Altered NMDAR signaling underlies autistic-like features in mouse models of CDKL5 deficiency disorder

Mouse models of CDKL5 deficiency disorder (CDD) recapitulate multiple clinical symptoms of CDD, such as intellectual disability and autism. Here, the authors show that selective loss of CDKL5 from GABAergic neurons leads to social deficits and stereotypic behaviors, which can be ameliorated through...

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Autores principales: Sheng Tang, Barbara Terzic, I-Ting Judy Wang, Nicolas Sarmiento, Katherine Sizov, Yue Cui, Hajime Takano, Eric D. Marsh, Zhaolan Zhou, Douglas A. Coulter
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Lenguaje:EN
Publicado: Nature Portfolio 2019
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Acceso en línea:https://doaj.org/article/fcc09e9d517f46139fc63936735506c3
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spelling oai:doaj.org-article:fcc09e9d517f46139fc63936735506c32021-12-02T14:35:56ZAltered NMDAR signaling underlies autistic-like features in mouse models of CDKL5 deficiency disorder10.1038/s41467-019-10689-w2041-1723https://doaj.org/article/fcc09e9d517f46139fc63936735506c32019-06-01T00:00:00Zhttps://doi.org/10.1038/s41467-019-10689-whttps://doaj.org/toc/2041-1723Mouse models of CDKL5 deficiency disorder (CDD) recapitulate multiple clinical symptoms of CDD, such as intellectual disability and autism. Here, the authors show that selective loss of CDKL5 from GABAergic neurons leads to social deficits and stereotypic behaviors, which can be ameliorated through inhibition of NMDAR signaling.Sheng TangBarbara TerzicI-Ting Judy WangNicolas SarmientoKatherine SizovYue CuiHajime TakanoEric D. MarshZhaolan ZhouDouglas A. CoulterNature PortfolioarticleScienceQENNature Communications, Vol 10, Iss 1, Pp 1-14 (2019)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Sheng Tang
Barbara Terzic
I-Ting Judy Wang
Nicolas Sarmiento
Katherine Sizov
Yue Cui
Hajime Takano
Eric D. Marsh
Zhaolan Zhou
Douglas A. Coulter
Altered NMDAR signaling underlies autistic-like features in mouse models of CDKL5 deficiency disorder
description Mouse models of CDKL5 deficiency disorder (CDD) recapitulate multiple clinical symptoms of CDD, such as intellectual disability and autism. Here, the authors show that selective loss of CDKL5 from GABAergic neurons leads to social deficits and stereotypic behaviors, which can be ameliorated through inhibition of NMDAR signaling.
format article
author Sheng Tang
Barbara Terzic
I-Ting Judy Wang
Nicolas Sarmiento
Katherine Sizov
Yue Cui
Hajime Takano
Eric D. Marsh
Zhaolan Zhou
Douglas A. Coulter
author_facet Sheng Tang
Barbara Terzic
I-Ting Judy Wang
Nicolas Sarmiento
Katherine Sizov
Yue Cui
Hajime Takano
Eric D. Marsh
Zhaolan Zhou
Douglas A. Coulter
author_sort Sheng Tang
title Altered NMDAR signaling underlies autistic-like features in mouse models of CDKL5 deficiency disorder
title_short Altered NMDAR signaling underlies autistic-like features in mouse models of CDKL5 deficiency disorder
title_full Altered NMDAR signaling underlies autistic-like features in mouse models of CDKL5 deficiency disorder
title_fullStr Altered NMDAR signaling underlies autistic-like features in mouse models of CDKL5 deficiency disorder
title_full_unstemmed Altered NMDAR signaling underlies autistic-like features in mouse models of CDKL5 deficiency disorder
title_sort altered nmdar signaling underlies autistic-like features in mouse models of cdkl5 deficiency disorder
publisher Nature Portfolio
publishDate 2019
url https://doaj.org/article/fcc09e9d517f46139fc63936735506c3
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