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.

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.

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.

Binocular combination of monocular neuronal responses involves response suppression for neurons more preferring one eye and response enhancement for neurons more preferring both eyes in macaque V1.

Having the eye open under the patch, even though this does not change the exogenous stimulation because the eye is occluded, will result in an enhanced short-term effect for ocular dominance due to the internal neural states.

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.

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.

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.