Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2009-11-16
pubmed:abstractText
The mitogen-activated protein kinase/extracellular regulated kinase (MAPK/ERK) pathway plays a key role in mediating estrogen actions in the brain and neuronal sensitization during inflammation. Estrogen status is a risk factor in chronic temporomandibular muscle/joint (TMJ) disorders; however, the basis for this relationship is not known. The present study tested the hypothesis that estrogen status acts through the MAPK/ERK signaling pathway to alter TMJ nociceptive processing. Single TMJ-responsive neurons were recorded in laminae I-II at the spinomedullary (Vc/C(1-2)) junction in naïve ovariectomized (OvX) female rats treated for 2 days with high-dose (20 microg/day; HE2) or low-dose estradiol (2 microg/day; LE2) and after chronic inflammation of the TMJ region by complete Freund's adjuvant for 12-14 days. Intra-TMJ injection of ATP (1 mM) was used to activate Vc/C(1-2) neurons. The MAPK/ERK inhibitor (PD98059, 0.01-1 mM) was applied topically to the dorsal Vc/C(1-2) surface at the site of recording 10 min prior to each ATP stimulus. In naïve HE2 rats, low-dose PD98059 caused a maximal inhibition of ATP-evoked activity, whereas even high doses had only minor effects on units in LE2 rats. By contrast, after chronic TMJ inflammation, PD98059 produced a marked and similar dose-related inhibition of ATP-evoked activity in HE2 and LE2 rats. These results suggested that E2 status and chronic inflammation acted, at least in part, through a common MAPK/ERK-dependent signaling pathway to enhance TMJ nociceptive processing by laminae I-II neurons at the spinomedullary junction region.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1873-7544
pubmed:author
pubmed:issnType
Electronic
pubmed:day
29
pubmed:volume
164
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1813-20
pubmed:dateRevised
2011-4-28
pubmed:meshHeading
pubmed-meshheading:19786077-Adenosine Triphosphate, pubmed-meshheading:19786077-Animals, pubmed-meshheading:19786077-Chronic Disease, pubmed-meshheading:19786077-Dose-Response Relationship, Drug, pubmed-meshheading:19786077-Enzyme Activation, pubmed-meshheading:19786077-Estradiol, pubmed-meshheading:19786077-Estrogens, pubmed-meshheading:19786077-Female, pubmed-meshheading:19786077-Inflammation, pubmed-meshheading:19786077-Mitogen-Activated Protein Kinases, pubmed-meshheading:19786077-Neurons, pubmed-meshheading:19786077-Ovariectomy, pubmed-meshheading:19786077-Pain, pubmed-meshheading:19786077-Rats, pubmed-meshheading:19786077-Rats, Sprague-Dawley, pubmed-meshheading:19786077-Signal Transduction, pubmed-meshheading:19786077-Skin, pubmed-meshheading:19786077-Temporomandibular Joint, pubmed-meshheading:19786077-Trigeminal Caudal Nucleus
pubmed:year
2009
pubmed:articleTitle
Chronic inflammation and estradiol interact through MAPK activation to affect TMJ nociceptive processing by trigeminal caudalis neurons.
pubmed:affiliation
Department of Diagnostic and Biological Sciences, University of Minnesota School of Dentistry, 18214 Moos Tower, Minneapolis, 515 Delaware Street SE, Minneapolis, MN 55455, USA. tashi004@umn.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural