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Open AccessJournal ArticleDOI

Loss of microRNAs in pyramidal neurons leads to specific changes in inhibitory synaptic transmission in the prefrontal cortex

TLDR
A vital role for miRNAs in governing essential aspects of inhibitory transmission and interneuron development in the mammalian nervous system is suggested.
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This article is published in Molecular and Cellular Neuroscience.The article was published on 2012-07-01 and is currently open access. It has received 51 citations till now. The article focuses on the topics: Interneuron & Prefrontal cortex.

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Journal ArticleDOI

MicroRNAs Shape the Neuronal Landscape

TL;DR: Here it is considered that recent advances in the study of microRNA-mediated regulation of synaptic form and function in mice are considered to be significant.
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MeCP2 Suppresses Nuclear MicroRNA Processing and Dendritic Growth by Regulating the DGCR8/Drosha Complex

TL;DR: It is reported that MeCP2 regulates gene expression posttranscriptionally by suppressing nuclear microRNA processing by binding directly to DiGeorge syndrome critical region 8 (DGCR8), a critical component of the nuclear micro RNA-processing machinery, and interferes with the assembly of Drosha and DG CR8 complex.
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Expression of microRNAs and Other Small RNAs in Prefrontal Cortex in Schizophrenia, Bipolar Disorder and Depressed Subjects

TL;DR: There was a significant inverse correlation between the fold-change of a given miRNA seen in schizophrenia and its synaptic enrichment ratio observed in controls, suggesting some deficit in miRNA biogenesis, transport, processing or turnover in schizophrenia that is selective for the synaptic compartment.
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MicroRNAs and synaptic plasticity--a mutual relationship.

TL;DR: How neuronal activity influences each step in the lifetime of miRNAs, including the regulation of transcription, maturation, gene regulatory function and turnover in mammals is summarized.
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MicroRNA Profiling of Neurons Generated Using Induced Pluripotent Stem Cells Derived from Patients with Schizophrenia and Schizoaffective Disorder, and 22q11.2 Del

TL;DR: Differentially expressed miRNAs previously identified using autopsy samples and peripheral cells, both of which have significant methodological problems, are indeed disrupted in neuropsychiatric disorders and likely have an underlying genetic basis.
References
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Journal ArticleDOI

microRNA expression in the prefrontal cortex of individuals with schizophrenia and schizoaffective disorder.

TL;DR: This study is the first to find altered miRNA profiles in postmortem prefrontal cortex from schizophrenia patients, and distinguished eight miRNAs distinguished by being expressed at lower microarray levels in schizophrenia samples versus comparison samples with quantitative RT-PCR.
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Types of neurons, synaptic connections and chemical characteristics of cells immunoreactive for calbindin-D28K, parvalbumin and calretinin in the neocortex

TL;DR: All, or the majority, of calbindin-, parvalbumin- and calretinin-immunoreactive cells are smooth nonpyramidal neurons (interneurons) which participate in a variety of complex cortical circuits that may differ depending on the species, cortical area or layer where they are located.
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Mice lacking Dlx1 show subtype-specific loss of interneurons, reduced inhibition and epilepsy.

TL;DR: The decrease in the number of interneurons was associated with a reduction of GABA-mediated inhibitory postsynaptic current in neocortex and hippocampus in vitro and cortical dysrhythmia in vivo and cell transplantation analysis demonstrates that interneuron loss reflects cell-autonomous functions of Dlx1.
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Genetic targeting of principal neurons in neocortex and hippocampus of NEX-Cre mice

TL;DR: A mouse line that expresses Cre recombinase under control of regulatory sequences of NEX, a gene that encodes a neuronal basic helix‐loop‐helix (bHLH) protein, will be a valuable tool for behavioral research and the conditional inactivation of target genes in pyramidal neurons of the dorsal telencephalon.
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Homeostatic regulation of MeCP2 expression by a CREB-induced microRNA.

TL;DR: It is found that MeCP2 translation is regulated by microRNA 132 (miR132) and this feedback loop may provide a mechanism for homeostatic control of Me CP2 expression.
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