AI Article Synopsis
- - The study shows that proper dendritic development relies on the active role of canonical Wnt signaling in certain neurons of the rat retrosplenial cortex during critical growth phases.
- - Reducing Wnt signaling early in development can cause lasting damage to dendritic structure, affecting spatial memory and navigation abilities later in life.
- - Neurotrophin-3 is identified as a key gene regulated by Wnt signaling that helps in spine formation and maturation during dendritic development.
Article Abstract
During development, the precise implementation of molecular programs is a key determinant of proper dendritic development. Here, we demonstrate that canonical Wnt signaling is active in dendritic bundle-forming layer II pyramidal neurons of the rat retrosplenial cortex during dendritic branching and spine formation. Transient downregulation of canonical Wnt transcriptional activity during the early postnatal period irreversibly reduces dendritic arbor architecture, leading to long-lasting deficits in spatial exploration and/or navigation and spatial memory in the adult. During the late phase of dendritogenesis, canonical Wnt-dependent transcription regulates spine formation and maturation. We identify neurotrophin-3 as canonical Wnt target gene in regulating dendritogenesis. Our findings demonstrate how temporary imbalance in canonical Wnt signaling during specific time windows can result in irreversible dendritic defects, leading to abnormal behavior in the adult.
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| http://dx.doi.org/10.1016/j.celrep.2019.04.026 | DOI Listing |
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