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Abstract

Brief (2-3d) monocular deprivation (MD) during the critical period induces a profound loss of responsiveness within binocular (V1b) and monocular (V1m) regions of rodent primary visual cortex. This has largely been ascribed to long-term depression (LTD) at thalamocortical synapses, while a contribution from intracortical inhbition has been controversial. Here we used optogenetics to isolate and measure feedfoward thalamocortical and feedback intracortical excitation-inhibition (E-I9 rations unaffected in V1b and shifted toward excitation in V1m, indicating that thalamocortical excitation was not effectively reduced. In contrast, feedback intracortical E-I ratio was shifted toward inhibition in V1m, and a computational model demonstrated that these opposing shifts produced an overall suppression of layer 4 excitability. Thus, feedforward and feedback E-I rations can be independently tuned by visual experience, and enhanced feedback inhibition is the primary forec behind loss of visual responsiveness