Abstract:
: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 α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors (AMPARs), the major excitatory neurotransmitter receptors in the brain. KIBRA knockdown accelerates the rate of AMPAR 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.
journal_name
Neuronjournal_title
Neuronauthors
Makuch L,Volk L,Anggono V,Johnson RC,Yu Y,Duning K,Kremerskothen J,Xia J,Takamiya K,Huganir RLdoi
10.1016/j.neuron.2011.08.017subject
Has Abstractpub_date
2011-09-22 00:00:00pages
1022-9issue
6eissn
0896-6273issn
1097-4199pii
S0896-6273(11)00738-0journal_volume
71pub_type
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