PET imaging of brain inflammation during early epileptogenesis in a rat model of temporal lobe epilepsy

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dc.contributor.authorDedeurwaerdere, Sen_AU
dc.contributor.authorCallaghan, PDen_AU
dc.contributor.authorPham, TQen_AU
dc.contributor.authorRahardjo, GLen_AU
dc.contributor.authorAmhaoul, Hen_AU
dc.contributor.authorBerghofer, PJen_AU
dc.contributor.authorQuinlivan, Men_AU
dc.contributor.authorMattner, Fen_AU
dc.contributor.authorLoc'h, Cen_AU
dc.contributor.authorKatsifis, Aen_AU
dc.contributor.authorGrégoire, MCen_AU
dc.date.accessioned2014-11-25T00:41:25Zen_AU
dc.date.available2014-11-25T00:41:25Zen_AU
dc.date.issued2012-11-08en_AU
dc.date.statistics2014-11-25en_AU
dc.description.abstractBackground Recently, inflammatory cascades have been suggested as a target for epilepsy therapy. Positron emission tomography (PET) imaging offers the unique possibility to evaluate brain inflammation longitudinally in a non-invasive translational manner. This study investigated brain inflammation during early epileptogenesis in the post-kainic acid-induced status epilepticus (KASE) model with post-mortem histology and in vivo with [18F]-PBR111 PET. Methods Status epilepticus (SE) was induced (N = 13) by low-dose injections of KA, while controls (N = 9) received saline. Translocator protein (TSPO) expression and microglia activation were assessed with [125I]-CLINDE autoradiography and OX-42 immunohistochemistry, respectively, 7 days post-SE. In a subgroup of rats, [18F]-PBR111 PET imaging with metabolite-corrected input function was performed before post-mortem evaluation. [18F]-PBR111 volume of distribution (V t) in volume of interests (VOIs) was quantified by means of kinetic modelling and a VOI/metabolite-corrected plasma activity ratio. Results Animals with substantial SE showed huge overexpression of TSPO in vitro in relevant brain regions such as the hippocampus and amygdala (P < 0.001), while animals with mild symptoms displayed a smaller increase in TSPO in amygdala only (P < 0.001). TSPO expression was associated with OX-42 signal but without obvious cell loss. Similar in vivo [18F]-PBR111 increases in V t and the simplified ratio were found in key regions such as the hippocampus (P < 0.05) and amygdala (P < 0.01). Conclusion Both post-mortem and in vivo methods substantiate that the brain regions important in seizure generation display significant brain inflammation during epileptogenesis in the KASE model. This work enables future longitudinal investigation of the role of brain inflammation during epileptogenesis and evaluation of anti-inflammatory treatments. © 2012, Springer.en_AU
dc.identifier.articlenumber60en_AU
dc.identifier.citationDedeurwaerdere, S., Callaghan, P. D., Pham, T., Rahardjo, G. L., Amhaoul, H., Berghofer, P., Quinlivan, M., Mattner, F., Loc'h, C., Katsifis, A. & Grégoire, M. C. (2012). PET imaging of brain inflammation during early epileptogenesis in a rat model of temporal lobe epilepsy. EJNMMI Research, 2, 60. doi:10.1186/2191-219X-2-60en_AU
dc.identifier.govdoc5704en_AU
dc.identifier.issn1619-7070en_AU
dc.identifier.issn2191-219Xen_AU
dc.identifier.issue60en_AU
dc.identifier.journaltitleEJNMMI Researchen_AU
dc.identifier.urihttp://dx.doi.org/10.1186/2191-219X-2-60en_AU
dc.identifier.urihttp://apo.ansto.gov.au/dspace/handle/10238/6063en_AU
dc.identifier.volume2en_AU
dc.language.isoenen_AU
dc.publisherSpringer-Velagen_AU
dc.subjectNervous system diseasesen_AU
dc.subjectEpilepsyen_AU
dc.subjectPositron computed tomographyen_AU
dc.subjectBrainen_AU
dc.subjectInflammationen_AU
dc.subjectIn vivoen_AU
dc.subjectRatsen_AU
dc.titlePET imaging of brain inflammation during early epileptogenesis in a rat model of temporal lobe epilepsyen_AU
dc.typeJournal Articleen_AU
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