Sensory experience is critical for the development and refinement of visual cortical networks, and alteration of sensory drive during a critical period (CP) can have dramatic effects on visual response properties. The rodent visual system is a premier model system for studying the effects of sensory experience on neuronal circuit function. Prior to eye opening, initial stages in circuit refinement are driven by spontaneous retinal activity. After eye opening, visual experience becomes a major factor driving refinement and alterations of sensory inputs during well-defined critical periods (CP). For instance, depriving one eye of vision drastically reduces the responsiveness of cortical neurons to that eye and potentiates neuronal responses to the non- deprived eye, leading to an ocular dominance shift (OD) in the binocular region of the visual cortex. Hebbian plasticity at excitatory synapses has been suggested to underlie this visual–deprivation (VD)- induced remodeling of responsiveness, but recently a role for plasticity at inhibitory synapses has begun to emerge. Previous work from our lab demonstrated that two days of monocular deprivation (MD) depresses the strength of fast-spiking (FS) GABAergic synapses onto star pyramids (SP) within layer 4 of the rat monocular primary visual cortex when begun during the pre-CP (P15), but potentiates this same synapse when performed during the CP (P20). Further, this specific synapse can undergo long-term potentiation of inhibition (LTPi). Prior visual deprivation using MD occludes LTPi, suggesting that LTPi is the underlying mechanism of MD-induced increase of inhibition during the CP. I found that the sign of plasticity at FS?RS synapses is developmentally regulated and concomitant with the transition between the pre-CP and the CP. Further, the switch in VD-induced change of FS?RS synaptic strength is correlated with the transition in plasticity at this synapse. Thus, maturation of inhibitory plasticity at FS synapses plays an important role in sensory-driven refinement of cortical circuit and initiation of CP plasticity.