Maternal Sleep Deprivation Induce Impairments Of Synaptic Plasticity And Cognition In The Offspring Rats

Objective:Through the establishment of late pregnancy sleep deprivation?MSD?animal model,taking the offspring as the research objection,we observed the effects of late maternal sleep deprivation on offspring's learning and memory and cognitive function,then made further researchment on the synaptic plasticity of hippocampal CA3-CA1 pathway and AMPAR expression in the hippocampal of the offspring rats.Finally,by injecting the synthesis peptide Tat-Glua2_3y?inhibitor of AMPAR?,we detected the variation of the cognitive function and hippocampal synaptic plasticity.Hence,this study is designed to explore the relevance between?-amino-3-hydroxy-5-methyl-isoxazole-4-propionicacidreceptors?AMPARs?and the damage of the offspring's hippocampal-dependent cognitive function caused by late maternal sleeping deprivation,and,at the same time,provide treatment theoretical basis for the offspring suffered from maternal sleep deprivation,even develop new drugs for clinical development in the future.Methods:In our research,when the pregnant rats were in the third trimester?gestational days 15-21?of pregnancy,we handled the rats gently to deprive their sleep for 6h persistently for 7 days.While the offsprings grow up to 5 weeks old,by peritoneal inject tat-GluA2_3yy peptide and control scr-GluA2_3yy peptide to them for 7 days,then the emotional and cognitive functions as well as hippocampal synaptic plasticity were tested in the offspring rats?postnatal days 42-56?.Results:Tat-GluA2_3yy rescued the impaired hippocampal-dependent spatial learning and memory,and increased depressive-and anxiety-like behaviors displayed by the offspring after the late maternal sleep deprivation.Tat-GluA2_3yy rescued the decresed subunit GluA2 in synaptic protein,but subunit GluA1 and GluA3 had no stastical difference viaration.Electrophysiological recording showed that Tat-GluA2_3yy improve the hippocampal CA3-CA1 impaired LTP and facilitated LTD.Conclusion:These results implied that inhibit the endocytosis of AMPA receptor by Tat-GluA2_3yy rescue the emotional and cognitive functions of the offsprings which is attributable to the suppression of hippocampal LTP and facilitated LTD due to late maternal sleep deprivation.