C J Woolf

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Neuroscience. It takes more than two to Nogo
    Clifford J Woolf
    Neural Plasticity Research Group, Department of Anesthesia, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA
    Science 297:1132-4. 2002
  2. pmc Exploiting microarrays to reveal differential gene expression in the nervous system
    Robert S Griffin
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    Genome Biol 4:105. 2003
  3. pmc Replicate high-density rat genome oligonucleotide microarrays reveal hundreds of regulated genes in the dorsal root ganglion after peripheral nerve injury
    Michael Costigan
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    BMC Neurosci 3:16. 2002
  4. pmc Transcriptional and posttranslational plasticity and the generation of inflammatory pain
    C J Woolf
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Massachusetts General Hospital East, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 96:7723-30. 1999
  5. ncbi request reprint Neuronal plasticity: increasing the gain in pain
    C J Woolf
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, MGH East, Charlestown, MA 02129, USA
    Science 288:1765-9. 2000
  6. ncbi request reprint Axonal injury-dependent induction of the peripheral benzodiazepine receptor in small-diameter adult rat primary sensory neurons
    Laurie A Karchewski
    Neural Plasticity Research Group, Department of Anaesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, MGH East, 149 13th Street, Rm 4309, Charlestown, MA 02129, USA
    Eur J Neurosci 20:671-83. 2004
  7. ncbi request reprint Runx1 determines nociceptive sensory neuron phenotype and is required for thermal and neuropathic pain
    Chih Li Chen
    Dana Farber Cancer Institute and Department of Neurobiology, Harvard Medical School, 1 Jimmy Fund Way, Boston, Massachusetts 02115, USA
    Neuron 49:365-77. 2006
  8. ncbi request reprint Disruption of ErbB receptor signaling in adult non-myelinating Schwann cells causes progressive sensory loss
    Suzhen Chen
    Division of Neuroscience, Children s Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, Massachusetts 02115, USA
    Nat Neurosci 6:1186-93. 2003
  9. ncbi request reprint p38 mitogen-activated protein kinase is activated after a spinal nerve ligation in spinal cord microglia and dorsal root ganglion neurons and contributes to the generation of neuropathic pain
    Shan Xue Jin
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
    J Neurosci 23:4017-22. 2003
  10. ncbi request reprint Direct activation of rat spinal dorsal horn neurons by prostaglandin E2
    H Baba
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 21:1750-6. 2001

Detail Information

Publications85

  1. ncbi request reprint Neuroscience. It takes more than two to Nogo
    Clifford J Woolf
    Neural Plasticity Research Group, Department of Anesthesia, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA
    Science 297:1132-4. 2002
  2. pmc Exploiting microarrays to reveal differential gene expression in the nervous system
    Robert S Griffin
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    Genome Biol 4:105. 2003
    ..This article highlights what is needed to get the most out of microarrays in terms of accurately and effectively revealing differential gene expression and regulation in the nervous system...
  3. pmc Replicate high-density rat genome oligonucleotide microarrays reveal hundreds of regulated genes in the dorsal root ganglion after peripheral nerve injury
    Michael Costigan
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    BMC Neurosci 3:16. 2002
    ..Two comparisons were made using two sets of triplicate microarrays, naïve versus naïve and naïve versus axotomy...
  4. pmc Transcriptional and posttranslational plasticity and the generation of inflammatory pain
    C J Woolf
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Massachusetts General Hospital East, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 96:7723-30. 1999
    ..Elucidation of the molecular mechanisms responsible provides new opportunities for therapeutic approaches to managing inflammatory pain...
  5. ncbi request reprint Neuronal plasticity: increasing the gain in pain
    C J Woolf
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, MGH East, Charlestown, MA 02129, USA
    Science 288:1765-9. 2000
    ....
  6. ncbi request reprint Axonal injury-dependent induction of the peripheral benzodiazepine receptor in small-diameter adult rat primary sensory neurons
    Laurie A Karchewski
    Neural Plasticity Research Group, Department of Anaesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, MGH East, 149 13th Street, Rm 4309, Charlestown, MA 02129, USA
    Eur J Neurosci 20:671-83. 2004
    ..DBI expression does not change with sciatic nerve transection. PBR acting on small-calibre neurons could play a role in the adaptive survival and growth responses of these cells to injury of their axons...
