Inactivation of Magel2 suppresses oxytocin neurons through synaptic excitation-inhibition imbalance

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dc.authorid0000-0003-4604-4765
dc.authorid0000-0002-3247-613X
dc.authorid0000-0002-3325-8820
dc.contributor.authorAteş, Tayfun
dc.contributor.authorÖncül, Merve
dc.contributor.authorDilsiz, Pelin
dc.contributor.authorTopçu, İskalen Cansu
dc.contributor.authorCıvaş, Cihan Civan
dc.contributor.authorAlp, Muhammed İkbal
dc.contributor.authorAklan, İltan
dc.contributor.authorÖz, Edanur Ateş
dc.contributor.authorYavuz, Yavuz
dc.contributor.authorYılmaz, Bayram
dc.contributor.authorAtasoy, Nilüfer Sayar
dc.contributor.authorAtasoy, Deniz
dc.date.accessioned10.07.201910:49:13
dc.date.accessioned2019-07-10T19:49:55Z
dc.date.available10.07.201910:49:13
dc.date.available2019-07-10T19:49:55Z
dc.date.issued2019
dc.departmentİstanbul Medipol Üniversitesi, Rektörlük, Rejeneratif ve Restoratif Tıp Araştırmaları Merkezi (REMER)
dc.descriptionWOS: 000452684700005
dc.descriptionPubMed ID: 30240706
dc.description.abstractPrader-Willi and the related Schaaf-Yang Syndromes (PWS/SYS) are rare neurodevelopmental disorders characterized by overlapping phenotypes of high incidence of autism spectrum disorders (ASD) and neonatal feeding difficulties. Based on clinical and basic studies, oxytocin pathway defects are suggested to contribute disease pathogenesis but the mechanism has been poorly understood. Specifically, whether the impairment in oxytocin system is limited to neuropeptide levels and how the functional properties of broader oxytocin neuron circuits affected in PWS/SYS have not been addressed. Using cell type specific electrophysiology, we investigated basic synaptic and cell autonomous properties of oxytocin neurons in the absence of MAGEL2; a hypothalamus enriched ubiquitin ligase regulator that is inactivated in both syndromes. We observed significant suppression of overall ex vivo oxytocin neuron activity, which was largely contributed by altered synaptic input profile; with reduced excitatory and increased inhibitory currents. Our results suggest that dysregulation of oxytocin system goes beyond altered neuropeptide expression and synaptic excitation inhibition imbalance impairs overall oxytocin pathway function.
dc.description.sponsorshipScientific and Technological Research Council of Turkey (TUBITAK) [214S361]en_US
dc.description.sponsorshipThis work is supported by The Scientific and Technological Research Council of Turkey (TUBITAK) funding to D.A. grant no: 214S361.en_US
dc.identifier.citationAteş, T., Öncül, M., Dilsiz, P., Topçu, İ. C., Cıvaş, C. C., Alp, M. İ. ... Atasoy, D. (2019). Inactivation of Magel2 suppresses oxytocin neurons through synaptic excitation-inhibition imbalance. Neurobiology of Disease, 121, 58-64. https://dx.doi.org/10.1016/j.nbd.2018.09.017
dc.identifier.doi10.1016/j.nbd.2018.09.017
dc.identifier.endpage64
dc.identifier.issn0969-9961
dc.identifier.issn1095-953X
dc.identifier.scopusqualityQ1
dc.identifier.startpage58
dc.identifier.urihttps://dx.doi.org/10.1016/j.nbd.2018.09.017
dc.identifier.urihttps://hdl.handle.net/20.500.12511/1820
dc.identifier.volume121
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherAcademic Press Inc Elsevier Science
dc.relation.ecinfo:eu-repo/grantAgreement/TUBITAK/SOBAG/214S361
dc.relation.ispartofNeurobiology of Diseaseen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectPrader Willi Syndrome
dc.subjectAutism
dc.subjectMagel2
dc.subjectOxytocin
dc.subjectAMPA
dc.subjectNMDA
dc.subjectElectrophysiology
dc.titleInactivation of Magel2 suppresses oxytocin neurons through synaptic excitation-inhibition imbalance
dc.typeArticle

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