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Article: Interleukin 1β facilitates bone cancer pain in rats by enhancing NMDA receptor NR-1 subunit phosphorylation

TitleInterleukin 1β facilitates bone cancer pain in rats by enhancing NMDA receptor NR-1 subunit phosphorylation
Authors
Issue Date2008
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscience
Citation
Neuroscience, 2008, v. 154 n. 4, p. 1533-1538 How to Cite?
AbstractIt has been shown that interleukin-1β (IL-1β) facilitates nociception during neuropathic and inflammatory pain, but its involvement in bone cancer pain and its mechanisms have not previously been established. This study is an investigation of IL-1β spinal expression and the N-methyl-D-aspartate (NMDA) receptor (NMDAR) NR1 subunit phosphorylation during cancer pain, co-localization of IL-1 receptor type I (IL-1RI) and NMDAR in the spinal cord, and the effects of IL-1 receptor antagonist (IL-1ra) on NMDAR1 (NR1) phosphorylation and hyperalgesia in a rat model of bone cancer pain. Cancer was induced by injecting AT-3.1 prostate cancer cells into the tibia of the male Copenhagen rat. Phosphorylation of NR1, an essential subunit of the NMDAR, is known to modulate NMDAR activity and facilitate pain. Mechanical hyperalgesia, established by a decrease in paw withdrawal pressure threshold (PWPT), was measured at baseline and 2 h after IL-1ra treatment. IL-1ra was given (i.t.) daily for 7 days between days 13 and 19 after the cancer cell inoculation. Spinal cords were removed for Western blot to measure IL-1β and NR1 phosphorylation and for double immunostaining of IL-1RI and NR1. The data showed that 1) spinal IL-1β was up-regulated and NR1 phosphorylation was increased, 2) IL-1ra at 0.1 mg/rat significantly (P<0.05) inhibited mechanical hyperalgesia, increasing PWPT on day 14 from 71.1±3.1-85.3±4.6 g and on day 19 from 73.5.0±3.5-87.1±3.7 g, and inhibited NR1 phosphorylation compared with saline control, and 3) IL-1RI is localized in NR1-immunoreactive neurons within the spinal cord. The results suggest that spinal IL-1β enhances NR1 phosphorylation to facilitate bone cancer pain. © 2008 IBRO.
Persistent Identifierhttp://hdl.handle.net/10722/188604
ISSN
2015 Impact Factor: 3.231
2015 SCImago Journal Rankings: 1.768
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, RXen_US
dc.contributor.authorLiu, Ben_US
dc.contributor.authorLi, Aen_US
dc.contributor.authorWang, Len_US
dc.contributor.authorRen, Ken_US
dc.contributor.authorQiao, JTen_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorLao, Len_US
dc.date.accessioned2013-09-03T04:10:32Z-
dc.date.available2013-09-03T04:10:32Z-
dc.date.issued2008en_US
dc.identifier.citationNeuroscience, 2008, v. 154 n. 4, p. 1533-1538en_US
dc.identifier.issn0306-4522en_US
dc.identifier.urihttp://hdl.handle.net/10722/188604-
dc.description.abstractIt has been shown that interleukin-1β (IL-1β) facilitates nociception during neuropathic and inflammatory pain, but its involvement in bone cancer pain and its mechanisms have not previously been established. This study is an investigation of IL-1β spinal expression and the N-methyl-D-aspartate (NMDA) receptor (NMDAR) NR1 subunit phosphorylation during cancer pain, co-localization of IL-1 receptor type I (IL-1RI) and NMDAR in the spinal cord, and the effects of IL-1 receptor antagonist (IL-1ra) on NMDAR1 (NR1) phosphorylation and hyperalgesia in a rat model of bone cancer pain. Cancer was induced by injecting AT-3.1 prostate cancer cells into the tibia of the male Copenhagen rat. Phosphorylation of NR1, an essential subunit of the NMDAR, is known to modulate NMDAR activity and facilitate pain. Mechanical hyperalgesia, established by a decrease in paw withdrawal pressure threshold (PWPT), was measured at baseline and 2 h after IL-1ra treatment. IL-1ra was given (i.t.) daily for 7 days between days 13 and 19 after the cancer cell inoculation. Spinal cords were removed for Western blot to measure IL-1β and NR1 phosphorylation and for double immunostaining of IL-1RI and NR1. The data showed that 1) spinal IL-1β was up-regulated and NR1 phosphorylation was increased, 2) IL-1ra at 0.1 mg/rat significantly (P<0.05) inhibited mechanical hyperalgesia, increasing PWPT on day 14 from 71.1±3.1-85.3±4.6 g and on day 19 from 73.5.0±3.5-87.1±3.7 g, and inhibited NR1 phosphorylation compared with saline control, and 3) IL-1RI is localized in NR1-immunoreactive neurons within the spinal cord. The results suggest that spinal IL-1β enhances NR1 phosphorylation to facilitate bone cancer pain. © 2008 IBRO.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscienceen_US
dc.relation.ispartofNeuroscienceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntirheumatic Agents - Pharmacologyen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshBone Neoplasms - Complicationsen_US
dc.subject.meshFluorescent Antibody Techniqueen_US
dc.subject.meshHyperalgesia - Physiopathologyen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshInterleukin 1 Receptor Antagonist Protein - Pharmacologyen_US
dc.subject.meshInterleukin-1Beta - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshNeurons - Drug Effects - Metabolismen_US
dc.subject.meshPain - Etiology - Physiopathologyen_US
dc.subject.meshPhosphorylationen_US
dc.subject.meshRatsen_US
dc.subject.meshReceptors, N-Methyl-D-Aspartate - Drug Effects - Metabolismen_US
dc.subject.meshSpinal Cord - Drug Effects - Metabolismen_US
dc.subject.meshUp-Regulationen_US
dc.titleInterleukin 1β facilitates bone cancer pain in rats by enhancing NMDA receptor NR-1 subunit phosphorylationen_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.doi10.1016/j.neuroscience.2008.04.072en_US
dc.identifier.pmid18554806-
dc.identifier.scopuseid_2-s2.0-45849117181en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-45849117181&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume154en_US
dc.identifier.issue4en_US
dc.identifier.spage1533en_US
dc.identifier.epage1538en_US
dc.identifier.isiWOS:000257677900036-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridZhang, RX=7404864527en_US
dc.identifier.scopusauthoridLiu, B=55720712900en_US
dc.identifier.scopusauthoridLi, A=16245342100en_US
dc.identifier.scopusauthoridWang, L=9036448600en_US
dc.identifier.scopusauthoridRen, K=7102272533en_US
dc.identifier.scopusauthoridQiao, JT=7103301572en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridLao, L=7005681883en_US

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