Dark exposure lowers the MMP9 activation threshold, and subsequent light stimulation to an amblyopic eye is sufficient to induce proteolysis at thalamo-cortical synapses in deprived mouse visual cortex.

Visual impairment caused by monocular deprivation early in life can be reversed rapidly at older ages by temporarily blocking all activity in the non-deprived eye.

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.

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.

Mice that viewed a visual stimulus whilst running showed recovery of the neuronal responses that had been lost due to early visual deprivation, with potential relevance for amblyopia.

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.

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.

Stimulus representation in primary visual cortex rebounds to its original state following therapeutic sensory deprivation in adults.

A new computational model explains how alternate rearing conditions affect the development of binocular vision.

A critical re-evaluation of some of the quintessential examples given as evidence for cortical reorganisation argues that, contrary to the prevalent view, any opportunities for functional change in cortical organisation are incremental and constrained by the underlying structural ‘blueprint'.