H
Hongmei Chen
Researcher at Baylor College of Medicine
Publications - 15
Citations - 2192
Hongmei Chen is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Neurotransmission & Excitatory postsynaptic potential. The author has an hindex of 12, co-authored 14 publications receiving 1898 citations. Previous affiliations of Hongmei Chen include Boston Children's Hospital.
Papers
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Journal ArticleDOI
Dysfunction in GABA signalling mediates autism-like stereotypies and Rett syndrome phenotypes
Hsiao-Tuan Chao,Hongmei Chen,Rodney C. Samaco,Mingshan Xue,Mingshan Xue,Maria H. Chahrour,Jong Yoo,Jeffrey L. Neul,Shiaoching Gong,Hui-Chen Lu,Nathaniel Heintz,Marc Ekker,John L.R. Rubenstein,Jeffrey L. Noebels,Christian Rosenmund,Christian Rosenmund,Huda Y. Zoghbi +16 more
TL;DR: It is shown that mice lacking Mecp2 from GABA-releasing neurons recapitulate numerous Rett syndrome and autistic features, including repetitive behaviours, and that subtle dysfunction of GABAergic neurons contributes to numerous neuropsychiatric phenotypes.
Journal ArticleDOI
SHANK3 overexpression causes manic-like behaviour with unique pharmacogenetic properties
Kihoon Han,Kihoon Han,J. Lloyd Holder,J. Lloyd Holder,Christian P. Schaaf,Christian P. Schaaf,Hui Lu,Hui Lu,Hongmei Chen,Hongmei Chen,Hyojin Kang,Hyojin Kang,Hyojin Kang,Jianrong Tang,Jianrong Tang,Zhenyu Wu,Zhenyu Wu,Shuang Hao,Shuang Hao,Sau Wai Cheung,Peng Yu,Peng Yu,Hao Sun,Hao Sun,Amy M. Breman,Ankita Patel,Hui-Chen Lu,Huda Y. Zoghbi +27 more
TL;DR: This article found that incorrect gene dosage of SHANK3 (a gene linked to some human neuropsychiatric disorders, including autism spectrum disorder) is associated with behavioural abnormalities including mania, possibly because of actin regulation problems in excitatory/inhibitory synapses.
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Reversal of phenotypes in MECP2 duplication mice using genetic rescue or antisense oligonucleotides
Yehezkel Sztainberg,Hongmei Chen,John W. Swann,John W. Swann,Shuang Hao,Bin Tang,Bin Tang,Zhenyu Wu,Zhenyu Wu,Jianrong Tang,Jianrong Tang,Ying-Wooi Wan,Ying-Wooi Wan,Zhandong Liu,Zhandong Liu,Frank Rigo,Huda Y. Zoghbi +16 more
TL;DR: In this paper, a conditional MECP2-overexpressing mouse model was used to study the effect of methyl-CpG-binding protein 2 (MeCP2) overexpression.
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Loss of MeCP2 in Parvalbumin-and Somatostatin-Expressing Neurons in Mice Leads to Distinct Rett Syndrome-like Phenotypes
TL;DR: Mecp2, the mouse homolog of the gene that causes Rett syndrome, is deleted from the two most populous subtypes, parvalbumin- positive (PV+) and somatostatin-positive (SOM+) neurons, indicating that PV+ and SOM+ neurons contribute complementary aspects of the Rett phenotype and may have modular roles in regulating specific behaviors.
Journal ArticleDOI
Complexins facilitate neurotransmitter release at excitatory and inhibitory synapses in mammalian central nervous system
Mingshan Xue,Alicja Stradomska,Hongmei Chen,Nils Brose,Weiqi Zhang,Christian Rosenmund,Kerstin Reim +6 more
TL;DR: It is shown that genetic deletion of all Cplxs expressed in the mouse brain causes a reduction in Ca2+-triggered and spontaneous neurotransmitter release at both excitatory and inhibitory synapses.