File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Interleukin-1ra inhibits Fos expression and hyperalgesia in rats

TitleInterleukin-1ra inhibits Fos expression and hyperalgesia in rats
Authors
Issue Date2007
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.neuroreport.com
Citation
Neuroreport, 2007, v. 18 n. 5, p. 495-498 How to Cite?
AbstractIt is known that interleukin-1β facilitates pain, but the mechanisms of this are not understood. This study investigated the role of interleukin-1β in the expression of Fos, a marker of neuronal activation, and hyperalgesia caused by injecting complete Freund's adjuvant into one hind paw of the rat. Interleukin-receptor antagonist (interleukin-1ra, 0.005 mg/rat) was given intrathecally twice, 24 h before complete Freund's adjuvant and immediately before complete Freund's adjuvant injection, to block interleukin-1β action. Fos expression was measured 2 h after complete Freund's adjuvant injection. Paw withdrawal latency was used to assess hyperalgesia. The findings were that interleukin-1ra inhibited inflammation-induced Fos expression and hyperalgesia, which suggests that endogenous interleukin-1β facilitates transmission of noxious messages at the spinal level by processes involving an enhanced Fos expression. © 2007 Lippincott Williams & Wilkins, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/188586
ISSN
2015 Impact Factor: 1.343
2015 SCImago Journal Rankings: 0.783
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Aen_US
dc.contributor.authorLao, Len_US
dc.contributor.authorWang, Yen_US
dc.contributor.authorZhang, Hen_US
dc.contributor.authorRen, Ken_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorZhang, Ren_US
dc.date.accessioned2013-09-03T04:10:27Z-
dc.date.available2013-09-03T04:10:27Z-
dc.date.issued2007en_US
dc.identifier.citationNeuroreport, 2007, v. 18 n. 5, p. 495-498en_US
dc.identifier.issn0959-4965en_US
dc.identifier.urihttp://hdl.handle.net/10722/188586-
dc.description.abstractIt is known that interleukin-1β facilitates pain, but the mechanisms of this are not understood. This study investigated the role of interleukin-1β in the expression of Fos, a marker of neuronal activation, and hyperalgesia caused by injecting complete Freund's adjuvant into one hind paw of the rat. Interleukin-receptor antagonist (interleukin-1ra, 0.005 mg/rat) was given intrathecally twice, 24 h before complete Freund's adjuvant and immediately before complete Freund's adjuvant injection, to block interleukin-1β action. Fos expression was measured 2 h after complete Freund's adjuvant injection. Paw withdrawal latency was used to assess hyperalgesia. The findings were that interleukin-1ra inhibited inflammation-induced Fos expression and hyperalgesia, which suggests that endogenous interleukin-1β facilitates transmission of noxious messages at the spinal level by processes involving an enhanced Fos expression. © 2007 Lippincott Williams & Wilkins, Inc.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.neuroreport.comen_US
dc.relation.ispartofNeuroReporten_US
dc.subject.meshAnimalsen_US
dc.subject.meshFreund's Adjuvanten_US
dc.subject.meshFunctional Laterality - Physiologyen_US
dc.subject.meshGene Expression Regulation - Drug Effectsen_US
dc.subject.meshHyperalgesia - Chemically Induced - Prevention & Controlen_US
dc.subject.meshInterleukin 1 Receptor Antagonist Protein - Therapeutic Useen_US
dc.subject.meshMaleen_US
dc.subject.meshPain Measurement - Methodsen_US
dc.subject.meshProto-Oncogene Proteins C-Fos - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.titleInterleukin-1ra inhibits Fos expression and hyperalgesia in ratsen_US
dc.typeArticleen_US
dc.identifier.emailLao, L: lxlao1@hku.hken_US
dc.identifier.authorityLao, L=rp01784en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/WNR.0b013e3280586839en_US
dc.identifier.pmid17496810-
dc.identifier.scopuseid_2-s2.0-34247593035en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34247593035&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume18en_US
dc.identifier.issue5en_US
dc.identifier.spage495en_US
dc.identifier.epage498en_US
dc.identifier.isiWOS:000245440900019-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLi, A=16245342100en_US
dc.identifier.scopusauthoridLao, L=7005681883en_US
dc.identifier.scopusauthoridWang, Y=7601488320en_US
dc.identifier.scopusauthoridZhang, H=51563012400en_US
dc.identifier.scopusauthoridRen, K=7102272533en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridZhang, R=7404864527en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats