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A novel critical period for inhibitory plasticity in rat somatosensory cortex


The cerebral cortex encodes sensory information with astonishing precision, but it is also confronted with the impressive task of reworking and rewiring its physiology in the face of a changing environment. Hubel and Weisel first characterized the impact of sensory deprivation on the development of cortical response properties, but there is still much we do not know about which forms of cortical plasticity are induced with sensory deprivation, as well as which cell types and synapses mediate plasticity. While traditional models of cortical plasticity proposed Hebbian ("use it or lose it") rules in excitatory circuits as the primary substrate for cortical plasticity, recent advances to the classical model include an important role for non- Hebbian forms of plasticity, and show that inhibitory circuits are a major site of sensory plasticity. A precisely regulated balance between cortical excitation and inhibition is crucial for sensory processing and plasticity, but our understanding of inhibitory synapse development is lacking. Here we investigate the impact of sensory experience on the development and function of inhibitory synapses in rat primary somatosensory cortex. I deprived the D-row of rat whiskers (beginning on the 7th postnatal day, P7) in order to probe how experience guides inhibitory synapse development. I found that deprivation reduced inhibitory currents at P15 in layer (L) 4 and at P21 in L2/3. Evoked inhibition was also reduced at P15 in L4. This reduction in inhibition constitutes a homeostatic form of plasticity, as it would ultimately increase excitatory activity in response to sensory deprivation. Surprisingly, inhibitory currents recovered to control (spared) levels after this one-day period. Our findings demonstrate that the development of inhibitory signaling in S1 during the first postnatal month occurs in a largely experience-independent fashion, but that sensory deprivation during this period causes a delayed and transient reduction in the efficacy of inhibitory signaling. Our results also reveal that these transient changes in mIPSC amplitude and frequency can be dissociated, meaning that they are mechanistically independent. These results add to the growing body of evidence that inhibitory circuits undergo homeostatic plasticity in response to sensory use and disuse in primary sensory cortex

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