The decline in ocular dominance plasticity observed over the course of postnatal development was previously thought to be irreversible. The developmental decline in ocular dominance plasticity constrains the ability of the adult visual system to recover from chronic monocular deprivation. Here we use chronic monocular deprivation from eye opening to adulthood to induce severe amblyopia in pigmented Long Evans rats, and demonstrate that dark exposure in adulthood promotes the experience-dependent recovery of spatial acuity in the chronically-deprived eye. We propose that dark exposure in adulthood reactivates anatomical and physiological plasticity at thalamocortical synapses, and delineate a series of experiments to isolate, characterize and optimize the recovery of thalamocortical synaptic transmission. We propose that dark exposure will enhance plasticity at thalamocortical synapses, which will promote experience-dependent visual perceptual learning and activity-dependent potentiation of the visually-evoked responses. Importantly, we propose that the enhancement of GABAergic inhibition with diazepam will block these reactivation of anatomical, physiological and behavioral plasticity by dark exposure. We propose to develop non-invasive methods to strengthen thalamocortical synapses in vivo, via visual tetanus (photic LTP) and visual perceptual learning. In addition, we propose to harness the experience-dependent potentiation of thalamocortical synaptic that is reactivated by dark exposure to accelerate the recovery of spatial acuity in our animal model of severe amblyopia.
Dark exposure in adulthood promotes the experience-dependent recovery of vision in a rodent model of severe amblyopia. We propose that dark exposure in adulthood reactivates anatomical and physiological plasticity at thalamocortical synapses, and delineate a series of experiments to isolate, characterize and optimize the recovery of thalamocortical synaptic transmission. We propose to harness the experience-dependent enhancement of thalamocortical synaptic reactivated by dark exposure to accelerate the recovery from severe amblyopia.
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