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Blockade of spinal glutamate recycling produces paradoxical antinociception in rats with orofacial inflammatory pain

DC FieldValueLanguage
dc.contributor.author김성택-
dc.date.accessioned2018-03-26T17:04:27Z-
dc.date.available2018-03-26T17:04:27Z-
dc.date.issued2015-
dc.identifier.issn0278-5846-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/157143-
dc.description.abstractIn our current study, we investigated the role of spinal glutamate recycling in the development of orofacial inflammatory pain. DL-threo-β-benzyloxyaspartate (TBOA) or methionine sulfoximine (MSO) was administered intracisternally to block spinal glutamate transporter and glutamine synthetase activity in astroglia. Intracisternal administration of high dose TBOA (10 μg) produced thermal hyperalgesia in naïve rats but significantly attenuated the thermal hyperalgesia in rats that had been pretreated with interleukin (IL)-1β or Complete Freund's Adjuvant (CFA). In contrast, intracisternal injection of MSO produced anti-hyperalgesic effects against thermal stimuli in CFA-treated rats only. To confirm the paradoxical antinociceptive effects of TBOA and MSO, we examined changes in c-Fos expression in the medullary dorsal horn produced by thermal stimulation in naïve, IL-1β-, or CFA-treated rats, after intracisternal injections of TBOA and MSO. Intracisternal administration of TBOA significantly increased c-Fos immunoreactivity in naïve rats. In contrast, intracisternal administration of TBOA significantly decreased the up-regulation of c-Fos immunoreactivity in the medullary dorsal horn of IL-1β- and CFA-treated rats. However, intracisternal injection of MSO blocked the up-regulation of c-Fos immunoreactivity in CFA-treated rats only. We also investigated the effects of botulinum toxin type A (BoNT-A) on TBOA-induced paradoxical antinociception in CFA-treated rats, as BoNT-A inhibits the release of neurotransmitters, including glutamate. BoNT-A treatment reversed behavioral responses produced by intracisternal administration of TBOA in CFA-treated rats. These results suggest that the paradoxical responses produced by blocking glutamate transporters under inflammatory pain conditions are mediated by the modulation of glutamate release from presynaptic terminals. Moreover, blockade of glutamate reuptake could represent a new therapeutic target for the treatment of chronic inflammatory pain conditions.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherPergamon Press-
dc.relation.isPartOfPROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAmino Acid Transport System X-AG/antagonists & inhibitors*-
dc.subject.MESHAnimals-
dc.subject.MESHAspartic Acid/administration & dosage-
dc.subject.MESHAspartic Acid/pharmacology*-
dc.subject.MESHAspartic Acid/therapeutic use-
dc.subject.MESHAstrocytes/drug effects-
dc.subject.MESHBotulinum Toxins, Type A/pharmacology-
dc.subject.MESHFacial Pain/drug therapy*-
dc.subject.MESHFreund's Adjuvant/antagonists & inhibitors-
dc.subject.MESHFreund's Adjuvant/pharmacology-
dc.subject.MESHGlutamate-Ammonia Ligase/antagonists & inhibitors-
dc.subject.MESHGlutamic Acid/metabolism*-
dc.subject.MESHHyperalgesia/chemically induced-
dc.subject.MESHHyperalgesia/drug therapy*-
dc.subject.MESHInjections, Intraventricular-
dc.subject.MESHInterleukin-1beta/antagonists & inhibitors-
dc.subject.MESHInterleukin-1beta/pharmacology-
dc.subject.MESHMale-
dc.subject.MESHMethionine Sulfoximine/administration & dosage-
dc.subject.MESHMethionine Sulfoximine/pharmacology*-
dc.subject.MESHMethionine Sulfoximine/therapeutic use-
dc.subject.MESHNociception/drug effects*-
dc.subject.MESHRats-
dc.subject.MESHSpinal Cord Dorsal Horn/drug effects-
dc.subject.MESHSpinal Cord Dorsal Horn/physiology-
dc.titleBlockade of spinal glutamate recycling produces paradoxical antinociception in rats with orofacial inflammatory pain-
dc.typeArticle-
dc.contributor.collegeCollege of Dentistry-
dc.contributor.departmentDept. of Oral Medicine-
dc.contributor.googleauthorKui Y. Yang-
dc.contributor.googleauthorJun H. Mun-
dc.contributor.googleauthorKi D. Park-
dc.contributor.googleauthorMin J. Kim-
dc.contributor.googleauthorJin S. Ju-
dc.contributor.googleauthorSeong T. Kim-
dc.contributor.googleauthorYong C. Bae-
dc.contributor.googleauthorDong K. Ahn-
dc.identifier.doi10.1016/j.pnpbp.2014.10.011-
dc.contributor.localIdA00588-
dc.relation.journalcodeJ02554-
dc.identifier.eissn1878-4216-
dc.identifier.pmid25445477-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0278584614002024-
dc.subject.keywordGlutamate-
dc.subject.keywordGlutamate transporter-
dc.subject.keywordGlutamine synthetase inhibitor-
dc.subject.keywordOrofacial pain-
dc.subject.keywordParadoxical antinociception-
dc.contributor.alternativeNameKim, Seong Taek-
dc.contributor.affiliatedAuthorKim, Seong Taek-
dc.citation.volume57-
dc.citation.startPage100-
dc.citation.endPage109-
dc.identifier.bibliographicCitationPROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY, Vol.57 : 100-109, 2015-
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Orofacial Pain and Oral Medicine (구강내과학교실) > 1. Journal Papers

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