Synapse-Selective Control of Cortical Maturation and Plasticity by Parvalbumin-Autonomous Action of SynCAM 1

摘要

Cortical plasticity peaks early in life and tapers inadulthood, as exemplified in the primary visual cortex(V1), wherein brief loss of vision in one eyereduces cortical responses to inputs from that eyeduring the critical period but not in adulthood. Thesynaptic locus of cortical plasticity and the cellautonomoussynaptic factors determining criticalperiods remain unclear. We here demonstrate thatthe immunoglobulin protein Synaptic Cell AdhesionMolecule 1 (SynCAM 1/Cadm1) is regulated by visualexperience and limits V1 plasticity. Loss of SynCAM1 selectively reduces the number of thalamocorticalinputs onto parvalbumin (PV+) interneurons, impairingthe maturation of feedforward inhibition in V1.SynCAM 1 acts in PV+ interneurons to activelyrestrict cortical plasticity, and brief PV+-specificknockdown of SynCAM 1 in adult visual cortex restoresjuvenile-like plasticity. These results identifya synapse-specific, cell-autonomous mechanismfor thalamocortical visual circuit maturation andclosure of the visual critical period.