Clifford J Woolf

Summary

Affiliation: Massachusetts General Hospital
Country: USA

Publications

  1. ncbi 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
  2. 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
  3. ncbi 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
  4. ncbi 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
  5. ncbi 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
  6. ncbi 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
  7. doi Mu and delta opioid receptors diverge
    Clifford J Woolf
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA
    Cell 137:987-8. 2009
  8. ncbi 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
  9. ncbi 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
  10. ncbi 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

Detail Information

Publications86

  1. ncbi 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...
  2. 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...
  3. ncbi 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...
  4. ncbi 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
  5. ncbi 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
  6. ncbi 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
    ....
  7. doi Mu and delta opioid receptors diverge
    Clifford J Woolf
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA
    Cell 137:987-8. 2009
    ..In mice, agonists for these receptors produce analgesia restricted to either noxious heat or mechanical stimuli, implying that the receptors act on distinct fibers to mediate completely different types of pain relief...
  8. ncbi 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...
  9. ncbi 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...
  10. ncbi 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...
  11. 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...
  12. ncbi 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...
  13. doi 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...
  14. ncbi 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
    ....
  15. 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...
  16. 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
    ....
  17. ncbi 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...
  18. ncbi 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...
  19. ncbi 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...
  20. ncbi 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...
  21. 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...
  22. ncbi 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...
  23. ncbi 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...
  24. ncbi 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
    ....
  25. ncbi 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...
  26. ncbi 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...
  27. pmc The BMP coreceptor RGMb promotes while the endogenous BMP antagonist noggin reduces neurite outgrowth and peripheral nerve regeneration by modulating BMP signaling
    Chi H E Ma
    F M Kirby Neurobiology Center, Children s Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 31:18391-400. 2011
    ..Our data suggest a positive modulatory contribution of RGMb and BMP signaling to neurite extension in vitro and early axonal regrowth after nerve injury in vivo and a negative effect of Noggin...
  28. ncbi 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...
  29. ncbi 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...
  30. ncbi 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...
  31. ncbi 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...
  32. ncbi 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
    ....
  33. ncbi 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...
  34. pmc Bacteria activate sensory neurons that modulate pain and inflammation
    Isaac M Chiu
    Kirby Neurobiology Center, Boston Children s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 501:52-7. 2013
    ..Thus, bacterial pathogens produce pain by directly activating sensory neurons that modulate inflammation, an unsuspected role for the nervous system in host-pathogen interactions. ..
  35. 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...
  36. 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...
  37. pmc Phenotyping the function of TRPV1-expressing sensory neurons by targeted axonal silencing
    Christian Brenneis
    F M Kirby Neurobiology Center, Children s Hospital Boston, Boston, Massachusetts 02115, USA
    J Neurosci 33:315-26. 2013
    ....
  38. 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...
  39. ncbi 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...
  40. 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...
  41. pmc Overexpression of the wild-type SPT1 subunit lowers desoxysphingolipid levels and rescues the phenotype of HSAN1
    Florian S Eichler
    Massachusetts General Hospital Neuroscience Center, Department of Neurology, Harvard Medical School, Boston, Massachusetts 02114, USA
    J Neurosci 29:14646-51. 2009
    ..This observation is consistent with the hypothesis that HSAN1 is the result of a gain-of-function mutation in SPTLC1 that leads to accumulation of a toxic metabolite...
  42. 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...
  43. ncbi 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...
  44. pmc Permeation and block of TRPV1 channels by the cationic lidocaine derivative QX-314
    Michelino Puopolo
    Dept of Neurobiology, Harvard Medical School, Boston, MA 02115, USA
    J Neurophysiol 109:1704-12. 2013
    ..We conclude that QX-314 is directly permeant in the "standard" pore formed by TRPV1 channels and does not require either pore dilation or activation of additional downstream channels for entry...
  45. 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...
  46. ncbi 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...
  47. 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...
  48. 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...
  49. pmc Coapplication of lidocaine and the permanently charged sodium channel blocker QX-314 produces a long-lasting nociceptive blockade in rodents
    Alexander M Binshtok
    Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Anesthesiology 111:127-37. 2009
