MECP2
雷特综合征
神经科学
兴奋性突触后电位
神经传递
海马结构
抑制性突触后电位
海马体
突触
突触可塑性
突触疲劳
小RNA
生物
表型
遗传学
受体
基因
作者
Patricia M. Horvath,Michelle K Piazza,Ege T. Kavalali,Lisa M. Monteggia
出处
期刊:Hippocampus
[Wiley]
日期:2022-07-19
卷期号:32 (8): 610-623
摘要
Rett syndrome is a leading cause of intellectual disability in females primarily caused by loss of function mutations in the transcriptional regulator MeCP2. Loss of MeCP2 leads to a host of synaptic phenotypes that are believed to underlie Rett syndrome pathophysiology. Synaptic deficits vary by brain region upon MeCP2 loss, suggesting distinct molecular alterations leading to disparate synaptic outcomes. In this study, we examined the contribution of MeCP2's newly described role in miRNA regulation to regional molecular and synaptic impairments. Two miRNAs, miR-101a and miR-203, were identified and confirmed as upregulated in MeCP2 KO mice in the hippocampus and cortex, respectively. miR-101a overexpression in hippocampal cultures led to opposing effects at excitatory and inhibitory synapses and in spontaneous and evoked neurotransmission, revealing the potential for a single miRNA to broadly regulate synapse function in the hippocampus. These results highlight the importance of regional alterations in miRNA expression and the specific impact on synaptic function with potential implications for Rett syndrome.
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