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Loss of MeCP2 in cholinergic neurons causes part of RTT- like phenotypes via α7 receptor in hippocampus
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Loss of MeCP2 in cholinergic neurons causes part of RTT- like phenotypes via α7 receptor in hippocampus
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Journal Article
Loss of MeCP2 in cholinergic neurons causes part of RTT- like phenotypes via α7 receptor in hippocampus
2016
Overview
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.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ alpha7 Nicotinic Acetylcholine Receptor - metabolism
/ Animals
/ Biomedical and Life Sciences
/ Bridged Bicyclo Compounds - pharmacology
/ Caudate Nucleus - metabolism
/ Cholinergic Neurons - metabolism
/ Male
/ Methyl-CpG-Binding Protein 2 - metabolism
/ Original
/ Rett Syndrome - complications
/ RTT
/ 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