    ..Because TRPV1 channels are also activated by lidocaine, the authors tested whether lidocaine can substitute for capsaicin to introduce QX-314 into nociceptors through TRPV1 channels and produce selective analgesia...
  50. pmc Capsaicin combined with local anesthetics preferentially prolongs sensory/nociceptive block in rat sciatic nerve
    Peter Gerner
    Department of Anesthesiology, Perioperative, and Pain Medicine, Brigham and Women s Hospital, Boston, MA 02115, USA
    Anesthesiology 109:872-8. 2008
    ..05% capsaicin, in a rat sciatic nerve block model...
  51. ncbi 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...
  52. pmc Activity-dependent silencing reveals functionally distinct itch-generating sensory neurons
    David P Roberson
    FM Kirby Neurobiology Center and Department of Neurology, Children s Hospital, Boston, Massachusetts, USA
    Nat Neurosci 16:910-8. 2013
    ....
  53. pmc Inflammation-induced decrease in voluntary wheel running in mice: a nonreflexive test for evaluating inflammatory pain and analgesia
    Enrique J Cobos
    Program in Neurobiology, F M Kirby Neurobiology Center, Children s Hospital Boston, Boston, MA 02115, USA
    Pain 153:876-84. 2012
    ....
  54. 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...
  55. pmc Accelerating axonal growth promotes motor recovery after peripheral nerve injury in mice
    Chi Him Eddie Ma
    Program in Neurobiology and F M Kirby Neurobiology Center, Children s Hospital Boston, and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts, USA
    J Clin Invest 121:4332-47. 2011
    ..Thus, absence of motor recovery after nerve damage may result from a failure of synapse reformation after prolonged denervation rather than a failure of axonal growth...
  56. ncbi 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...
  57. ncbi Mutant SPTLC1 dominantly inhibits serine palmitoyltransferase activity in vivo and confers an age-dependent neuropathy
    Alexander McCampbell
    Day Laboratory for Neuromuscular Research, Massachusetts General Hospital and Harvard Medical School, Charlestown, 02129, USA
    Hum Mol Genet 14:3507-21. 2005
    ..These mice represent a novel mouse model of peripheral neuropathy and confirm the link between mutant SPT and neuronal dysfunction...
  58. ncbi 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...
  59. ncbi RNAi blocks DYT1 mutant torsinA inclusions in neurons
    Norman Kock
    Departments of Neurology and Radiology, Massachusetts General Hospital, and Neuroscience Program, Harvard Medical School, Boston, USA
    Neurosci Lett 395:201-5. 2006
    ..Vector-delivered siRNAs have the potential to decrease the adverse effects of this mutant protein in neurons without affecting wild-type protein...
  60. ncbi Central sensitization and LTP: do pain and memory share similar mechanisms?
    Ru Rong Ji
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA
    Trends Neurosci 26:696-705. 2003
    ....
  61. pmc Analgesia by inhibiting tetrahydrobiopterin synthesis
    Michael Costigan
    FM Kirby Neurobiology Center, Children s Hospital Boston, and Department of Neurobiology, Harvard Medical School, 3 Blackfan Circle, CLS 12260, Boston, MA 02115, USA
    Curr Opin Pharmacol 12:92-9. 2012
    ..SPR is part of the BH4 synthesis cascade and is also upregulated by nerve injury. Inhibiting SPR will reduce BH4 levels and therefore should act as an analgesic. We propose SSZ as a novel anti-neuropathic pain medicine...
  62. pmc Deconstructing the neuropathic pain phenotype to reveal neural mechanisms
    Christian A von Hehn
    FM Kirby Neurobiology Center, Children s Hospital Boston, and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA
    Neuron 73:638-52. 2012
    ..The pain phenotype can serve therefore, as a window on underlying pathophysiological neural mechanisms and as a guide for developing personalized pain medicine...
  63. ncbi 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...
  64. 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...
  65. ncbi 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...
  66. pmc A novel tool for the assessment of pain: validation in low back pain
    Joachim Scholz
    Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, Massachusetts, United States of America
    PLoS Med 6:e1000047. 2009
    ..We have developed a tool for a standardized assessment of pain-related symptoms and signs that differentiates pain phenotypes independent of etiology...
  67. ncbi 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
    ....
  68. ncbi 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
    ....
  69. 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...
  70. ncbi 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...
  71. ncbi 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...
  72. ncbi 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...
  73. ncbi 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
    ....
  74. ncbi 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
  75. pmc BACE1 regulates voltage-gated sodium channels and neuronal activity
    Doo Yeon Kim
    Neurobiology of Disease Laboratory, Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Nat Cell Biol 9:755-64. 2007
    ..BACE1, by cleaving beta2, thus regulates Na(v)1 alpha-subunit levels and controls cell-surface sodium current densities. BACE1 inhibitors may normalize membrane excitability in Alzheimer's disease patients with elevated BACE1 activity...
  76. ncbi 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...
  77. ncbi 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...
  78. ncbi 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...
  79. ncbi 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
    ....
  80. ncbi 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. 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
    ....
  82. ncbi 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
    ....
  83. ncbi 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 The development and maintenance of human visceral pain hypersensitivity is dependent on the N-methyl-D-aspartate receptor
    Robert Paul Willert
    GI Science Group, Hope Hospital, Salford, United Kingdom
    Gastroenterology 126:683-92. 2004
    ..Our aims were to determine whether the development and maintenance of human visceral hypersensitivity is NMDA receptor mediated...
  85. ncbi 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...
  86. ncbi 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...