期刊
NEURON
卷 71, 期 6, 页码 1022-1029出版社
CELL PRESS
DOI: 10.1016/j.neuron.2011.08.017
关键词
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资金
- National Institute of Health [MH64856, NS36715, T32MH15330]
- Howard Hughes Medical Institute
- International Human Frontier Science Program [LT00399/2008-L]
- Australian National Health and Medical Research Council [477108]
- Grants-in-Aid for Scientific Research [22300122] Funding Source: KAKEN
KIBRA has recently been identified as a gene associated with human memory performance. Despite the elucidation of the role of KIBRA in several diverse processes in nonneuronal cells, the molecular function of KIBRA in neurons is unknown. We found that KIBRA directly binds to the protein interacting with C-kinase 1 (PICK1) and forms a complex with alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors (AMPARs), the major excitatory neurotransmitter receptors in the brain. KIBRA knockdown accelerates the rate of AM PAR recycling following N-methyl-D-aspartate receptor-induced internalization. Genetic deletion of KIBRA in mice impairs both long-term depression and long-term potentiation at hippocampal Schaffer collateral-CA1 synapses. Moreover, KIBRA knockout mice have severe deficits in contextual fear learning and memory. These results indicate that KIBRA regulates higher brain function by regulating AMPAR trafficking and synaptic plasticity.
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