Loss of MeCP2 in cholinergic neurons causes part of RTT- like phenotypes via α7 receptor in hippocampus

Mutations in the X-linked MECP2 gene cause Rett syndrome （RTT）, an autism spectrum disorder characterized by impaired social interactions, motor abnormalities, cognitive defects and a high risk of epilepsy. Here, we showed that conditional deletion of Mecp2 in cholinergic neurons caused part of RTT-...

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Published inCell research Vol. 26; no. 6; pp. 728 - 742
Main Authors Zhang, Ying, Cao, Shu-Xia, Sun, Peng, He, Hai-Yang, Yang, Ci-Hang, Chen, Xiao-Juan, Shen, Chen-Jie, Wang, Xiao-Dong, Chen, Zhong, Berg, Darwin K, Duan, Shumin, Li, Xiao-Ming
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.06.2016
Nature Publishing Group
Subjects
631/378/1595/1554
631/45/612/1239
631/80/86
692/699/476
alpha7 Nicotinic Acetylcholine Receptor - metabolism
Animals
Benzamides - pharmacology
Biomedical and Life Sciences
Bridged Bicyclo Compounds - pharmacology
Caudate Nucleus - metabolism
Cell Biology
Cholinergic Neurons - metabolism
Disease Susceptibility
Gene Deletion
Hippocampus - drug effects
Hippocampus - metabolism
Life Sciences
Male
Methyl-CpG-Binding Protein 2 - metabolism
Mice, Inbred C57BL
Mice, Knockout
Models, Biological
Nicotine - pharmacology
Original
original-article
Phenotype
Prosencephalon - metabolism
Rett Syndrome - complications
Rett Syndrome - metabolism
Rett Syndrome - pathology
RTT
Seizures - complications
Seizures - pathology
Signal Transduction - drug effects
乙酰胆碱受体
基因突变
海马
社会关系
胆碱乙酰转移酶
胆碱能神经元
表型
MeCP2
RTT-like phenotypes
cholinergic system
Rett syndrome
Online AccessGet full text

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Abstract Mutations in the X-linked MECP2 gene cause Rett syndrome （RTT）, an autism spectrum disorder characterized by impaired social interactions, motor abnormalities, cognitive defects and a high risk of epilepsy. Here, we showed that conditional deletion of Mecp2 in cholinergic neurons caused part of RTT-like phenotypes, which could be rescued by re-expressing Mecp2 in the basal forebrain （BF） eholinergic neurons rather than in the caudate putamen of conditional knockout （Chat-Mecp2-/y） mice. We found that choline acetyltransferase expression was decreased in the BF and that α7 nicotine acetylcholine receptor signaling was strongly impaired in the hippocampus of Chat-Mecp2^-/y mice, which is sufficient to produce neuronal hyperexcitation and increase seizure susceptibility. Application of PNU282987 or nicotine in the hippocampus rescued these phenotypes in Chat-Mecp2^-/y mice. Taken together, our findings suggest that MeCP2 is critical for normal function of cholinergic neurons and dysfunction of cholinergic neurons can contribute to numerous neuropsychiatric phenotypes.
AbstractList Mutations in the X-linked MECP2 gene cause Rett syndrome (RTT), an autism spectrum disorder characterized by impaired social interactions, motor abnormalities, cognitive defects and a high risk of epilepsy. Here, we showed that conditional deletion of Mecp2 in cholinergic neurons caused part of RTT-like phenotypes, which could be rescued by re-expressing Mecp2 in the basal forebrain (BF) cholinergic neurons rather than in the caudate putamen of conditional knockout (Chat-Mecp2(-/y)) mice. We found that choline acetyltransferase expression was decreased in the BF and that α7 nicotine acetylcholine receptor signaling was strongly impaired in the hippocampus of Chat-Mecp2(-/y) mice, which is sufficient to produce neuronal hyperexcitation and increase seizure susceptibility. Application of PNU282987 or nicotine in the hippocampus rescued these phenotypes in Chat-Mecp2(-/y) mice. Taken together, our findings suggest that MeCP2 is critical for normal function of cholinergic neurons and dysfunction of cholinergic neurons can contribute to numerous neuropsychiatric phenotypes.
Mutations in the X-linked MECP2 gene cause Rett syndrome (RTT), an autism spectrum disorder characterized by impaired social interactions, motor abnormalities, cognitive defects and a high risk of epilepsy. Here, we showed that conditional deletion of Mecp2 in cholinergic neurons caused part of RTT-like phenotypes, which could be rescued by re-expressing Mecp2 in the basal forebrain (BF) cholinergic neurons rather than in the caudate putamen of conditional knockout ( Chat-Mecp2 −/y ) mice. We found that choline acetyltransferase expression was decreased in the BF and that α7 nicotine acetylcholine receptor signaling was strongly impaired in the hippocampus of Chat-Mecp2 −/y mice, which is sufficient to produce neuronal hyperexcitation and increase seizure susceptibility. Application of PNU282987 or nicotine in the hippocampus rescued these phenotypes in Chat-Mecp2 −/y mice. Taken together, our findings suggest that MeCP2 is critical for normal function of cholinergic neurons and dysfunction of cholinergic neurons can contribute to numerous neuropsychiatric phenotypes.
Mutations in the X-linked MECP2 gene cause Rett syndrome （RTT）, an autism spectrum disorder characterized by impaired social interactions, motor abnormalities, cognitive defects and a high risk of epilepsy. Here, we showed that conditional deletion of Mecp2 in cholinergic neurons caused part of RTT-like phenotypes, which could be rescued by re-expressing Mecp2 in the basal forebrain （BF） eholinergic neurons rather than in the caudate putamen of conditional knockout （Chat-Mecp2-/y） mice. We found that choline acetyltransferase expression was decreased in the BF and that α7 nicotine acetylcholine receptor signaling was strongly impaired in the hippocampus of Chat-Mecp2^-/y mice, which is sufficient to produce neuronal hyperexcitation and increase seizure susceptibility. Application of PNU282987 or nicotine in the hippocampus rescued these phenotypes in Chat-Mecp2^-/y mice. Taken together, our findings suggest that MeCP2 is critical for normal function of cholinergic neurons and dysfunction of cholinergic neurons can contribute to numerous neuropsychiatric phenotypes.
Author Ying Zhang Shu-Xia Cao Peng Sun Hai-Yang He Ci-Hang Yang Xiao-Juan Chen Chen-Jie Shen Xiao-Dong Wang Zhong Chen Darwin K Berg Shumin Duan Xiao-Ming Li
AuthorAffiliation Department of Neurobiology, Institute of Neuroscienee, Key Laboratory of Medical Neurobiology of the Ministry of Health of Chi- na, Collaborative Innovation Center for Brain Science, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China Neurobiology Section, Division of Biological Sciences and Center for Neural Circuits and Behavior, University of California, San Diego, La Jolla, CA 92093-0357, USA Soft Matter Research Center, Zhejiang University, Hangzhou, Zhejiang, China
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DocumentTitleAlternate Loss of MeCP2 in cholinergic neurons causes part of RTT- like phenotypes via α7 receptor in hippocampus
α7 receptors as a potential target for RTT treatment
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RTT-like phenotypes
cholinergic system
Rett syndrome
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Notes 31-1568
MeCP2; cholinergic system; Rett syndrome; RTT-Iike phenotypes
Mutations in the X-linked MECP2 gene cause Rett syndrome （RTT）, an autism spectrum disorder characterized by impaired social interactions, motor abnormalities, cognitive defects and a high risk of epilepsy. Here, we showed that conditional deletion of Mecp2 in cholinergic neurons caused part of RTT-like phenotypes, which could be rescued by re-expressing Mecp2 in the basal forebrain （BF） eholinergic neurons rather than in the caudate putamen of conditional knockout （Chat-Mecp2-/y） mice. We found that choline acetyltransferase expression was decreased in the BF and that α7 nicotine acetylcholine receptor signaling was strongly impaired in the hippocampus of Chat-Mecp2^-/y mice, which is sufficient to produce neuronal hyperexcitation and increase seizure susceptibility. Application of PNU282987 or nicotine in the hippocampus rescued these phenotypes in Chat-Mecp2^-/y mice. Taken together, our findings suggest that MeCP2 is critical for normal function of cholinergic neurons and dysfunction of cholinergic neurons can contribute to numerous neuropsychiatric phenotypes.
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These two authors contributed equally to this work.
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Snippet Mutations in the X-linked MECP2 gene cause Rett syndrome （RTT）, an autism spectrum disorder characterized by impaired social interactions, motor abnormalities,...
Mutations in the X-linked MECP2 gene cause Rett syndrome (RTT), an autism spectrum disorder characterized by impaired social interactions, motor abnormalities,...
Mutations in the X-linked MECP2 gene cause Rett syndrome (RTT), an autism spectrum disorder characterized by impaired social interactions, motor abnormalities,...
SourceID pubmedcentral
proquest
crossref
pubmed
springer
chongqing
SourceType Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage 728
SubjectTerms 631/378/1595/1554
631/45/612/1239
631/80/86
692/699/476
alpha7 Nicotinic Acetylcholine Receptor - metabolism
Animals
Benzamides - pharmacology
Biomedical and Life Sciences
Bridged Bicyclo Compounds - pharmacology
Caudate Nucleus - metabolism
Cell Biology
Cholinergic Neurons - metabolism
Disease Susceptibility
Gene Deletion
Hippocampus - drug effects
Hippocampus - metabolism
Life Sciences
Male
Methyl-CpG-Binding Protein 2 - metabolism
Mice, Inbred C57BL
Mice, Knockout
Models, Biological
Nicotine - pharmacology
Original
original-article
Phenotype
Prosencephalon - metabolism
Rett Syndrome - complications
Rett Syndrome - metabolism
Rett Syndrome - pathology
RTT
Seizures - complications
Seizures - pathology
Signal Transduction - drug effects
乙酰胆碱受体
基因突变
海马
社会关系
胆碱乙酰转移酶
胆碱能神经元
表型
Title Loss of MeCP2 in cholinergic neurons causes part of RTT- like phenotypes via α7 receptor in hippocampus
URI http://lib.cqvip.com/qk/85240X/201606/669671117.html
https://link.springer.com/article/10.1038/cr.2016.48
https://www.ncbi.nlm.nih.gov/pubmed/27103432
https://search.proquest.com/docview/1793908423
https://pubmed.ncbi.nlm.nih.gov/PMC4897179
Volume 26
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