Poststroke dendritic arbor regrowth requires the actin nucleator Cobl

Yuanyuan Ji, Dennis Koch, Jule González Delgado, Madlen Günther, Otto W Witte, Michael M Kessels, Christiane Frahm and Britta Qualmann

PLOS Biology, 2021, vol. 19, issue 12, 1-35

Abstract: Ischemic stroke is a major cause of death and long-term disability. We demonstrate that middle cerebral artery occlusion (MCAO) in mice leads to a strong decline in dendritic arborization of penumbral neurons. These defects were subsequently repaired by an ipsilateral recovery process requiring the actin nucleator Cobl. Ischemic stroke and excitotoxicity, caused by calpain-mediated proteolysis, significantly reduced Cobl levels. In an apparently unique manner among excitotoxicity-affected proteins, this Cobl decline was rapidly restored by increased mRNA expression and Cobl then played a pivotal role in poststroke dendritic arbor repair in peri-infarct areas. In Cobl knockout (KO) mice, the dendritic repair window determined to span day 2 to 4 poststroke in wild-type (WT) strikingly passed without any dendritic regrowth. Instead, Cobl KO penumbral neurons of the primary motor cortex continued to show the dendritic impairments caused by stroke. Our results thereby highlight a powerful poststroke recovery process and identified causal molecular mechanisms critical during poststroke repair.Ischemic stroke is a major cause of death and long-term disability. This study reveals that, in mice, stroke-induced damage to dendritic arborization in the area around an infarct is rapidly repaired via dendritic regrowth; this plasticity requires the actin nucleator Cobl.

Date: 2021
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Persistent link: https://EconPapers.repec.org/RePEc:plo:pbio00:3001399

DOI: 10.1371/journal.pbio.3001399

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