  7. ncbi request reprint Runx1 determines nociceptive sensory neuron phenotype and is required for thermal and neuropathic pain
    Chih Li Chen
    Dana Farber Cancer Institute and Department of Neurobiology, Harvard Medical School, 1 Jimmy Fund Way, Boston, Massachusetts 02115, USA
    Neuron 49:365-77. 2006
    ..Moreover, mice lacking Runx1 exhibit specific defects in thermal and neuropathic pain. Thus, Runx1 coordinates the phenotype of a large cohort of nociceptors, a finding with implications for pain therapy...
  8. ncbi request reprint Disruption of ErbB receptor signaling in adult non-myelinating Schwann cells causes progressive sensory loss
    Suzhen Chen
    Division of Neuroscience, Children s Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, Massachusetts 02115, USA
    Nat Neurosci 6:1186-93. 2003
    ....
  9. ncbi request reprint p38 mitogen-activated protein kinase is activated after a spinal nerve ligation in spinal cord microglia and dorsal root ganglion neurons and contributes to the generation of neuropathic pain
    Shan Xue Jin
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
    J Neurosci 23:4017-22. 2003
    ..Coactivation of p38 in DRG neurons and spinal microglia may contribute to later phases of neuropathic pain...
  10. ncbi request reprint Direct activation of rat spinal dorsal horn neurons by prostaglandin E2
    H Baba
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 21:1750-6. 2001
    ..Moreover, these findings imply an involvement of spinal cord-generated prostanoids in modulating sensory processing through an alteration in dorsal horn neuronal excitability...
  11. doi request reprint Ro5-4864 promotes neonatal motor neuron survival and nerve regeneration in adult rats
    Charles Mills
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    Eur J Neurosci 27:937-46. 2008
    ..Furthermore, although Ro5-4864 is only a very weak promoter of survival in adult neurons, it significantly enhances regeneration and functional recovery in adults...
  12. pmc Detection of cold pain, cold allodynia and cold hyperalgesia in freely behaving rats
    Andrew J Allchorne
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 13th Street, Building 149 4309, Charlestown, MA 02129, USA
    Mol Pain 1:36. 2005
    ..To expand our understanding of cold induced pain states we have studied cold pain behaviors over a range of temperatures in several animal models of chronic pain...
  13. ncbi request reprint Selective up-regulation of the growth arrest DNA damage-inducible gene Gadd45 alpha in sensory and motor neurons after peripheral nerve injury
    Katia Befort
    Neural Plasticity Research Group, Department of Anaesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA
    Eur J Neurosci 18:911-22. 2003
    ..Gadd45a is a specific marker of the presence of peripheral axonal injury in adult primary sensory and motor neurons...
  14. ncbi request reprint Nociceptive-specific activation of ERK in spinal neurons contributes to pain hypersensitivity
    R R Ji
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Rm 4309, Charlestown, Massachusetts 02129, USA
    Nat Neurosci 2:1114-9. 1999
    ..ERK signaling within the spinal cord is therefore involved in generating pain hypersensitivity. Because of its rapid activation, this effect probably involves regulation of neuronal excitability without changes in transcription...
  15. ncbi request reprint The transcription factor ATF-3 promotes neurite outgrowth
    Rhona Seijffers
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    Mol Cell Neurosci 32:143-54. 2006
    ..Furthermore, ATF-3 promotes long sparsely branched neurites. ATF-3 overexpression did not increase c-Jun expression. ATF-3 may contribute, therefore, to neurite outgrowth by orchestrating the gene expression responses in injured neurons...
  16. ncbi request reprint Removal of GABAergic inhibition facilitates polysynaptic A fiber-mediated excitatory transmission to the superficial spinal dorsal horn
    Hiroshi Baba
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    Mol Cell Neurosci 24:818-30. 2003
    ..This NMDA receptor-dependent phenomenon may contribute to bicuculline-induced allodynia or hyperalgesia, as well as the hypersensitivity observed in neuropathic pain patients...
