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

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, <5 min after bath-applied NMDA, F-actin depolymerizes within spines and polymerizes into stable filaments within the dendrite shaft and soma. A similar actinification occurs after experimental ischemia in culture, and photothrombotic stroke in mouse. Following transient NMDA incubation, actinification spontaneously reverses. Na⁺, Cl^-, water, and Ca²⁺ influx, and spine F-actin depolymerization are all necessary, but not i

SUBMITTER: Calabrese B 

PROVIDER: S-EPMC9558009 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature