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dc.contributor.author Park, Dongseok -
dc.contributor.author Kim, Seungjoon -
dc.contributor.author Kim, Hyeonho -
dc.contributor.author Shin, Jungsu -
dc.contributor.author Jung, Hyeji -
dc.contributor.author Um, Ji Won -
dc.date.accessioned 2021-01-22T06:41:51Z -
dc.date.available 2021-01-22T06:41:51Z -
dc.date.created 2020-07-17 -
dc.date.issued 2020-12 -
dc.identifier.issn 0894-1491 -
dc.identifier.uri http://hdl.handle.net/20.500.11750/12572 -
dc.description.abstract IQSEC3, a guanine nucleotide exchange factor for ADP-ribosylation factors (ARF-GEFs) is specifically expressed at GABAergic synapses, and its loss increases seizure susceptibility in mice. However, the contribution of microglia to initiation and/or progression of seizures in IQSEC3-deficient mice has not been investigated. In the current study, we show that mice with hippocampal dentate gyrus (DG)-specific IQSEC3 knockdown (KD) exhibit microglial activation and death of DG granule cell. Furthermore, treatment of IQSEC3-KD mice with minocycline, an inhibitor of microglial activation, blocks DG granule neuron cell death and the occurrence of spontaneous seizures without affecting GABAergic synapse deficits or loss of somatostatin. Our results suggest that microglial activation is involved in a subset of IQSEC3-KD-induced epileptogenesis stages, and that its regulation could be an alternative strategy for managing epilepsy. © 2020 Wiley Periodicals LLC -
dc.language English -
dc.publisher John Wiley & Sons Inc. -
dc.title Seizure progression triggered byIQSEC3loss is mitigated by reducing activated microglia in mice -
dc.type Article -
dc.identifier.doi 10.1002/glia.23876 -
dc.identifier.scopusid 2-s2.0-85087705835 -
dc.identifier.bibliographicCitation GLIA, v.68, no.12, pp.2661 - 2673 -
dc.description.isOpenAccess FALSE -
dc.subject.keywordAuthor GABA -
dc.subject.keywordAuthor inhibitory synapse -
dc.subject.keywordAuthor IQSEC3 -
dc.subject.keywordAuthor microglia -
dc.subject.keywordAuthor minocycline -
dc.subject.keywordAuthor seizure -
dc.subject.keywordPlus BRAIN INFLAMMATION -
dc.subject.keywordPlus ANIMAL-MODELS -
dc.subject.keywordPlus MINOCYCLINE -
dc.subject.keywordPlus EPILEPSY -
dc.subject.keywordPlus EPILEPTOGENESIS -
dc.subject.keywordPlus MECHANISMS -
dc.subject.keywordPlus INNATE -
dc.citation.endPage 2673 -
dc.citation.number 12 -
dc.citation.startPage 2661 -
dc.citation.title GLIA -
dc.citation.volume 68 -
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Department of Brain Sciences Synapse Disorder Laboratory 1. Journal Articles

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