  17. ncbi request reprint Peripheral axonal injury results in reduced mu opioid receptor pre- and post-synaptic action in the spinal cord
    Tatsuro Kohno
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Charlestown, Boston, MA 02129, USA
    Pain 117:77-87. 2005
    ..Axotomy-induced changes in MOR may contribute to opioid- insensitive components of neuropathic pain while the absence of these changes in intact afferents may contribute to the opioid sensitive components...
  18. pmc Nociceptors are interleukin-1beta sensors
    Alexander M Binshtok
    Neural Plasticity Research Group, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 28:14062-73. 2008
    ..By acting as an IL-1beta sensor, nociceptors can directly signal the presence of ongoing tissue inflammation...
  19. ncbi request reprint DRAGON: a member of the repulsive guidance molecule-related family of neuronal- and muscle-expressed membrane proteins is regulated by DRG11 and has neuronal adhesive properties
    Tarek A Samad
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
    J Neurosci 24:2027-36. 2004
    ..The dynamic expression, ordered spatial localization, and adhesive properties of the RGM-related family of membrane-associated proteins are compatible with specific roles in development...
  20. ncbi request reprint Repulsive guidance molecule (RGMa), a DRAGON homologue, is a bone morphogenetic protein co-receptor
    Jodie L Babitt
    Program in Membrane Biology and Division of Nephrology, Department of Medicine, Harvard Medical School, Boston, MA 02129, USA
    J Biol Chem 280:29820-7. 2005
    ..Finally, we demonstrate that BMP signaling occurs in neurons that express RGMa in vivo. These data are consistent with a role for RGMa as a BMP co-receptor...
  21. ncbi request reprint Partial peripheral nerve injury promotes a selective loss of GABAergic inhibition in the superficial dorsal horn of the spinal cord
    Kimberly A Moore
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 22:6724-31. 2002
    ..Both of these mechanisms could reduce presynaptic GABA levels and promote a functional loss of GABAergic transmission in the superficial dorsal horn...
  22. ncbi request reprint Peripheral noxious stimulation induces phosphorylation of the NMDA receptor NR1 subunit at the PKC-dependent site, serine-896, in spinal cord dorsal horn neurons
    Gary J Brenner
    Neural Plasticity Research Group, Department of Anaesthesia and Critical Care, Massachusetts General Hospital, Boston, MA 02110, USA
    Eur J Neurosci 20:375-84. 2004
    ..These data provide evidence for an activity-dependent NMDAR phosphorylation at the PKC-dependent site, serine-896, in spinal cord dorsal horn neurons initiated by peripheral noxious stimuli...
  23. ncbi request reprint Dynamic changes in glypican-1 expression in dorsal root ganglion neurons after peripheral and central axonal injury
    Stefan Bloechlinger
    Department of Anaesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, MGH East, 149 13th Street, Rm 4309, Charlestown, MA 02129, USA
    Eur J Neurosci 19:1119-32. 2004
    ..Glypican-1 is coexpressed with robo 2 and its up-regulation after axonal injury may contribute to an altered sensitivity to axonal growth or guidance cues...
  24. pmc Localization and action of Dragon (repulsive guidance molecule b), a novel bone morphogenetic protein coreceptor, throughout the reproductive axis
    Yin Xia
    Reproductive Endocrine Unit, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    Endocrinology 146:3614-21. 2005
    ..The overlap between Dragon expression and the functional BMP signaling system suggests that Dragon may play a role in mammalian reproduction...
  25. ncbi request reprint The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity
    Fumimasa Amaya
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 26:12852-60. 2006
    ..9-/- mice. Na(v)1.9 is, we conclude, an effector of the hypersensitivity produced by multiple inflammatory mediators on nociceptor peripheral terminals and therefore plays a key role in mediating peripheral sensitization...
  26. pmc Periganglionic inflammation elicits a distally radiating pain hypersensitivity by promoting COX-2 induction in the dorsal root ganglion
    Fumimasa Amaya
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, USA
    Pain 142:59-67. 2009
    ....
  27. ncbi request reprint Can we conquer pain?
