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INF2-mediated actin filament reorganization confers intrinsic resilience to neuronal ischemic injury

Author

Listed:
  • Barbara Calabrese

    (University of California, San Diego, and Sanford Consortium for Regenerative Medicine)

  • Steven L. Jones

    (University of Pennsylvania)

  • Yoko Shiraishi-Yamaguchi

    (Japan Science and Technology Agency (JST))

  • Michael Lingelbach

    (Stanford University)

  • Uri Manor

    (The Salk Institute for Biological Studies)

  • Tatyana M. Svitkina

    (University of Pennsylvania)

  • Henry N. Higgs

    (Geisel School of Medicine)

  • Andy Y. Shih

    (Seattle Children’s Research Institute
    Medical University of South Carolina)

  • Shelley Halpain

    (University of California, San Diego, and Sanford Consortium for Regenerative Medicine)

Abstract

During early ischemic brain injury, glutamate receptor hyperactivation mediates neuronal death via osmotic cell swelling. Here we show that ischemia and excess NMDA receptor activation cause actin to rapidly and extensively reorganize within the somatodendritic compartment. Normally, F-actin is concentrated within dendritic spines. However,

Suggested Citation

  • Barbara Calabrese & Steven L. Jones & Yoko Shiraishi-Yamaguchi & Michael Lingelbach & Uri Manor & Tatyana M. Svitkina & Henry N. Higgs & Andy Y. Shih & Shelley Halpain, 2022. "INF2-mediated actin filament reorganization confers intrinsic resilience to neuronal ischemic injury," Nature Communications, Nature, vol. 13(1), pages 1-20, December.
    • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-33268-y
    DOI: 10.1038/s41467-022-33268-y
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