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시냅스뇌질환연구단
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Increased excitatory synaptic transmission of dentate granule neurons in mice lacking PSD-95-interacting adhesion molecule Neph2/Kirrel3 during the early postnatal period.

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dc.contributor.authorJunyeop Daniel Roh-
dc.contributor.authorSu-Yeon Choi-
dc.contributor.authorYi Sul Cho-
dc.contributor.authorTae-Yong Choi-
dc.contributor.authorJong-Sil Park-
dc.contributor.authorTyler Cutforth-
dc.contributor.authorWoosuk Chung-
dc.contributor.authorHanwool Park-
dc.contributor.authorDongsoo Lee-
dc.contributor.authorMyeong-Heui Kim-
dc.contributor.authorYeunkum Lee-
dc.contributor.authorSeojung Mo-
dc.contributor.authorJeong-Seop Rhee-
dc.contributor.authorHyun Kim-
dc.contributor.authorJaewon Ko-
dc.contributor.authorSe-Young Choi-
dc.contributor.authorYong Chul Bae-
dc.contributor.authorKang Shen-
dc.contributor.authorEunjoon Kim-
dc.contributor.authorKihoon Han-
dc.date.available2017-05-19T01:12:43Z-
dc.date.created2017-03-22-
dc.date.issued2017-03-
dc.identifier.issn1662-5099-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/3455-
dc.description.abstractCopy number variants and point mutations of NEPH2 (also called KIRREL3) gene encoding an immunoglobulin (Ig) superfamily adhesion molecule have been linked to autism spectrum disorders, intellectual disability and neurocognitive delay associated with Jacobsen syndrome, but the physiological roles of Neph2 in the mammalian brain remain largely unknown. Neph2 is highly expressed in the dentate granule (DG) neurons of the hippocampus and is localized in both dendrites and axons. It was recently shown that Neph2 is required for the formation of mossy fiber filopodia, the axon terminal structure of DG neurons forming synapses with GABAergic neurons of CA3. In contrast, however, it is unknown whether Neph2 also has any roles in the postsynaptic compartments of DG neurons. We here report that, through its C-terminal PDZ domain-binding motif, Neph2 directly interacts with postsynaptic density (PSD)-95, an abundant excitatory postsynaptic scaffolding protein. Moreover, Neph2 protein is detected in the brain PSD fraction and interacts with PSD-95 in synaptosomal lysates. Functionally, loss of Neph2 in mice leads to age-specific defects in the synaptic connectivity of DG neurons. Specifically, Neph2−/− mice show significantly increased spontaneous excitatory synaptic events in DG neurons at postnatal week 2 when the endogenous Neph2 protein expression peaks, but show normal excitatory synaptic transmission at postnatal week 3. The evoked excitatory synaptic transmission and synaptic plasticity of medial perforant pathway (MPP)-DG synapses are also normal in Neph2−/− mice at postnatal week 3, further confirming the age-specific synaptic defects. Together, our results provide some evidence for the postsynaptic function of Neph2 in DG neurons during the early postnatal period, which might be implicated in neurodevelopmental and cognitive disorders caused by NEPH2 mutations. Copyright © 2017 Roh, Choi, Cho, Choi, Park, Cutforth, Chung, Park, Lee, Kim, Lee, Mo, Rhee, Kim, Ko, Choi, Bae, Shen, Kim and Han. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. © 2017 Roh, Choi, Cho, Choi, Park, Cutforth, Chung, Park, Lee, Kim, Lee, Mo, Rhee, Kim, Ko, Choi, Bae, Shen, Kim and Han. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. Frontiers-
dc.description.uri1-
dc.language영어-
dc.publisherFRONTIERS MEDIA SA-
dc.subjectKirrel3-
dc.subjectNeph2-
dc.subjectPSD-95-
dc.subjectdentate granule neuron-
dc.subjectexcitatory synapse-
dc.titleIncreased excitatory synaptic transmission of dentate granule neurons in mice lacking PSD-95-interacting adhesion molecule Neph2/Kirrel3 during the early postnatal period.-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000397084000001-
dc.identifier.scopusid2-s2.0-85018895494-
dc.identifier.rimsid59079ko
dc.date.tcdate2018-10-01-
dc.contributor.affiliatedAuthorSu-Yeon Choi-
dc.contributor.affiliatedAuthorHanwool Park-
dc.contributor.affiliatedAuthorDongsoo Lee-
dc.contributor.affiliatedAuthorYeunkum Lee-
dc.contributor.affiliatedAuthorEunjoon Kim-
dc.identifier.doi10.3389/fnmol.2017.00081-
dc.identifier.bibliographicCitationFRONTIERS IN MOLECULAR NEUROSCIENCE, v.10, pp.81 - 81-
dc.citation.titleFRONTIERS IN MOLECULAR NEUROSCIENCE-
dc.citation.volume10-
dc.citation.startPage81-
dc.citation.endPage81-
dc.date.scptcdate2018-10-01-
dc.description.wostc3-
dc.description.scptc2-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.subject.keywordAuthorDentate granule neuron-
dc.subject.keywordAuthorExcitatory synapse-
dc.subject.keywordAuthorKirrel3-
dc.subject.keywordAuthorNeph2-
dc.subject.keywordAuthorPSD-95-
Appears in Collections:
Center for Synaptic Brain Dysfunctions(시냅스 뇌질환 연구단) > 1. Journal Papers (저널논문)
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