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Synaptotagmin-3 drives AMPA receptor endocytosis, depression of synapse strength, and forgetting.

Science. 2019-01; 
AwasthiAnkit,RamachandranBinu,AhmedSaheeb,BenitoEva,ShinodaYo,NitzanNoam,HeukampAlina,RannioSabine,MartensHenrik,BarthJonas,BurkKatja,WangYu Tian,FischerAndre,DeanC
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Mutagenesis Services The calcium-binding deficient mutant of Syt3 was generated by GenScript by mutagenesis of D386, 388N and D520, 522 N, corresponding to the calcium-binding sites of syt1: D230, 232 N and D363, 365 N Get A Quote

摘要

Forgetting is important. Without it, the relative importance of acquired memories in a changing environment is lost. We discovered that synaptotagmin-3 (Syt3) localizes to postsynaptic endocytic zones and removes AMPA receptors from synaptic plasma membranes in response to stimulation. AMPA receptor internalization, long-term depression (LTD), and decay of long-term potentiation (LTP) of synaptic strength required calcium-sensing by Syt3 and were abolished through Syt3 knockout. In spatial memory tasks, mice in which Syt3 was knocked out learned normally but exhibited a lack of forgetting. Disrupting Syt3:GluA2 binding in a wild-type background mimicked the lack of LTP decay and lack of forgetting, an... More

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