    Joachim Scholz
    Neural Plasticity Research Group, Department of Anesthesia, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
    Nat Neurosci 5:1062-7. 2002
    ..Elucidation of these mechanisms is key to the development of treatments that specifically target underlying causes rather than just symptoms. This new approach promises to revolutionize pain diagnosis and management...
  28. pmc Multiple chronic pain states are associated with a common amino acid-changing allele in KCNS1
    Michael Costigan
    F M Kirby Neurobiology Centre, Children s Hospital Boston and Harvard Medical School, Boston, MA 02115, USA
    Brain 133:2519-27. 2010
    ..Screening for this allele could help define those individuals prone to a transition to persistent pain, and thus requiring therapeutic strategies or lifestyle changes that minimize nerve injury...
  29. ncbi request reprint Hsp27 upregulation and phosphorylation is required for injured sensory and motor neuron survival
    Susanna C Benn
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Charlestown, MA 02129, USA
    Neuron 36:45-56. 2002
    ..Transcriptional and posttranslational regulation of Hsp27 is necessary for sensory and motor neuron survival following peripheral nerve injury...
  30. ncbi request reprint Neuronal plasticity and signal transduction in nociceptive neurons: implications for the initiation and maintenance of pathological pain
    R R Ji
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, Massachusetts 02129, USA
    Neurobiol Dis 8:1-10. 2001
    ..Pharmacological intervention targeted specifically at the signal transduction pathways in nociceptive neurons may provide, therefore, new therapeutic opportunities for pathological pain...
  31. ncbi request reprint Developmental expression of the TTX-resistant voltage-gated sodium channels Nav1.8 (SNS) and Nav1.9 (SNS2) in primary sensory neurons
    S C Benn
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 21:6077-85. 2001
    ....
  32. pmc Semaphorin 3A growth cone collapse requires a sequence homologous to tarantula hanatoxin
    O Behar
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 96:13501-5. 1999
    ..Our data support an important role for Ca(2+) in mediating the Sema 3A response and suggest that Sema 3A may produce its effects by causing the opening of Ca(2+) channels...
  33. ncbi request reprint Prostanoids and pain: unraveling mechanisms and revealing therapeutic targets
    Tarek A Samad
    Neural Plasticity Research Group, Dept of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA
    Trends Mol Med 8:390-6. 2002
    ....
  34. ncbi request reprint DRAGON, a bone morphogenetic protein co-receptor
    Tarek A Samad
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
    J Biol Chem 280:14122-9. 2005
    ..The direct interaction of DRAGON with BMP ligands and receptors indicates that it is a BMP co-receptor that potentiates BMP signaling...
  35. ncbi request reprint Complement induction in spinal cord microglia results in anaphylatoxin C5a-mediated pain hypersensitivity
    Robert S Griffin
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 27:8699-708. 2007
    ..We conclude that induction of the complement cascade in spinal cord microglia after peripheral nerve injury contributes to neuropathic pain through the release and action of the C5a anaphylatoxin peptide...
  36. ncbi request reprint Nociceptors--noxious stimulus detectors
    Clifford J Woolf
    Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Neuron 55:353-64. 2007
    ....
  37. doi request reprint Overcoming obstacles to developing new analgesics
    Clifford J Woolf
    Neurobiology Center and Program in Neurobiology, Department of Neurology, Children s Hospital Boston, Boston, Massachusetts, USA
    Nat Med 16:1241-7. 2010
    ..Nevertheless, the chances of success could increase if analgesic drug development strategy changed. To achieve such a paradigm shift we must understand why development of drugs for pain relief is so challenging...
  38. pmc What is this thing called pain?
    Clifford J Woolf
    Department of Neurology, Children s Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Clin Invest 120:3742-4. 2010
    ....
  39. ncbi request reprint Blocking caspase activity prevents transsynaptic neuronal apoptosis and the loss of inhibition in lamina II of the dorsal horn after peripheral nerve injury
    Joachim Scholz
    Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 25:7317-23. 2005
    ..Preventing nerve injury-induced apoptosis of dorsal horn neurons by blocking caspase activity maintains inhibitory transmission in lamina II and reduces pain hypersensitivity...
