Unique functions of kainate receptors in the brain are determined by the auxiliary subunit Neto1

Ionotropic glutamate receptors principally mediate fast excitatory transmission in the brain. Among the three classes of ionotropic glutamate receptors, kainate receptors (KARs) display a categorical brain distribution, which has been historically defined by 3H-radiolabeled kainate binding. Compared...

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Main Authors: Straub, Christoph, Hunt, David L., Yamasaki, Miwako, Kim, Kwang S., Watanabe, Masahiko, Castillo, Pablo E., Tomita, Susumu
Format: Online
Language:English
Published: 2011
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3125417/
id pubmed-3125417
recordtype oai_dc
spelling pubmed-31254172012-01-01 Unique functions of kainate receptors in the brain are determined by the auxiliary subunit Neto1 Straub, Christoph Hunt, David L. Yamasaki, Miwako Kim, Kwang S. Watanabe, Masahiko Castillo, Pablo E. Tomita, Susumu Article Ionotropic glutamate receptors principally mediate fast excitatory transmission in the brain. Among the three classes of ionotropic glutamate receptors, kainate receptors (KARs) display a categorical brain distribution, which has been historically defined by 3H-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 unique KAR properties remain unclear. Here we found that both the distinct high affinity biding 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 determines both KAR high affinity binding pattern and the distinctively slow kinetics of postsynaptic KARs. By regulating KAR-EPSC kinetics, Neto1 can control synaptic temporal summation, spike generation and fidelity. 2011-05-29 /pmc/articles/PMC3125417/ /pubmed/21623363 http://dx.doi.org/10.1038/nn.2837 Text en Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Straub, Christoph
Hunt, David L.
Yamasaki, Miwako
Kim, Kwang S.
Watanabe, Masahiko
Castillo, Pablo E.
Tomita, Susumu
spellingShingle Straub, Christoph
Hunt, David L.
Yamasaki, Miwako
Kim, Kwang S.
Watanabe, Masahiko
Castillo, Pablo E.
Tomita, Susumu
Unique functions of kainate receptors in the brain are determined by the auxiliary subunit Neto1
author_facet Straub, Christoph
Hunt, David L.
Yamasaki, Miwako
Kim, Kwang S.
Watanabe, Masahiko
Castillo, Pablo E.
Tomita, Susumu
author_sort Straub, Christoph
title Unique functions of kainate receptors in the brain are determined by the auxiliary subunit Neto1
title_short Unique functions of kainate receptors in the brain are determined by the auxiliary subunit Neto1
title_full Unique functions of kainate receptors in the brain are determined by the auxiliary subunit Neto1
title_fullStr Unique functions of kainate receptors in the brain are determined by the auxiliary subunit Neto1
title_full_unstemmed Unique functions of kainate receptors in the brain are determined by the auxiliary subunit Neto1
title_sort unique functions of kainate receptors in the brain are determined by the auxiliary subunit neto1
description Ionotropic glutamate receptors principally mediate fast excitatory transmission in the brain. Among the three classes of ionotropic glutamate receptors, kainate receptors (KARs) display a categorical brain distribution, which has been historically defined by 3H-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 unique KAR properties remain unclear. Here we found that both the distinct high affinity biding 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 determines both KAR high affinity binding pattern and the distinctively slow kinetics of postsynaptic KARs. By regulating KAR-EPSC kinetics, Neto1 can control synaptic temporal summation, spike generation and fidelity.
publishDate 2011
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3125417/
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