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

Barbara Calabrese, Steven L. Jones, Yoko Shiraishi-Yamaguchi, Michael Lingelbach, Uri Manor, Tatyana M. Svitkina, Henry N. Higgs, Andy Y. Shih and Shelley Halpain ()
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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
Shelley Halpain: University of California, San Diego, and Sanford Consortium for Regenerative Medicine

Nature Communications, 2022, vol. 13, issue 1, 1-20

Abstract: 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,

Date: 2022
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DOI: 10.1038/s41467-022-33268-y

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