  40. ncbi request reprint Role of the peripheral benzodiazepine receptor in sensory neuron regeneration
    Charles D Mills
    Neural Plasticity Research Group, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Mol Cell Neurosci 30:228-37. 2005
    ..These results show that PBR has a role in the early regenerative response of small caliber sensory axons, the preconditioning effect, and that PBR agonists enhance sensory axon regeneration...
  41. ncbi request reprint p38 MAPK activation by NGF in primary sensory neurons after inflammation increases TRPV1 levels and maintains heat hyperalgesia
    Ru Rong Ji
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA
    Neuron 36:57-68. 2002
    ....
  42. pmc Central sensitization: implications for the diagnosis and treatment of pain
    Clifford J Woolf
    FM Kirby Neurobiology Center, Children s Hospital Boston, Department of Neurobiology, Harvard Medical School, Boston, MA, USA
    Pain 152:S2-15. 2011
    ....
  43. ncbi request reprint Ionotropic and metabotropic receptors, protein kinase A, protein kinase C, and Src contribute to C-fiber-induced ERK activation and cAMP response element-binding protein phosphorylation in dorsal horn neurons, leading to central sensitization
    Yasuhiko Kawasaki
    Pain Research Center, Department of Anesthesiology, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 24:8310-21. 2004
    ....
  44. ncbi request reprint TRPA1 contributes to cold, mechanical, and chemical nociception but is not essential for hair-cell transduction
    Kelvin Y Kwan
    Department of Neurobiology and Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Neuron 50:277-89. 2006
    ..TRPA1 is apparently not essential for hair-cell transduction but contributes to the transduction of mechanical, cold, and chemical stimuli in nociceptor sensory neurons...
  45. ncbi request reprint ERK MAP kinase activation in superficial spinal cord neurons induces prodynorphin and NK-1 upregulation and contributes to persistent inflammatory pain hypersensitivity
    Ru Rong Ji
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
    J Neurosci 22:478-85. 2002
    ..Activation of the ERK pathway in a subset of nociceptive spinal neurons contributes, therefore, to persistent pain hypersensitivity, possibly via transcriptional regulation of genes, such as prodynorphin and NK-1...
  46. ncbi request reprint Utilization of an HSV-based amplicon vector encoding the axonal marker hPLAP to follow neurite outgrowth in cultured DRG neurons
    Rhona Seijffers
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Room 4309, Charlestown, MA 02129, USA
    J Neurosci Methods 132:169-76. 2004
    ..Using this reporter, the effect of GAP-43 on neurite outgrowth in transduced DRG neurons could be demonstrated. HSV-based amplicon vectors can contribute to the study of axonal growth and guidance in cultured neurons...
  47. pmc Bradykinin enhances AMPA and NMDA receptor activity in spinal cord dorsal horn neurons by activating multiple kinases to produce pain hypersensitivity
    Tatsuro Kohno
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 28:4533-40. 2008
    ..We conclude that bradykinin, by activating multiple kinases in dorsal horn neurons, potentiates glutamatergic synaptic transmission to produce pain hypersensitivity...
  48. ncbi request reprint High basal expression and injury-induced down regulation of two regulator of G-protein signaling transcripts, RGS3 and RGS4 in primary sensory neurons
    Michael Costigan
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 13th Street, Building 149 4309, Charlestown, MA 02129, USA
    Mol Cell Neurosci 24:106-16. 2003
    ..Decreased levels of RGS3 and RGS4 in injured sensory neurons is likely to result in an increased GPCR sensitivity, and therefore contribute to alterations in cellular function seen after such lesions...
  49. pmc Central sensitization: a generator of pain hypersensitivity by central neural plasticity
    Alban Latremoliere
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, USA
    J Pain 10:895-926. 2009
    ..Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations...
  50. pmc Peripheral nerve injury alters excitatory synaptic transmission in lamina II of the rat dorsal horn
    Tatsuro Kohno
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Physiol 548:131-8. 2003
    ..Thus, excitatory synaptic transmission is subject to divergent plasticity in different peripheral nerve injury models, reflecting the complexity of responses to different forms of deafferentation...
