Nogo Receptor 1 Limits Ocular Dominance Plasticity but not Turnover of Axonal Boutons in a Model of Amblyopia

The formation and stabilityof dendritic spines on excitatory cortical neurons are correlated with adult visual plasticity, yet how the formation, loss, and stability of postsynaptic spines register with that of presynaptic axonal varicosities is unknown. Monocular deprivation has been demonstrated to increase the rate of formation of dendritic spines in visual cortex. However, we find that monocular deprivation does not alter the dynamics of intracortical axonal boutons in visual cortex of either adult wild-type (WT) miceoradultNgR1mutant (ngr1−/−) mice thatretain criticalperiod visual plasticity. Restoringnormalvision for a week following long-term monocular deprivation (LTMD), a model of amblyopia, partially restores ocular dominance (OD) in WT and ngr1−/− mice but does not alter the formation or stability of axonal boutons. Both WT and ngr1−/− mice displayed a rapid return of normal OD within 8 days after LTMD as measured with optical imaging of intrinsic signals. In contrast, singleunit recordings revealed that ngr1−/− exhibited greater recovery of OD by 8 days post-LTMD. Our findings support a model of structural plasticityin whichchangesin synapticconnectivityare largelypostsynaptic.In contrast,axonalboutonsappearto be stable during changes in cortical circuit function.