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Conference Paper: Dexmedetomidine enhances cerebral cortex GIRK1 protein expression and attenuates acute postoperative pain in rats

TitleDexmedetomidine enhances cerebral cortex GIRK1 protein expression and attenuates acute postoperative pain in rats
Authors
KeywordsBiology
Issue Date2015
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The 2015 Annual Meeting of Experimental Biology (EB 2015), Boston, MA., 28 March-1 April 2015. In The FASEB Journal, 2015, v. 29 meeting abstracts, abstract no. LB503 How to Cite?
AbstractDexmedetomidine (DEX), a highly selective α2-adrenoceptor agonist, produces both sedative and antinociceptive action. However, the mechanism for DEX analgesia remains unclear. Opening of G protein-activated inwardly rectifying K+ (GIRK) channels at spinal sites are involved in antinociception induced by opioid and no-opioid receptor agonists (Pain. 2013;154(12):2853-9). We investigated the antihyperalgesic effects induced by intravenous administration of DEX in acute incisional pain model in rats and its potential effect on the expression of GIRK1 at the supraspinal sites. The hyperalgesic effects induced by the plantar incision were verified by a significant and transient decrease in the mechanical paw withdrawal threshold for 24 hours (h) after hindpaw incision. The decreases of paw withdrawal threshold at 0.5h, 1h, 2h, 4h after incision were significantly suppressed by intravenous pre-administration of 5 or 10 ug/kg of DEX. Furthermore, pretreatment with DEX increased the expression of GIRK1 in the cerebral cortex at 2h and 4h after plantar incision as assessed by immunofluorescence and western blotting. It is concluded that administration of DEX before surgery induces antihyperalgesic effects in rats suffering from acute incision pain and that stimulation of GIRK1 expression in the cerebral cortex may represent a mechanism whereby DEX confers antinociception in acute postoperative pain.
DescriptionSession: Pharmacology - Central Nervous System Pharmacology
Open Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/219017
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorWang, LZ-
dc.contributor.authorWu, ZK-
dc.contributor.authorLiu, SM-
dc.contributor.authorLi, H-
dc.contributor.authorXia, Z-
dc.contributor.authorHuang, HS-
dc.date.accessioned2015-09-18T07:10:28Z-
dc.date.available2015-09-18T07:10:28Z-
dc.date.issued2015-
dc.identifier.citationThe 2015 Annual Meeting of Experimental Biology (EB 2015), Boston, MA., 28 March-1 April 2015. In The FASEB Journal, 2015, v. 29 meeting abstracts, abstract no. LB503-
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/219017-
dc.descriptionSession: Pharmacology - Central Nervous System Pharmacology-
dc.descriptionOpen Access Journal-
dc.description.abstractDexmedetomidine (DEX), a highly selective α2-adrenoceptor agonist, produces both sedative and antinociceptive action. However, the mechanism for DEX analgesia remains unclear. Opening of G protein-activated inwardly rectifying K+ (GIRK) channels at spinal sites are involved in antinociception induced by opioid and no-opioid receptor agonists (Pain. 2013;154(12):2853-9). We investigated the antihyperalgesic effects induced by intravenous administration of DEX in acute incisional pain model in rats and its potential effect on the expression of GIRK1 at the supraspinal sites. The hyperalgesic effects induced by the plantar incision were verified by a significant and transient decrease in the mechanical paw withdrawal threshold for 24 hours (h) after hindpaw incision. The decreases of paw withdrawal threshold at 0.5h, 1h, 2h, 4h after incision were significantly suppressed by intravenous pre-administration of 5 or 10 ug/kg of DEX. Furthermore, pretreatment with DEX increased the expression of GIRK1 in the cerebral cortex at 2h and 4h after plantar incision as assessed by immunofluorescence and western blotting. It is concluded that administration of DEX before surgery induces antihyperalgesic effects in rats suffering from acute incision pain and that stimulation of GIRK1 expression in the cerebral cortex may represent a mechanism whereby DEX confers antinociception in acute postoperative pain.-
dc.languageeng-
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journal-
dc.subjectBiology-
dc.titleDexmedetomidine enhances cerebral cortex GIRK1 protein expression and attenuates acute postoperative pain in rats-
dc.typeConference_Paper-
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hk-
dc.identifier.authorityXia, Z=rp00532-
dc.identifier.hkuros252697-
dc.identifier.volume29-
dc.identifier.issuemeeting abstracts-
dc.publisher.placeUnited States-

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