AMPAR-Dependent Synaptic Plasticity Initiates Cortical Remapping and Adaptive Behaviors during Sensory Experience

Cortical plasticity improves behaviors and helps recover lost functions after injury. However, the underlying synaptic mechanisms remain unclear. In mice, we show that trimming all but one whisker enhances sensory responses from the spared whisker in the barrel cortex and occludes whisker-mediated synaptic potentiation (w-Pot) in vivo. In addition, whisker-dependent behaviors that are initially impaired by single-whisker experience (SWE) rapidly recover when associated cortical regions remap. Cross-linking the surface GluA2 subunit of AMPA receptors (AMPARs) suppresses the expression of w-Pot, presumably by blocking AMPAR surface diffusion, in mice with all whiskers intact, indicating that synaptic potentiation in vivo requires AMPAR trafficking. We use this approach to demonstrate that w-Pot is required for SWE-mediated strengthening of synaptic inputs and initiates the recovery of previously learned skills during the early phases of SWE. Taken together, our data reveal that w-Pot mediates cortical remapping and behavioral improvement upon partial sensory deafferentation.