  51. pmc Low-dose methotrexate reduces peripheral nerve injury-evoked spinal microglial activation and neuropathic pain behavior in rats
    Joachim Scholz
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Room 4309, Charlestown, MA 02129, USA
    Pain 138:130-42. 2008
    ..We confirm that microglial activation is crucial for the development of pain after nerve injury, and demonstrates that suppression of this cellular immune response is a promising approach for preventing neuropathic pain...
  52. ncbi request reprint The neuropathic pain triad: neurons, immune cells and glia
    Joachim Scholz
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Nat Neurosci 10:1361-8. 2007
    ....
  53. pmc Loss of inhibitory interneurons in the dorsal spinal cord and elevated itch in Bhlhb5 mutant mice
    Sarah E Ross
    Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA
    Neuron 65:886-98. 2010
    ..Our findings suggest that Bhlhb5 is required for the survival of a specific population of inhibitory interneurons that regulate pruritus, and provide evidence that the loss of inhibitory synaptic input results in abnormal itch...
  54. ncbi request reprint No Nogo: now where to go?
    Clifford J Woolf
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA
    Neuron 38:153-6. 2003
    ..Three independent labs have now produced Nogo knockout mice with, quite unexpectedly, three different regeneration phenotypes...
  55. pmc COX2 in CNS neural cells mediates mechanical inflammatory pain hypersensitivity in mice
    Daniel Vardeh
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02129, USA
    J Clin Invest 119:287-94. 2009
    ..Mechanical pain is a major symptom of most inflammatory conditions, such as postoperative pain and arthritis, and induction of COX2 in neural cells in the CNS seems to contribute to this...
  56. pmc Neuropathic pain: a maladaptive response of the nervous system to damage
    Michael Costigan
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
    Annu Rev Neurosci 32:1-32. 2009
    ..Treatment needs to move from merely suppressing symptoms to a disease-modifying strategy aimed at both preventing maladaptive plasticity and reducing intrinsic risk...
  57. ncbi request reprint Inhibition of nociceptors by TRPV1-mediated entry of impermeant sodium channel blockers
    Alexander M Binshtok
    Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Nature 449:607-10. 2007
    ....
  58. pmc GDNF selectively promotes regeneration of injury-primed sensory neurons in the lesioned spinal cord
    Charles D Mills
    Neural Plasticity Research Group, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Mol Cell Neurosci 36:185-94. 2007
    ..We conclude that peripheral nerve injury upregulates GDNF signaling pathway components and that exogenous GDNF treatment selectively promotes axonal growth of injury-primed sensory neurons in a concentration-dependent fashion...
  59. ncbi request reprint ERK is sequentially activated in neurons, microglia, and astrocytes by spinal nerve ligation and contributes to mechanical allodynia in this neuropathic pain model
    Zhi Ye Zhuang
    Pain Research Center, Department of Anesthesiology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Pain 114:149-59. 2005
    ..The sequential activation of ERK in dorsal horn microglia and then in astrocytes might reflect distinct roles for these two subtypes of glia in the temporal evolution of neuropathic pain...
  60. ncbi request reprint Bradykinin and peripheral sensitization
    Haibin Wang
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    Biol Chem 387:11-4. 2006
    ....
  61. ncbi request reprint ATF3 increases the intrinsic growth state of DRG neurons to enhance peripheral nerve regeneration
    Rhona Seijffers
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 27:7911-20. 2007
    ..We conclude that ATF3 contributes to nerve regeneration by increasing the intrinsic growth state of injured neurons...
  62. ncbi request reprint Bradykinin produces pain hypersensitivity by potentiating spinal cord glutamatergic synaptic transmission
    Haibin Wang
    Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 25:7986-92. 2005
    ..We conclude that bradykinin is released in the spinal cord in response to nociceptor inputs and acts as a synaptic neuromodulator, potentiating glutamatergic synaptic transmission to produce pain hypersensitivity...
