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. ► Turnover of synaptic anatomy is accelerated in the brain of mice lacking NgR1 ► Deletion of NgR1 in adult mice restores juvenile levels of anatomical plasticity ► NgR1 functions cell-autonomously to limit anatomical plasticity in vivo ► NgR1 expression limits the anatomical response to somatosensory input Experience rearranges connectivity, but anatomical plasticity is restricted in adults. Akbik et al. demonstrate that Nogo Receptor 1 is required continuously and cell-autonomously to limit adult dendritic spine turnover. NgR1 determines the low set point for synaptic turnover in adult cerebral cortex.