Disruption of Coordinated Presynaptic and Postsynaptic Maturation Underlies the Defects in Hippocampal Synapse Stability and Plasticity in Abl2/Arg-Deficient Mice

Abstract

Synapses mature in vitro from high-release probability (Pr) GluN2B(+) to low-Pr, GluN2B(-), but it is unknown why this happens or whether it occurs in vivo High-Pr, GluN2B(+) synapses persist into early adulthood in Arg-deficient mice in vivo and have elevated NMDA receptor currents and increased structural plasticity. The persistence of these high-Pr, GluN2B(+) synapses is associated with a net synapse loss and significant disruption of normal synaptic plasticity by early adulthood. Together, these observations suggest that the maturation of high-Pr, GluN2B(+) synapses to predominantly low-Pr, GluN2B(-) synapses may be essential to preserving a larger dynamic range for plasticity while ensuring that connectivity is distributed among a greater number of synapses for optimal circuit function.