Amblyopia is widespread form of human visual disability caused by a disparity in visual quality between the two eyes during early postnatal life. This disparity drives ocular dominance plasticity in the visual cortex to favor the stronger eye at the expense of the weaker (amblyopic) eye. Consequently, synapses in the visual cortex downstream of the amblyopic eye are weakened, a process that is difficult to reverse unless treatment is initiated during infancy or early childhood. Recent work in animal models has suggested several strategies for promoting recovery from amblyopia. While the pathophysiology underlying amblyopia has been well studied, the synaptic and cellular conditions underlying recovery are less clear. This proposal focuses on a treatment strategy that rapidly promotes visual recovery following experimental amblyopia via temporary inactivation of the retinas. A temporary period of retinal inactivation leads of a stable enhancement of visual cortical responses once vision is restored. The goal of this proposal is to identify how retinal inactivation alters synaptic, cellular, and circuit-level properties to promote visual cortical enhancement. The long-term objective of this research is to understand how cortical plasticity is engaged to promote recovery and to inform clinical interventions for treating human amblyopia.
Amblyopia is common neurodevelopmental form of visual disability with limited treatment options, especially in medically-underserved communities. The proposed research seeks to understand how neural plasticity can be harnessed to enhance visual ability, and to suggest new treatment options for human amblyopia.
