Global Synpatic Plasticity Mechanisms in Visual Cortex

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Project Summary While experience-dependent cortical plasticity is most prominent during early postnatal development, the adult brain retains some level of plasticity. In particular, synapses in the superficial layers of primary sensory cortices, including the primary visual cortex (V1), remain plastic throughout adulthood. We previously reported that a short duration of visual deprivation or auditory deprivation in adult mice produces a rather robust plasticity in V1, which results in distinct plasticity of feedforward and intracortical synapses onto principal neurons. V1 layer 2/3 (L2/3) not only receives feedforward information transmitted from the visual thalamus (dLGN) through L4, but it also receives intracortical feedback projections from other cortical areas that provide context to bottom-up visual information. We found that visual deprivation preferentially potentiates intracortical synapses, while auditory deprivation leads to potentiation of the feedforward circuit in adult V1. Such adaptation might underlie activation of V1 by Braille reading or speech in blind individuals or enhancement of visual processing reported in deaf subjects. Here we will examine how such circuit-level plasticity is established by changes in recruitment of inhibitory circuits, and how it could alter activation of adult V1 through feedforward and intracortical inputs. Recent studies demonstrate that transient changes in the recruitment of inhibitory circuits play a role in enabling cortical plasticity in juveniles. There are largely two distinct inhibitory circuits in V1, one that involves parvalbumin (PV) interneurons and another that involves somatostatin (SOM) interneurons. The former has been shown to play a pivotal role in mediating visual experience-dependent plasticity, while the latter is targeted by top-down circuits. Here we will test the hypothesis that differential recruitment of PV and SOM circuits underlie adult V1 plasticity induced by visual and auditory deprivation. In addition, we hypothesize the circuit level plasticity induced by visual or auditory deprivation will lead to differential activation of adult V1 by feedforward and intracortical inputs. To test these hypotheses, we will determine how recruitment of PV and SOM circuits in adult V1 L2/3 undergo plasticity by visual versus auditory deprivation (Aim 1), and how V1 activation patterns from feedforward inputs (Aim 2) or long-range intracortical inputs (Aim 3) are altered following visual or auditory deprivation. Our results will provide much needed mechanistic information on adult V1 plasticity, and suggest how transient visual or auditory deprivation could be leveraged to enhance the distinct functionality of the adult V1.