NgR1 Improves Brain Plasticity in Adult Mice
Experience rearranges anatomical connectivity in the brain, but such plasticity is suppressed in adulthood. We examined the turnover of dendritic spines and axonal varicosities in the somatosensory cortex of mice lacking Nogo Receptor 1 (NgR1). Through adolescence, the anatomy and plasticity of ngr1 null mice are indistinguishable from control, but suppression of turnover after age 26 days fails to occur in ngr1−/− mice. Adolescent anatomical plasticity can be restored to 1-year-old mice by conditional deletion of ngr1. Suppression of anatomical dynamics by NgR1 is cell autonomous and is phenocopied by deletion of Nogo-A ligand. Whisker removal deprives the somatosensory cortex of experience-dependent input and reduces dendritic spine turnover in adult ngr1−/− mice to control levels, while an acutely enriched environment increases dendritic spine dynamics in control mice to the level of ngr1−/− mice in a standard environment. Thus, NgR1 determines the low set point for synaptic turnover in adult cerebral cortex.
Feras V. Akbik, Sarah M. Bhagat, William B.J. Cafferty, Pujan R. Patel, Stephen M. Strittmatter, Anatomical Plasticity of Adult Brain Is Titrated by Nogo Receptor (6 March 2013)
Notes
The plasticity lost from our youth is revived in mice by deletion of Nogo-A ligand.
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Mice The plasticity, Adolescent anatomical plasticity, dendritic spine turnover, somatosensory cortex, null mice, Nogo-A ligand, 1-year-old mice, adult cerebral cortex, Brain Plasticity, control mice, ngr1−/− mice, acutely enriched environment
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low set point, dendritic spines, synaptic turnover, conditional deletion, anatomical connectivity, anatomical dynamics, axonal varicosities, Nogo Receptor, Whisker removal, spine dynamics, experience-dependent input, control levels, standard environment, suppression, adulthood, adolescence, increases