Journal
NATURE NEUROSCIENCE
Volume 14, Issue 7, Pages 866-U83Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.2837
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Funding
- US National Institutes of Health/National Institute of Mental Health [R01 MH085080, R01 MH081935]
- Boehringer-Ingelheim PhD fellowship
- Ministry of Education, Culture, Sports, Science and Technology of Japan [19100005]
- Grants-in-Aid for Scientific Research [19100005] Funding Source: KAKEN
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Ionotropic glutamate receptors principally mediate fast excitatory transmission in the brain. Among the three classes of ionotropic glutamate receptors, kainate receptors (KARs) have a unique brain distribution, which has been historically defined by H-3-radiolabeled kainate binding. Compared with recombinant KARs expressed in heterologous cells, synaptic KARs exhibit characteristically slow rise-time and decay kinetics. However, the mechanisms responsible for these distinct KAR properties remain unclear. We found that both the high-affinity binding pattern in the mouse brain and the channel properties of native KARs are determined by the KAR auxiliary subunit Neto1. Through modulation of agonist binding affinity and off-kinetics of KARs, but not trafficking of KARs, Neto1 determined both the KAR high-affinity binding pattern and the distinctively slow kinetics of postsynaptic KARs. By regulating KAR excitatory postsynaptic current kinetics, Neto1 can control synaptic temporal summation, spike generation and fidelity.
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