CaMKH binding to GluN2B is critical for memory consolidation
作者单位：Departments of Pharmacology and Psychiatry and NeurosurgeryRoy J.and Lucille A.Carver College of MedicineUniversity of IowaIowa CityIA 52242USA Department of NeurobiologySemel InstituteDepartment of PsychologyBrain Research InstituteUniversity of CaliforniaLos AngelesCalifornia90095USA
会议名称：《中国生理学会第23届全国会员代表大会暨生理学学术大会》
会议日期：2010年
学科分类：0710[理学-生物学] 07[理学] 071006[理学-神经生物学]
摘 要：Memory is essential for our normal daily lives and our sense of ***,our knowledge of molecular and cellular mechanisms of memory formation and retention is *** influx through the NMDA-type glutamate receptor(NMDAR) and the ensuing activation of the Ca and calmodulin-dependent protein kinase(CaMKII) are required for memory formation and its physiological correlate,long-term potentiation(LTP).The Ca influx induces CaMKII binding to the NMDAR to strategically recruit CaMKII to synapses that are undergoing potentiation. We show that mice with two point mutations that impair CaMKII binding to the NMDAR GluN2B subunit initially learn the Morris water maze and acquire contextual fear conditioning under standard conditions to the same degree as wild type mice but show deficiency during the period of early memory consolidation in these ***, the activity-driven interaction of CaMKII with the NMDAR is important for imprinting memory traces.