  63. pmc Targeting of sodium channel blockers into nociceptors to produce long-duration analgesia: a systematic study and review
    D P Roberson
    FM Kirby Neurobiology Center and Department of Neurology, Children s Hospital, Boston, MA 02115, USA
    Br J Pharmacol 164:48-58. 2011
    ..This involves co-administration of QX-314 and a TRPV1 agonist to produce a long-lasting local analgesia. For potential clinical use we propose using lidocaine as the TRPV1 agonist, because it activates TRPV1 at clinical doses...
  64. ncbi request reprint Gabapentin-- actions on adult superficial dorsal horn neurons
    K A Moore
    Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston 02129, USA
    Neuropharmacology 43:1077-81. 2002
    ..Thus, in adult rat dorsal horn, synaptic and extrasynaptic NMDA receptors may be differentially regulated by GBP perhaps due to differences in subunit composition...
  65. ncbi request reprint Bone morphogenetic protein signaling by hemojuvelin regulates hepcidin expression
    Jodie L Babitt
    Program in Membrane Biology and Nephrology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Genet 38:531-9. 2006
    ..Our data suggest a mechanism by which HFE2 mutations cause hemochromatosis: hemojuvelin dysfunction decreases BMP signaling, thereby lowering hepcidin expression...
  66. ncbi request reprint Dissecting out mechanisms responsible for peripheral neuropathic pain: implications for diagnosis and therapy
    Clifford J Woolf
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA
    Life Sci 74:2605-10. 2004
    ..This review highlights some of the mechanisms underlying neuropathic pain and the novel targets they reveal for future putative analgesics...
  67. ncbi request reprint No DREAM, No pain. Closing the spinal gate
    Michael Costigan
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Massachusetts General Hospital East, Charlestown, MA 02129, USA
    Cell 108:297-300. 2002
    ..Knocking out DREAM results in sufficient dynorphin expression to produce a strong reduction in generalized pain behavior, highlighting the role that intracellular molecules play in modulating pain gating in the spinal cord...
  68. ncbi request reprint Pain: moving from symptom control toward mechanism-specific pharmacologic management
    Clifford J Woolf
    Neural Plasticity Research Group, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Ann Intern Med 140:441-51. 2004
  69. ncbi request reprint Pain TRPs
    Haibin Wang
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Neuron 46:9-12. 2005
    ....
  70. ncbi request reprint Central sensitization: uncovering the relation between pain and plasticity
    Clifford J Woolf
    Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Anesthesiology 106:864-7. 2007
  71. ncbi request reprint Implications of recent advances in the understanding of pain pathophysiology for the assessment of pain in patients
    C J Woolf
    Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown 02129, USA
    Pain . 1999
    ....
  72. ncbi request reprint Transport and localization of the DEG/ENaC ion channel BNaC1alpha to peripheral mechanosensory terminals of dorsal root ganglia neurons
    J Garcia-Anoveros
    Howard Hughes Medical Institute and Department of Neurobiology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA
    J Neurosci 21:2678-86. 2001
    ..Accordingly, BNaC1alpha channels might participate in the transduction of touch and painful mechanical stimuli...
  73. ncbi request reprint Cyclooxygenase 2 expression in the spared nerve injury model of neuropathic pain
    D C Broom
    Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    Neuroscience 124:891-900. 2004
    ..The pain hypersensitivity produced by the SNI model is not COX-2-dependent...
  74. ncbi request reprint Use and abuse of opioid analgesics: potential methods to prevent and deter non-medical consumption of prescription opioids
    Clifford J Woolf
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Curr Opin Investig Drugs 5:61-6. 2004
    ..This review highlights the extent of the illicit use of prescribed opiate analgesics and some of the steps, legal, educational and pharmaceutical, that can be taken to potentially reduce the risk of their misuse or diversion for abuse...
  75. ncbi request reprint Differential analgesic sensitivity of two distinct neuropathic pain models
    Isabelle Decosterd
    Anesthesiology Pain Research Group, Department of Anesthesiology and DBCM, University of Lausanne, Bugnon 9, 1005 Lausanne, Switzerland
    Anesth Analg 99:457-63, table of contents. 2004
    ..Multiple models are required, therefore, to study the mechanisms that contribute to neuropathic pain and to predict analgesic efficacy for different components of the neuropathic pain syndrome...
