| Social isolation is an objective reflection of a shrinking social network or lack of social contact,and isolated individuals are at increased risk of depression,schizophrenia,and memory deterioration,but the exact mechanism is unknown.Previous studies in our laboratory have shown that the C-terminal tails of AMPA receptor GluA1 and GluA2participate in the formation of different forms of synaptic plasticity and memory behaviors.In the present study,we found that compared to grouped mice,isolated A2C1KI mice exhibited normal social memory formation and impairment in memory maintenance,but isolated WT and A1C2KI mice had normal social memory.In addition,we also found that in the vCA1region of isolated A2C1KI mice,basic synaptic transmission and LTP were impaired,and PKC and GluA1-S831 phosphorylation caused by social stimulation were also inhibited.Finally,we used adeno-associated virus to specifically knock down GluA2 in the vCA1 region of the hippocampus,which also induced deficits in social memory maintenance after social isolation.In conclusion,Our study explored the role of GluA2 and its C-terminal tails in the formation and maintenance of social memory after social isolation from the perspectives of animal behavior,electrophysiology,and molecular biology.Our research provides experimental basis and theoretical basis for the mechanism of memory impairment caused by social isolation. |