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Genomes and Genes | C J WoolfSummaryAffiliation: Harvard University Country: USA Publications
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Publications
Neuroscience. It takes more than two to NogoClifford 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
Exploiting microarrays to reveal differential gene expression in the nervous systemRobert 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...- Replicate high-density rat genome oligonucleotide microarrays reveal hundreds of regulated genes in the dorsal root ganglion after peripheral nerve injuryMichael 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... - Transcriptional and posttranslational plasticity and the generation of inflammatory painC 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... - Neuronal plasticity: increasing the gain in painC 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.... - Axonal injury-dependent induction of the peripheral benzodiazepine receptor in small-diameter adult rat primary sensory neuronsLaurie 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... - Runx1 determines nociceptive sensory neuron phenotype and is required for thermal and neuropathic painChih 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... - Disruption of ErbB receptor signaling in adult non-myelinating Schwann cells causes progressive sensory lossSuzhen Chen
Division of Neuroscience, Children s Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, Massachusetts 02115, USA
Nat Neurosci 6:1186-93. 2003.... - 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 painShan-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... - Direct activation of rat spinal dorsal horn neurons by prostaglandin E2H 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... 
Ro5-4864 promotes neonatal motor neuron survival and nerve regeneration in adult ratsCharles 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...- Detection of cold pain, cold allodynia and cold hyperalgesia in freely behaving ratsAndrew 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... - Selective up-regulation of the growth arrest DNA damage-inducible gene Gadd45 alpha in sensory and motor neurons after peripheral nerve injuryKatia 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... - Nociceptive-specific activation of ERK in spinal neurons contributes to pain hypersensitivityR 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... - The transcription factor ATF-3 promotes neurite outgrowthRhona 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... - Removal of GABAergic inhibition facilitates polysynaptic A fiber-mediated excitatory transmission to the superficial spinal dorsal hornHiroshi 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... - Peripheral axonal injury results in reduced mu opioid receptor pre- and post-synaptic action in the spinal cordTatsuro 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... - Nociceptors are interleukin-1beta sensorsAlexander 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... - 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 propertiesTarek 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... - Repulsive guidance molecule (RGMa), a DRAGON homologue, is a bone morphogenetic protein co-receptorJodie 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... - Partial peripheral nerve injury promotes a selective loss of GABAergic inhibition in the superficial dorsal horn of the spinal cordKimberly 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... - Peripheral noxious stimulation induces phosphorylation of the NMDA receptor NR1 subunit at the PKC-dependent site, serine-896, in spinal cord dorsal horn neuronsGary 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... - Dynamic changes in glypican-1 expression in dorsal root ganglion neurons after peripheral and central axonal injuryStefan 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... - Localization and action of Dragon (repulsive guidance molecule b), a novel bone morphogenetic protein coreceptor, throughout the reproductive axisYin 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... - The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivityFumimasa 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... - Periganglionic inflammation elicits a distally radiating pain hypersensitivity by promoting COX-2 induction in the dorsal root ganglionFumimasa Amaya
Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, USA
Pain 142:59-67. 2009.... - 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... - Multiple chronic pain states are associated with a common amino acid-changing allele in KCNS1Michael 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... - Hsp27 upregulation and phosphorylation is required for injured sensory and motor neuron survivalSusanna 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... - Neuronal plasticity and signal transduction in nociceptive neurons: implications for the initiation and maintenance of pathological painR 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... - Developmental expression of the TTX-resistant voltage-gated sodium channels Nav1.8 (SNS) and Nav1.9 (SNS2) in primary sensory neuronsS 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.... - Semaphorin 3A growth cone collapse requires a sequence homologous to tarantula hanatoxinO 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... - Prostanoids and pain: unraveling mechanisms and revealing therapeutic targetsTarek 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.... - DRAGON, a bone morphogenetic protein co-receptorTarek 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... - Complement induction in spinal cord microglia results in anaphylatoxin C5a-mediated pain hypersensitivityRobert 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... - Nociceptors--noxious stimulus detectorsClifford 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.... - Overcoming obstacles to developing new analgesicsClifford 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... - 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.... - Blocking caspase activity prevents transsynaptic neuronal apoptosis and the loss of inhibition in lamina II of the dorsal horn after peripheral nerve injuryJoachim 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... - Role of the peripheral benzodiazepine receptor in sensory neuron regenerationCharles 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... - p38 MAPK activation by NGF in primary sensory neurons after inflammation increases TRPV1 levels and maintains heat hyperalgesiaRu 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.... - Central sensitization: implications for the diagnosis and treatment of painClifford J Woolf
FM Kirby Neurobiology Center, Children s Hospital Boston, Department of Neurobiology, Harvard Medical School, Boston, MA, USA
