Research Topics
Genomes and Genes | Michael CostiganSummaryAffiliation: Massachusetts General Hospital Country: USA Publications
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Publications
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...
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...
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...
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...
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...
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...
Analgesia by inhibiting tetrahydrobiopterin synthesisMichael 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...
The BMP coreceptor RGMb promotes while the endogenous BMP antagonist noggin reduces neurite outgrowth and peripheral nerve regeneration by modulating BMP signalingChi 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...
GCH1, BH4 and painAlban Latremoliere
FM Kirby Neurobiology Center, Children s Hospital Boston, Harvard Medical School, Boston, MA 02115, USA
Curr Pharm Biotechnol 12:1728-41. 2011..We explain the nature of the GCH1 reduced-function haplotype and set out the potential for a ' BH4 blocking' drug as a novel analgesic...
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...
Accelerating axonal growth promotes motor recovery after peripheral nerve injury in miceChi 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...
GTP cyclohydrolase and tetrahydrobiopterin regulate pain sensitivity and persistenceIrmgard Tegeder
Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Room 4309, Charlestown, Massachusetts 02129, USA
Nat Med 12:1269-77. 2006..BH4 is therefore an intrinsic regulator of pain sensitivity and chronicity, and the GTP cyclohydrolase haplotype is a marker for these traits...
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...
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...
Research Grants
- The genetic basis of pain sensitivityMichael Costigan; Fiscal Year: 2006....