  76. pmc Delayed sympathetic dependence in the spared nerve injury (SNI) model of neuropathic pain
    Marie Pertin
    Anesthesiology Pain Research Unit, Department of Anesthesiology, University Hospital Center and University of Lausanne, Lausanne, Switzerland
    Mol Pain 3:21. 2007
    ..We investigated whether neuropathic pain-related behavior in the spared nerve injury (SNI) rat model is dependent on the sympathetic nervous system...
  77. ncbi request reprint Prostaglandin E2 receptor EP4 contributes to inflammatory pain hypersensitivity
    Chung Ren Lin
    Department of Anesthesiology, Chang Gung Memorial Hospital, Kaohsiung Medical Center, Chung Gang University, Taiwan, Republic of China
    J Pharmacol Exp Ther 319:1096-103. 2006
    ..AH23848 also reduces the PGE(2)-mediated sensitization of capsaicin-evoked currents in DRG neurons in vitro. These data suggest that EP4 is a potential target for the pharmacological treatment of inflammatory pain...
  78. ncbi request reprint The pattern of expression of the voltage-gated sodium channels Na(v)1.8 and Na(v)1.9 does not change in uninjured primary sensory neurons in experimental neuropathic pain models
    Isabelle Decosterd
    Department of Anesthesiology, Centre Hospitalier Universitaire Vaudois, 1011, Lausanne, Switzerland
    Pain 96:269-77. 2002
    ....
  79. ncbi request reprint Progressive tactile hypersensitivity after a peripheral nerve crush: non-noxious mechanical stimulus-induced neuropathic pain
    Isabelle Decosterd
    Anesthesiology Pain Research Group, Department of Anesthesiology, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland
    Pain 100:155-62. 2002
    ..Tactile stimulation of regenerating afferents but not spared non-injured afferents, can induce, therefore, PTH and such a stimulus-induced alteration in pain processing may contribute to clinical neuropathic pain...
  80. ncbi request reprint Upregulation of the voltage-gated sodium channel beta2 subunit in neuropathic pain models: characterization of expression in injured and non-injured primary sensory neurons
    Marie Pertin
    Anesthesiology Pain Research Group, Department of Anesthesiology, Lausanne University Hospital, CH 1011 Lausanne, Switzerland
    J Neurosci 25:10970-80. 2005
    ....
  81. ncbi request reprint Development of neuropathic pain in the rat spared nerve injury model is not prevented by a peripheral nerve block
    Marc R Suter
    Anesthesiology Pain Research Group, University Hospital Lausanne, Switzerland
    Anesthesiology 99:1402-8. 2003
    ....
  82. pmc Cannabinoids mediate analgesia largely via peripheral type 1 cannabinoid receptors in nociceptors
    Nitin Agarwal
    Institute for Pharmacology, University of Heidelberg, Im Neuenheimer Feld, Heidelberg, 69120 Germany
    Nat Neurosci 10:870-9. 2007
    ....
  83. ncbi request reprint A conditional deletion of the NR1 subunit of the NMDA receptor in adult spinal cord dorsal horn reduces NMDA currents and injury-induced pain
    Samantha M South
    Department of Pharmacology, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Neurosci 23:5031-40. 2003
    ....
  84. ncbi request reprint The prostaglandin E2 receptor-1 (EP-1) mediates acid-induced visceral pain hypersensitivity in humans
    Sanchoy Sarkar
    Department of GI Science, Clinical Sciences Building, University of Manchester, Hope Hospital, Salford M6 8HD, UK
    Gastroenterology 124:18-25. 2003
    ..The purpose of this study was to determine whether acid-induced pain hypersensitivity within the non-acid-exposed esophagus (secondary hyperalgesia) is mediated by PGE(2) activation of the EP-1 receptor...
  85. ncbi request reprint Adult neuron survival strategies--slamming on the brakes
    Susanna C Benn
    Day Neuromuscular Research Lab, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
    Nat Rev Neurosci 5:686-700. 2004
    ..Loss or reduced activity of these intrinsic anti-apoptotic 'brakes' might contribute to or accelerate neurodegeneration, whereas their activation might rescue neurons from injury or genetic abnormalities...