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Seizure susceptibility in immature brain due to lack of COX-2-induced PGF2α.

DC Field Value Language
dc.contributor.authorChung, JI-
dc.contributor.authorKim, AY-
dc.contributor.authorLee, SH-
dc.contributor.authorBaik, EJ-
dc.date.accessioned2014-04-28T05:15:53Z-
dc.date.available2014-04-28T05:15:53Z-
dc.date.issued2013-
dc.identifier.issn0014-4886-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/9850-
dc.description.abstractThe immature brain is prone to seizure; however, the mechanism underlying this vulnerability has not been clarified. Febrile seizure is common in young children, and the use of non-steroidal anti-inflammatory drugs for febrile seizure is not recommended. In previous studies, we established that prostaglandin (PG) F2α, a product of cyclooxygenase (COX), acts as an endogenous anticonvulsant in the adult mouse. Therefore, we assumed that COX-2 activity was involved with seizure susceptibility in early life. In the present study, immature mice (postnatal day 9) were far more prone to kainic acid (KA)-induced seizures than mature mice (after postnatal day 35). Seizure activity began later in immature mice, but was more severe and was unaffected by a potent COX inhibitor, indomethacin; in contrast, indomethacin aggravated seizure activity in mature mice. Immature mouse brains exhibited little basal COX-2 expression and little KA-induced COX-2 induction, while KA-induced COX-2 expression and PGF2α release were prominent in mature brains. During brain development, COX expression was increased and glycosylated in an age-dependent manner, which was necessary for COX enzyme activity. Intracisternal PGF2α administration also reduced KA-induced seizure activity and mortality. Taken together, low COX activity and the resulting deficiency of PGF2α may be an essential cause of increased seizure susceptibility in the immature brain.-
dc.language.isoen-
dc.subject.MESHAge Factors-
dc.subject.MESHAnimals-
dc.subject.MESHAnimals, Newborn-
dc.subject.MESHBrain/drug effects/*growth & development/*metabolism-
dc.subject.MESHCells, Cultured-
dc.subject.MESHCyclooxygenase 2/*biosynthesis-
dc.subject.MESHDinoprost/administration & dosage/*biosynthesis-
dc.subject.MESHDisease Susceptibility-
dc.subject.MESHGlycosylation-
dc.subject.MESHMice-
dc.subject.MESHSeizures/*metabolism-
dc.subject.MESHUp-Regulation/physiology-
dc.titleSeizure susceptibility in immature brain due to lack of COX-2-induced PGF2α.-
dc.typeArticle-
dc.identifier.pmid24005111-
dc.identifier.urlhttp://linkinghub.elsevier.com/retrieve/pii/S0014-4886(13)00254-9-
dc.contributor.affiliatedAuthor이, 수환-
dc.contributor.affiliatedAuthor백, 은주-
dc.type.localJournal Papers-
dc.identifier.doi10.1016/j.expneurol.2013.08.014-
dc.citation.titleExperimental neurology-
dc.citation.volume249-
dc.citation.date2013-
dc.citation.startPage95-
dc.citation.endPage103-
dc.identifier.bibliographicCitationExperimental neurology, 249:95-103, 2013-
dc.identifier.eissn1090-2430-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
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