Linked Life Data

16600520

Source:http://linkedlifedata.com/resource/pubmed/id/16600520

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-5-29
pubmed:abstractText
S100beta is a calcium-binding peptide produced mainly by astrocytes that exerts paracrine and autocrine effects on neurons and glia. We have previously shown that S100beta is markedly elevated at the mRNA level in the spinal cord following peripheral inflammation, intraplantar administration of complete Freund's adjuvant in the rat. The purpose of the present study was to further investigate the role of astrocytic S100beta in mediating behavioral hypersensitivity in rodent models of persistent pain. First, we assessed the lumbar spinal cord expression of S100beta at the mRNA and protein level using real-time RT-PCR, Western blot and immunohistochemistry analysis following L5 spinal nerve transection in rats, a rodent model of neuropathic pain. Second, we assessed behavioral hypersensitivity (mechanical allodynia) in wild type and genetically modified mice lacking or overexpressing S100beta following L5 spinal nerve transection. Third, we assessed the expression level of S100beta protein in the CD1 wild type mice after nerve injury. We report that lumbar spinal S100beta mRNA steadily increased from days 4-28 after nerve injury. S100beta protein in the lumbar spinal cord was significantly increased in both rats and mice at day 14 following nerve injury as compared with sham control groups. S100beta genetically deficient mice displayed significantly increased tactile thresholds (reduced response to non-noxious stimuli) after nerve injury as compared with the wild type group. S100beta overexpressing mice displayed significantly decreased tactile threshold responses (enhanced response to non-noxious stimuli). Together, these results from both series of experiments using a peripheral nerve injury model in two different species implicate the involvement of glial-derived S100beta in the pathophysiology of neuropathic pain.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
140
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1003-10
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16600520-Animals, pubmed-meshheading:16600520-Astrocytes, pubmed-meshheading:16600520-Behavior, Animal, pubmed-meshheading:16600520-Disease Models, Animal, pubmed-meshheading:16600520-Female, pubmed-meshheading:16600520-Glial Fibrillary Acidic Protein, pubmed-meshheading:16600520-Gliosis, pubmed-meshheading:16600520-Hyperalgesia, pubmed-meshheading:16600520-Immunohistochemistry, pubmed-meshheading:16600520-Male, pubmed-meshheading:16600520-Mice, pubmed-meshheading:16600520-Mice, Knockout, pubmed-meshheading:16600520-Mice, Transgenic, pubmed-meshheading:16600520-Nerve Growth Factors, pubmed-meshheading:16600520-Neuralgia, pubmed-meshheading:16600520-Pain Threshold, pubmed-meshheading:16600520-Peripheral Nervous System Diseases, pubmed-meshheading:16600520-Physical Stimulation, pubmed-meshheading:16600520-Posterior Horn Cells, pubmed-meshheading:16600520-RNA, Messenger, pubmed-meshheading:16600520-Rats, pubmed-meshheading:16600520-Rats, Sprague-Dawley, pubmed-meshheading:16600520-S100 Proteins, pubmed-meshheading:16600520-Spinal Nerves, pubmed-meshheading:16600520-Up-Regulation
pubmed:year
2006
pubmed:articleTitle
Role of astrocytic S100beta in behavioral hypersensitivity in rodent models of neuropathic pain.
pubmed:affiliation
Department of Anesthesiology, Dartmouth Medical School, Lebanon, NH 03756, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural