cytokine-induced hyperalgesia , 1994, Brain Research.

[52]  R. Zinkernagel,et al.  Mice lacking the tumour necrosis factor receptor 1 are resistant to IMF-mediated toxicity but highly susceptible to infection by Listeria monocytogenes , 1993, Nature.

[53]  P. Ricciardi-Castagnoli,et al.  Central effects of tumor necrosis factor α and interleukin-1α on nociceptive thresholds and spontaneous locomotor activity , 1992, Neuroscience Letters.

[54]  F. Cunha,et al.  The pivotal role of tumour necrosis factor α in the development of inflammatory hyperalgesia , 1992 .

[55]  S. Ferreira,et al.  Interleukin-1β as a potent hyperalgesic agent antagonized by a tripeptide analogue , 1988, Nature.

[56]  R. Tsien,et al.  A new generation of Ca2+ indicators with greatly improved fluorescence properties. , 1985, The Journal of biological chemistry.

[57]  D. Julius,et al.  The vanilloid receptor: a molecular gateway to the pain pathway. , 2001, Annual review of neuroscience.

[58]  M. Hosoi,et al.  Intracerebroventricular Injection of Tumor Necrosis Factor-αInduces Thermal Hyperalgesia in Rats , 1996 .

[59]  N. Rothwell,et al.  Cytokines and their receptors in the central nervous system: physiology, pharmacology, and pathology. , 1996, Pharmacology & therapeutics.