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.authorLee, Hyejinko
dc.contributor.authorShin, Wangyongko
dc.contributor.authorKim, Kyungdeokko
dc.contributor.authorLee, Suhoko
dc.contributor.authorLee, Eun-Jaeko
dc.contributor.authorKim, Jihyeko
dc.contributor.authorKweon, Hanseulko
dc.contributor.authorLee, Euneeko
dc.contributor.authorPark, Haramko
dc.contributor.authorKang, Muwonko
dc.contributor.authorYang, Estherko
dc.contributor.authorKim, Hyunko
dc.contributor.authorKim, Eunjoonko
dc.date.accessioned2019-07-23T07:20:04Z-
dc.date.available2019-07-23T07:20:04Z-
dc.date.created2019-07-23-
dc.date.created2019-07-23-
dc.date.issued2019-06-
dc.identifier.citationPLOS BIOLOGY, v.17, no.6-
dc.identifier.issn1544-9173-
dc.identifier.urihttp://hdl.handle.net/10203/263750-
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, alpha-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 3 beta (GSK3 beta) 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/GSK3 beta signaling, LTD, and locomotive and cognitive behaviors.-
dc.languageEnglish-
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.identifier.wosid000473675900002-
dc.identifier.scopusid2-s2.0-85067477026-
dc.type.rimsART-
dc.citation.volume17-
dc.citation.issue6-
dc.citation.publicationnamePLOS BIOLOGY-
dc.identifier.doi10.1371/journal.pbio.2005326-
dc.contributor.localauthorKim, Eunjoon-
dc.contributor.nonIdAuthorLee, Hyejin-
dc.contributor.nonIdAuthorLee, Suho-
dc.contributor.nonIdAuthorLee, Eun-Jae-
dc.contributor.nonIdAuthorKim, Jihye-
dc.contributor.nonIdAuthorKweon, Hanseul-
dc.contributor.nonIdAuthorLee, Eunee-
dc.contributor.nonIdAuthorPark, Haram-
dc.contributor.nonIdAuthorKang, Muwon-
dc.contributor.nonIdAuthorYang, Esther-
dc.contributor.nonIdAuthorKim, Hyun-
dc.description.isOpenAccessY-
dc.type.journalArticleArticle-
dc.subject.keywordPlusPROTEIN-TYROSINE PHOSPHATASES-
dc.subject.keywordPlusSYNAPTIC ADHESION MOLECULES-
dc.subject.keywordPlusAMPA RECEPTOR TRAFFICKING-
dc.subject.keywordPlusPTP-DELTA-
dc.subject.keywordPlusMICE LACKING-
dc.subject.keywordPlusMATRIX METALLOPROTEINASES-
dc.subject.keywordPlusMULTIPLE-SCLEROSIS-
dc.subject.keywordPlusLAR-RPTPS-
dc.subject.keywordPlusNMDA-
dc.subject.keywordPlusAKT-
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