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Spreading depression as an innate antiseizure mechanism

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  • Isra Tamim

    (Massachusetts General Hospital, Harvard Medical School
    Charité–Universitätsmedizin Berlin, Klinik und Hochschulambulanz für Neurologie und Centrum für Schlaganfallforschung Berlin (CSB))

  • David Y. Chung

    (Massachusetts General Hospital, Harvard Medical School
    Department of Neurology, Massachusetts General Hospital, Harvard Medical School)

  • Andreia Lopes Morais

    (Massachusetts General Hospital, Harvard Medical School)

  • Inge C. M. Loonen

    (Massachusetts General Hospital, Harvard Medical School)

  • Tao Qin

    (Massachusetts General Hospital, Harvard Medical School)

  • Amrit Misra

    (Department of Neurology, Massachusetts General Hospital, Harvard Medical School)

  • Frieder Schlunk

    (Charité–Universitätsmedizin Berlin, Klinik und Hochschulambulanz für Neurologie und Centrum für Schlaganfallforschung Berlin (CSB))

  • Matthias Endres

    (Charité–Universitätsmedizin Berlin, Klinik und Hochschulambulanz für Neurologie und Centrum für Schlaganfallforschung Berlin (CSB))

  • Steven J. Schiff

    (The Pennsylvania State University)

  • Cenk Ayata

    (Massachusetts General Hospital, Harvard Medical School
    Department of Neurology, Massachusetts General Hospital, Harvard Medical School)

Abstract

Spreading depression (SD) is an intense and prolonged depolarization in the central nervous systems from insect to man. It is implicated in neurological disorders such as migraine and brain injury. Here, using an in vivo mouse model of focal neocortical seizures, we show that SD may be a fundamental defense against seizures. Seizures induced by topical 4-aminopyridine, penicillin or bicuculline, or systemic kainic acid, culminated in SDs at a variable rate. Greater seizure power and area of recruitment predicted SD. Once triggered, SD immediately suppressed the seizure. Optogenetic or KCl-induced SDs had similar antiseizure effect sustained for more than 30 min. Conversely, pharmacologically inhibiting SD occurrence during a focal seizure facilitated seizure generalization. Altogether, our data indicate that seizures trigger SD, which then terminates the seizure and prevents its generalization.

Suggested Citation

  • Isra Tamim & David Y. Chung & Andreia Lopes Morais & Inge C. M. Loonen & Tao Qin & Amrit Misra & Frieder Schlunk & Matthias Endres & Steven J. Schiff & Cenk Ayata, 2021. "Spreading depression as an innate antiseizure mechanism," Nature Communications, Nature, vol. 12(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-22464-x
    DOI: 10.1038/s41467-021-22464-x
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    Cited by:

    1. John-Sebastian Mueller & Fabio C. Tescarollo & Trong Huynh & Daniel A. Brenner & Daniel J. Valdivia & Kanyin Olagbegi & Sahana Sangappa & Spencer C. Chen & Hai Sun, 2023. "Ictogenesis proceeds through discrete phases in hippocampal CA1 seizures in mice," Nature Communications, Nature, vol. 14(1), pages 1-17, December.

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