Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2001-5-24
pubmed:abstractText
Metabotropic glutamate receptors are expressed abundantly in the spinal cord and have been shown to play important roles in the modulation of nociceptive transmission and plasticity. Most previous studies have focused on the group I metabotropic glutamate receptors (mGluR1 and mGluR5) and activation of phospholipase C signaling by these receptors in modulating nociception. Recently, it was shown that the extracellular signal-regulated kinases (ERKs)/mitogen-activated protein kinases are activated in spinal cord dorsal horn neurons in response to stimulation of nociceptors and that ERK signaling is involved in nociceptive plasticity. In the present studies, we sought to test the hypothesis that group I mGluRs modulate nociceptive transmission or plasticity via modulation of ERK signaling in dorsal horn neurons. We show that activation of mGluR1 and mGluR5 leads to activation of ERK1 and ERK2 in the spinal cord. Furthermore, we find that inflammation-evoked ERK activation, which is required for nociceptive plasticity, is downstream of mGluR1 and mGluR5. Finally, we show colocalization of group I mGluRs with activated ERK in dorsal horn neurons. These results show that mGluR1 and mGluR5 are activated in dorsal horn neurons in response to peripheral inflammation and that activation of these group I mGluRs leads to activation of ERK1 and ERK2, resulting in enhanced pain sensitivity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/3,5-dihydroxyphenylglycine, http://linkedlifedata.com/resource/pubmed/chemical/Excitatory Amino Acid Agonists, http://linkedlifedata.com/resource/pubmed/chemical/Excitatory Amino Acid Antagonists, http://linkedlifedata.com/resource/pubmed/chemical/Formaldehyde, http://linkedlifedata.com/resource/pubmed/chemical/Glycine, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 1, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 3, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Metabotropic Glutamate, http://linkedlifedata.com/resource/pubmed/chemical/Resorcinols, http://linkedlifedata.com/resource/pubmed/chemical/metabotropic glutamate receptor 5, http://linkedlifedata.com/resource/pubmed/chemical/metabotropic glutamate receptor...
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3771-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11356865-Alternative Splicing, pubmed-meshheading:11356865-Animals, pubmed-meshheading:11356865-Behavior, Animal, pubmed-meshheading:11356865-Enzyme Activation, pubmed-meshheading:11356865-Excitatory Amino Acid Agonists, pubmed-meshheading:11356865-Excitatory Amino Acid Antagonists, pubmed-meshheading:11356865-Formaldehyde, pubmed-meshheading:11356865-Glycine, pubmed-meshheading:11356865-Hindlimb, pubmed-meshheading:11356865-Immunohistochemistry, pubmed-meshheading:11356865-Inflammation, pubmed-meshheading:11356865-Mice, pubmed-meshheading:11356865-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:11356865-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:11356865-Mitogen-Activated Protein Kinases, pubmed-meshheading:11356865-Neuronal Plasticity, pubmed-meshheading:11356865-Pain Measurement, pubmed-meshheading:11356865-Posterior Horn Cells, pubmed-meshheading:11356865-Receptors, Metabotropic Glutamate, pubmed-meshheading:11356865-Resorcinols, pubmed-meshheading:11356865-Signal Transduction
pubmed:year
2001
pubmed:articleTitle
Metabotropic glutamate receptor subtypes 1 and 5 are activators of extracellular signal-regulated kinase signaling required for inflammatory pain in mice.
pubmed:affiliation
Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't