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- W2044844304 abstract "A current model posits that cofilin-dependent actin severing negatively impacts dendritic spine volume. Studies suggested that increased cofilin activity underlies activity-dependent spine shrinkage, and that reduced cofilin activity induces activity-dependent spine growth. We suggest instead that both types of structural plasticity correlate with decreased cofilin activity. However, the mechanism of inhibition determines the outcome for spine morphology. RNAi in rat hippocampal cultures demonstrates that cofilin is essential for normal spine maintenance. Cofilin-F-actin binding and filament barbed-end production decrease during the early phase of activity-dependent spine shrinkage; cofilin concentration also decreases. Inhibition of the cathepsin B/L family of proteases prevents both cofilin loss and spine shrinkage. Conversely, during activity-dependent spine growth, LIM kinase stimulates cofilin phosphorylation, which activates phospholipase D-1 to promote actin polymerization. These results implicate novel molecular mechanisms and prompt a revision of the current model for how cofilin functions in activity-dependent structural plasticity." @default.
- W2044844304 created "2016-06-24" @default.
- W2044844304 creator A5020763202 @default.
- W2044844304 creator A5054843881 @default.
- W2044844304 creator A5089753548 @default.
- W2044844304 date "2014-04-16" @default.
- W2044844304 modified "2023-09-27" @default.
- W2044844304 title "Activity-Dependent Dendritic Spine Shrinkage and Growth Involve Downregulation of Cofilin via Distinct Mechanisms" @default.
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- W2044844304 doi "https://doi.org/10.1371/journal.pone.0094787" @default.
- W2044844304 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3989342" @default.
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