期刊
SCIENCE
卷 363, 期 6422, 页码 44-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aav1483
关键词
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资金
- Sofja Kovalevskaja grant from the Alexander von Humboldt Foundation
- European Research Council (ERC) starting grant SytActivity [FP7 260916]
- Deutsche Forschungsgemeinschaft (DFG) [DE1951/1, DE1951-3]
- Center for Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB)
- DFG research group KFO241/PsyCourse [Fi981-4/Fi981 11-1]
- DFG [179/1-1/2013]
- ERC [DEPICODE 648898]
- BMBF project ENERGI [01GQ1421A]
- BMBF project Intergrament [01ZX1314D]
- German Center for Neurodegenerative Diseases
- Canadian Institute for Health Research [FDN-154286]
- Dorothea Schloezer fellowship
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, and these effects were occluded in the Syt3 knockout background. Our findings provide evidence for a molecular mechanism in which Syt3 internalizes AMPA receptors to depress synaptic strength and promote forgetting.
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