Hippocampal Lnx1–NMDAR multiprotein complex mediates initial social memory

• DOI: 10.1038/s41380-019-0606-y
• Publication Date: 2019-11-26T13:02:33Z
• Authors: Xian-Dong Liu; Peng-Hui Ai; Xiao-Na Zhu; Yuan-Bo Pan; Michael M. Halford; Mark Henkemeyer; Dong-Fu Feng; Tian-Le Xu; Suya Sun; Nan-Jie Xu
• Keywords: Multiprotein complex

Abstract Social interaction and communication are evolutionary conserved behaviours that developed in mammals to establish partner cognition. Deficit sociability has been represented human patients animal models of neurodevelopmental disorders, which connected with genetic variants synaptic glutamate receptors associated PDZ-binding proteins. However, it remains elusive how these key proteins specialized the cellular level for initial social behaviour during postnatal developmental stage. Here we identify a hippocampal CA3 specifically expressed PDZ scaffold protein Lnx1 required behaviour. Through gene targeting find deficiency led subregional disorder neuronal activity memory impairments discrimination observed juvenile mice also show cognitive defects adult We further demonstrate deletion causes NMDA receptor (NMDAR) hypofunction this is attributable decreased GluN2B expression PSD compartment disruption Lnx1–NMDAR–EphB2 complex. Specific restoration or EphB2 area −/− rescues defective function memory. These findings thus reveal crucial roles postsynaptic NMDAR multiprotein complex regulates formation adolescent period.