GluN2B-containing NMDA receptors promote glutamate synapse development in hippocampal interneurons
In postnatal development, GluN2B-containing NMDARs are critical for the functional maturation of glutamatergic synapses. GluN2B-containing NMDARs prevail until the second postnatal week when GluN2A subunits are progressively added, conferring mature properties to NMDARs. In cortical principal neuron...
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Published in | The Journal of neuroscience Vol. 34; no. 48; pp. 16022 - 16030 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Society for Neuroscience
26.11.2014
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Subjects | |
Online Access | Get full text |
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Summary: | In postnatal development, GluN2B-containing NMDARs are critical for the functional maturation of glutamatergic synapses. GluN2B-containing NMDARs prevail until the second postnatal week when GluN2A subunits are progressively added, conferring mature properties to NMDARs. In cortical principal neurons, deletion of GluN2B results in an increase in functional AMPAR synapses, suggesting that GluN2B-containing NMDARs set a brake on glutamate synapse maturation. The function of GluN2B in the maturation of glutamatergic inputs to cortical interneurons is not known. To examine the function of GluN2B in interneurons, we generated mutant mice with conditional deletion of GluN2B in interneurons (GluN2B(ΔGAD67)). In GluN2B(ΔGAD67) mice interneurons distributed normally in cortical brain regions. After the second postnatal week, GluN2B(ΔGAD67) mice developed hippocampal seizures and died shortly thereafter. Before the onset of seizures, GluN2B-deficient hippocampal interneurons received fewer glutamatergic synaptic inputs than littermate controls, indicating that GluN2B-containing NMDARs positively regulate the maturation of glutamatergic input synapses in interneurons. These findings suggest that GluN2B-containing NMDARs keep the circuit activity under control by promoting the maturation of excitatory synapses in interneurons. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author contributions: W.K., S.W., Z.L., O.S., C.G., and H.M. designed research; W.K., S.W., Z.L., O.S., A.H., and C.G. performed research; W.K., A.H., and H.M. contributed unpublished reagents/analytic tools; W.K., S.W., Z.L., O.S., A.H., and C.G. analyzed data; W.K., S.W., O.S., C.G., and H.M. wrote the paper. W.K., Z.L., and S.W. contributed equally to this work. Z. Li's present address: Department of Neurology, Tongji Hospital, Huazhong University of Science and Technology, 430030 Hubei, China. |
ISSN: | 0270-6474 1529-2401 1529-2401 |
DOI: | 10.1523/JNEUROSCI.1210-14.2014 |