The effect of visual deprivation on the development of visual responsiveness in cortical neurons has been investigated intensively. The analyses conducted in primary visual cortex (V1) have indicated that the changes in visual responsiveness are mainly ascribed to altered neural circuits in V1. Although similar experience-dependent changes occur in secondary visual cortex (V2), it remains unresolved whether the modifications in V2 are ascribed to the changes in visual inputs from V1 or those in the neural circuits in V2. In order to address this issue, we conducted unit recordings from V1 and V2 in rats which were reared in a normal visual environment or with binocular deprivation by lid suture from the day of eye opening. The visual response properties were analyzed under anesthesia using drifting sinusoidal gratings of various spatial frequencies and orientations. In V1 cells, the optimal spatial frequency and orientation selectivity were both significantly lower in deprived than control rats. In V2 cells, deprivation impaired response selectivity less, but decreased the strength of visual responses far more, compared with V1 cells. To reveal the modifications in cortical circuits underlying these changes, we performed morphological analyses of long-range projections and physiological analyses of local neural circuits. We visualized the projections from V1 to V2 using rats injected with AAV-GFP in V1 and found that the layer-specific projection pattern was disordered in deprived rats. To examine the functional local circuits, we conducted whole-cell recordings from layer 2/3 pyramidal cells, sending output signals to other cortical areas, in V1 and V2 using slice preparations, and analyzed the excitatory postsynaptic currents (EPSCs) evoked by laser-scanning photostimulation of nearby cortical cells using caged glutamate. The visual deprivation decreased the number and amplitude of EPSCs coming from the cells in layer 2/3 and 4 in V2 but not in V1. These results suggest that visual experience regulates the maturation of visual responsiveness of V2 cells through the modifications of inputs from V1 and local circuits in V2.