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dc.contributor.author Roh, Junyeop D. -
dc.contributor.author Choi, Su-Yeon -
dc.contributor.author Cho, Yi Sul -
dc.contributor.author Choi, Tae-Yong -
dc.contributor.author Park, Jong-Sil -
dc.contributor.author Cutforth, Tyler -
dc.contributor.author Chung, Woosuk -
dc.contributor.author Park, Hanwool -
dc.contributor.author Lee, Dongsoo -
dc.contributor.author Kim, Myeong-Heui -
dc.contributor.author Lee, Yeunkum -
dc.contributor.author Mo, Seojung -
dc.contributor.author Rhee, Jeong-Seop -
dc.contributor.author Kim, Hyun -
dc.contributor.author Ko, Jaewon -
dc.contributor.author Choi, Se-Young -
dc.contributor.author Bae, Yong Chul -
dc.contributor.author Shen, Kang -
dc.contributor.author Kim, Eunjoon -
dc.contributor.author Han, Kihoon -
dc.date.available 2017-08-10T08:15:43Z -
dc.date.created 2017-08-09 -
dc.date.issued 2017-03 -
dc.identifier.issn 1662-5099 -
dc.identifier.uri http://hdl.handle.net/20.500.11750/4211 -
dc.description.abstract Copy 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. © 2017 Roh, Choi, Cho, Choi, Park, Cutforth, Chung, Park, Lee, Kim, Lee, Mo, Rhee, Kim, Ko, Choi, Bae, Shen, Kim and Han. -
dc.publisher Frontiers Research Foundation -
dc.title Increased Excitatory Synaptic Transmission of Dentate Granule Neurons in Mice Lacking PSD-95-Interacting Adhesion Molecule Neph2/Kirrel3 during the Early Postnatal Period -
dc.type Article -
dc.identifier.doi 10.3389/fnmol.2017.00081 -
dc.identifier.scopusid 2-s2.0-85018895494 -
dc.identifier.bibliographicCitation Frontiers in Molecular Neuroscience, v.10 -
dc.description.isOpenAccess FALSE -
dc.subject.keywordAuthor Neph2 -
dc.subject.keywordAuthor Kirrel3 -
dc.subject.keywordAuthor PSD-95 -
dc.subject.keywordAuthor excitatory synapse -
dc.subject.keywordAuthor dentate granule neuron -
dc.subject.keywordPlus Dentate Granule Neuron -
dc.subject.keywordPlus Excitatory Synapse -
dc.subject.keywordPlus Intellectual Disability -
dc.subject.keywordPlus Kirrel3 -
dc.subject.keywordPlus LAR RPTPs -
dc.subject.keywordPlus Mutations -
dc.subject.keywordPlus Neph2 -
dc.subject.keywordPlus Neuroligins -
dc.subject.keywordPlus Protein CASK -
dc.subject.keywordPlus PSD 95 -
dc.subject.keywordPlus Rat Brain -
dc.subject.keywordPlus Receptor -
dc.subject.keywordPlus Specificity -
dc.subject.keywordPlus Synapses -
dc.citation.title Frontiers in Molecular Neuroscience -
dc.citation.volume 10 -
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Appears in Collections:
Department of Brain Sciences Laboratory of Synapse Formation and Function 1. Journal Articles

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