How retinal silencing restores synaptic strength in visual cortex of adult amblyopia

Amblyopia is a prevalent form of visual disability that arises during infancy and early childhood when inputs to the visual cortex from the two eyes are poorly balanced (for example, by misalignment of the eyes, asymmetric refraction, or blocked vision of one eye). Characteristics of amblyopia are poor visual acuity in one eye, and an attendant loss of depth perception. The need for improved treatments for amblyopia is widely acknowledged. Animal studies over the past 50 years have uncovered the pathophysiology of amblyopia. It is well documented that temporary monocular deprivation alters the strength of synapses in primary visual cortex that renders cortical neurons unresponsive to stimulation of the deprived eye. However, much less is known about the mechanisms that serve recovery from amblyopia. We recently discovered that temporary local anesthesia of the retina sets in motion changes in the brain that enable complete recovery from the effect of early life monocular deprivation. Our objectives are to uncover the mechanism for how this recovery occurs, and to determine if this knowledge can be translated into new and better treatments for amblyopia.