Activity of cortical inhibitory interneurons is rapidly reduced in response to monocular deprivation during the critical period for ocular dominance plasticity and in response to salient events encountered during learning. In the case of primary sensory cortex, a decrease in mean evoked firing rate of parvalbumin-positive (PV) inhibitory neurons is causally linked to a reorganization of excitatory networks following sensory perturbation. Converging evidence indicates that it is deprivation, and not an imbalance between open and closed eye inputs, that triggers rapid plasticity in PV neurons. However, this has not been directly tested in-vivo. Using two-photon guided cell-attached recording we examined the impact of closing both eyes for 24 hours on PV neuron response properties in mouse primary visual cortex. We found that binocular deprivation induces a 30% reduction in stimulus-evoked mean firing rate, and that this reduction is specific to critical period-aged mice. In contrast to evoked mean firing rate, measurements of trial-to-trial variability revealed that stimulus-driven decreases in variability are significantly dampened by deprivation during both the critical period and the post-critical period. These data establish that open-eye inputs are not required to drive the deprivation-induced weakening of PV neuron evoked activity that defines critical period plasticity, and that other aspects of in-vivo PV neuron activity are malleable throughout life.
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