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시냅스뇌질환연구단
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NGL-3 in the regulation of brain development, Akt/GSK3b signaling, long-term depression, and locomotive and cognitive behaviors

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dc.contributor.authorHyejin Lee-
dc.contributor.authorWangyong Shin-
dc.contributor.authorKyungdeok Kim-
dc.contributor.authorSuho Lee-
dc.contributor.authorEun-Jae Lee-
dc.contributor.authorJihye Kim-
dc.contributor.authorHanseul Kweon-
dc.contributor.authorEunee Lee-
dc.contributor.authorHaram Park-
dc.contributor.authorMuwon Kang-
dc.contributor.authorEsther Yang-
dc.contributor.authorHyun Kim-
dc.contributor.authorEunjoon Kim-
dc.date.available2019-08-21T06:20:22Z-
dc.date.created2019-07-23-
dc.date.issued2019-06-
dc.identifier.issn1544-9173-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/6065-
dc.description.abstractNetrin-G ligand-3 (NGL-3) is a postsynaptic adhesion molecule known to directly interact with the excitatory postsynaptic scaffolding protein postsynaptic density-95 (PSD-95) and trans-synaptically with leukocyte common antigen-related (LAR) family receptor tyrosine phosphatases to regulate presynaptic differentiation. Although NGL-3 has been implicated in the regulation of excitatory synapse development by in vitro studies, whether it regulates synapse development or function, or any other features of brain development and function, is not known. Here, we report that mice lacking NGL-3 (Ngl3-/- mice) show markedly suppressed normal brain development and postnatal survival and growth. A change of the genetic background of mice from pure to hybrid minimized these developmental effects but modestly suppressed N-methyl-D-aspartate (NMDA) receptor (NMDAR)-mediated synaptic transmission in the hippocampus without affecting synapse development, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (AMPAR)-mediated basal transmission, and presynaptic release. Intriguingly, long-term depression (LTD) was near-completely abolished in Ngl3-/- mice, and the Akt/glycogen synthase kinase 3β (GSK3β) signaling pathway, known to suppress LTD, was abnormally enhanced. In addition, pharmacological inhibition of Akt, but not activation of NMDARs, normalized the suppressed LTD in Ngl3-/- mice, suggesting that Akt hyperactivity suppresses LTD. Ngl3-/- mice displayed several behavioral abnormalities, including hyperactivity, anxiolytic-like behavior, impaired spatial memory, and enhanced seizure susceptibility. Among them, the hyperactivity was rapidly improved by pharmacological NMDAR activation. These results suggest that NGL-3 regulates brain development, Akt/GSK3β signaling, LTD, and locomotive and cognitive behaviors. © 2019 Lee et al.-
dc.description.uri1-
dc.language영어-
dc.publisherPUBLIC LIBRARY SCIENCE-
dc.titleNGL-3 in the regulation of brain development, Akt/GSK3b signaling, long-term depression, and locomotive and cognitive behaviors-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000473675900002-
dc.identifier.scopusid2-s2.0-85067477026-
dc.identifier.rimsid68939-
dc.contributor.affiliatedAuthorHyejin Lee-
dc.contributor.affiliatedAuthorSuho Lee-
dc.contributor.affiliatedAuthorJihye Kim-
dc.contributor.affiliatedAuthorEunee Lee-
dc.contributor.affiliatedAuthorEunjoon Kim-
dc.identifier.doi10.1371/journal.pbio.2005326-
dc.identifier.bibliographicCitationPLOS BIOLOGY, v.17, no.6, pp.e2005326-
dc.citation.titlePLOS BIOLOGY-
dc.citation.volume17-
dc.citation.number6-
dc.citation.startPagee2005326-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
Appears in Collections:
Center for Synaptic Brain Dysfunctions(시냅스 뇌질환 연구단) > 1. Journal Papers (저널논문)
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