Inhibitory innervation in the dorsolateral geniculate nucleus is crucial for adult thalamic and cortical ocular dominance plasticity, highlighting potential thalamic involvement in conditions like amblyopia and learning disabilities.

Parvalbumin-containing inhibitory neurons are crucial for expression of plasticity in adult visual cortex that supports visual recognition memory, but not for expression of ocular dominance plasticity that results from monocular deprivation.

A series of experiments suggest that the fronto-parietal attentional network is involved in controlling eye-based attention, and FEF plays a crucial causal role in generating the attention-induced ocular dominance shift.

Neuromodulation of the expression of Hebbian plasticity enables rapid cortical sensory-induced remodeling in post-critical period adults, and can rescue deficits induced by prolonged sensory deprivation.

The study of sleep following monocular deprivation has shown that sleep slow oscillations and spindles occurring during non-REM sleep have a role in homeostatic ocular dominance plasticity even in the adulthood, beyond synaptic homeostatic hypothesis that applies to Hebbian phenomena.

Short-term monocular deprivation effects are widespread in the visual cortex and extend subcortically to the ventral pulvinar, while sparing the dorsal pulvinar and the lateral geniculate nucleus.

Light reintroduction (LRx) after dark exposure reactivates structural and functional plasticity in the adult mouse visual cortex by increasing the activity of MMP-9 at thalamo-cortical synapses.

In vivo and ex vivo analysis of the activity-regulated gene Rem2 in the mouse visual system sheds new light on the contribution of intrinsic excitability in circuit plasticity.

A new form of brain plasticity extends the known limits for how much early sensory input can alter the brain.

Two hour deprivation of vision in one eye transiently boosts the representation of the deprived eye (suppressing the non-deprived eye) in adult human V1 and along the ventral pathway.