Pain 152:S2-15. 2011.... - 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 sensitizationYasuhiko 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.... - TRPA1 contributes to cold, mechanical, and chemical nociception but is not essential for hair-cell transductionKelvin 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... - ERK MAP kinase activation in superficial spinal cord neurons induces prodynorphin and NK-1 upregulation and contributes to persistent inflammatory pain hypersensitivityRu 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... - Utilization of an HSV-based amplicon vector encoding the axonal marker hPLAP to follow neurite outgrowth in cultured DRG neuronsRhona 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... - Bradykinin enhances AMPA and NMDA receptor activity in spinal cord dorsal horn neurons by activating multiple kinases to produce pain hypersensitivityTatsuro 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... - High basal expression and injury-induced down regulation of two regulator of G-protein signaling transcripts, RGS3 and RGS4 in primary sensory neuronsMichael 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... - Central sensitization: a generator of pain hypersensitivity by central neural plasticityAlban 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.... - Peripheral nerve injury alters excitatory synaptic transmission in lamina II of the rat dorsal hornTatsuro 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... - Low-dose methotrexate reduces peripheral nerve injury-evoked spinal microglial activation and neuropathic pain behavior in ratsJoachim 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... - The neuropathic pain triad: neurons, immune cells and gliaJoachim 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.... - Loss of inhibitory interneurons in the dorsal spinal cord and elevated itch in Bhlhb5 mutant miceSarah 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... - 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... - COX2 in CNS neural cells mediates mechanical inflammatory pain hypersensitivity in miceDaniel 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... - Neuropathic pain: a maladaptive response of the nervous system to damageMichael 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... - Inhibition of nociceptors by TRPV1-mediated entry of impermeant sodium channel blockersAlexander M Binshtok
Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
Nature 449:607-10. 2007.... - GDNF selectively promotes regeneration of injury-primed sensory neurons in the lesioned spinal cordCharles 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... - ERK is sequentially activated in neurons, microglia, and astrocytes by spinal nerve ligation and contributes to mechanical allodynia in this neuropathic pain modelZhi-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... - Bradykinin and peripheral sensitizationHaibin 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.... - ATF3 increases the intrinsic growth state of DRG neurons to enhance peripheral nerve regenerationRhona 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... - Bradykinin produces pain hypersensitivity by potentiating spinal cord glutamatergic synaptic transmissionHaibin 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... - Targeting of sodium channel blockers into nociceptors to produce long-duration analgesia: a systematic study and reviewD 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... - Gabapentin-- actions on adult superficial dorsal horn neuronsK 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... - Bone morphogenetic protein signaling by hemojuvelin regulates hepcidin expressionJodie 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... - Dissecting out mechanisms responsible for peripheral neuropathic pain: implications for diagnosis and therapyClifford 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... - No DREAM, No pain. Closing the spinal gateMichael 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... - Pain: moving from symptom control toward mechanism-specific pharmacologic managementClifford J Woolf
Neural Plasticity Research Group, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
Ann Intern Med 140:441-51. 2004 - Pain TRPsHaibin 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.... - Central sensitization: uncovering the relation between pain and plasticityClifford J Woolf
Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
Anesthesiology 106:864-7. 2007 - Implications of recent advances in the understanding of pain pathophysiology for the assessment of pain in patientsC J Woolf
Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown 02129, USA
Pain . 1999.... - Transport and localization of the DEG/ENaC ion channel BNaC1alpha to peripheral mechanosensory terminals of dorsal root ganglia neuronsJ 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... - Cyclooxygenase 2 expression in the spared nerve injury model of neuropathic painD 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... - Use and abuse of opioid analgesics: potential methods to prevent and deter non-medical consumption of prescription opioidsClifford 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... - Differential analgesic sensitivity of two distinct neuropathic pain modelsIsabelle 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... - Delayed sympathetic dependence in the spared nerve injury (SNI) model of neuropathic painMarie 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... - Prostaglandin E2 receptor EP4 contributes to inflammatory pain hypersensitivityChung-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... - 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 modelsIsabelle Decosterd
Department of Anesthesiology, Centre Hospitalier Universitaire Vaudois, 1011, Lausanne, Switzerland
Pain 96:269-77. 2002.... - Progressive tactile hypersensitivity after a peripheral nerve crush: non-noxious mechanical stimulus-induced neuropathic painIsabelle 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... - Upregulation of the voltage-gated sodium channel beta2 subunit in neuropathic pain models: characterization of expression in injured and non-injured primary sensory neuronsMarie Pertin
Anesthesiology Pain Research Group, Department of Anesthesiology, Lausanne University Hospital, CH 1011 Lausanne, Switzerland
J Neurosci 25:10970-80. 2005.... - Development of neuropathic pain in the rat spared nerve injury model is not prevented by a peripheral nerve blockMarc R Suter
Anesthesiology Pain Research Group, University Hospital Lausanne, Switzerland
Anesthesiology 99:1402-8. 2003..It is unlikely that injury discharge at the time of nerve damage or the early onset of ectopic discharges arising from the injury site contributes significantly to the persistence of stimulus-evoked neuropathic pain in this model... - Cannabinoids mediate analgesia largely via peripheral type 1 cannabinoid receptors in nociceptorsNitin Agarwal
Institute for Pharmacology, University of Heidelberg, Im Neuenheimer Feld, Heidelberg, 69120 Germany
Nat Neurosci 10:870-9. 2007.... - A conditional deletion of the NR1 subunit of the NMDA receptor in adult spinal cord dorsal horn reduces NMDA currents and injury-induced painSamantha M South
Department of Pharmacology, Weill Medical College of Cornell University, New York, New York 10021, USA
J Neurosci 23:5031-40. 2003.... - The prostaglandin E2 receptor-1 (EP-1) mediates acid-induced visceral pain hypersensitivity in humansSanchoy Sarkar
Department of GI Science, Clinical Sciences Building, University of Manchester, Hope Hospital, Salford M6 8HD, UK
Gastroenterology 124:18-25. 2003..CONCLUSIONS: The attenuation of secondary esophageal hyperalgesia by ZD6416 suggests that PGE(2), via the EP-1 receptor, contributes to human visceral pain hypersensitivity... - Adult neuron survival strategies--slamming on the brakesSusanna 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...