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    Astrocyte proliferation and morphology across disease progression in viral encephalitis-induced epilepsy (2025)

    Art
    Poster
    Autoren
    Egilmez, A. (WE 14)
    Weiß, E. (WE 14)
    Pauletti, A. (WE 14)
    Bröer, S. C. (WE 14)
    Kongress
    Neuroscience 2025
    San Diego, CA, USA, 15. – 19.11.2025
    Quelle
    Neuroscience 2025 : Abstracts — Society of Neuroscience (Hrsg.)
    — S. 25
    Sprache
    Englisch
    Verweise
    URL (Volltext): https://www.sfn.org/-/media/SfN/Documents/NEW-SfN/Meetings/Neuroscience-2025/Abstracts-and-Sessions/Abstract-PDFs/SFN25_Abstracts-PDF-Posters_SUN_AM_Final.pdf
    Kontakt
    Institut für Pharmakologie und Toxikologie

    Koserstr. 20
    14195 Berlin
    +49 30 838 53221
    pharmakologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Viral encephalitis represents a major cause of infection-induced seizures and subsequent epileptogenesis. Astrocytes are central players in CNS inflammation and undergo functional alterations after seizures, such as morphological changes, and increase in numbers.
    This reactive astrogliosis may result from proliferation of existing astrocytes or seizure-induced switches in neural stem cell fate. This phenomenon has been demonstrated robustly in chemical epilepsy models, however there is no data on infection-induced seizures. This study characterizes astrocyte proliferation and morphological changes across disease phases using the Theiler’s Murine Encephalomyelitis Virus (TMEV) model. Adult C57BL/6J mice were infected intracerebrally, and BrdU was administered during the following acute phase of encephalitis to label proliferating cells. Seizures were monitored via EEG and behavioral observations. Mice were sacrificed at various time points post-infection. TMEV-infected animals demonstrated increased astrocyte reactivity in the acute phase of encephalitis, and astrocyte density was positively correlated with seizure activity. Proliferation of radial glia was reduced, and proliferation of mature astrocytes was increased. Morphological assessment showed regional variation but no between-group differences except larger astrocytes in seizure animals' molecula layer. This study reveals temporal astrocyte proliferation and morphological changes during viral encephalitis-induced seizures. Ongoing studies aim to characterize complete temporal profiles (28 and 90 dpi) to identify the mechanisms underlying the transition from acute inflammation to chronic epilepsy.