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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

Reciprocal actions of REST and a microRNA promote neuronal identity.

TL;DR: It is shown that REST regulates the expression of a family of miRNAs, including brain-specific miR-124a, and the combined transcriptional and posttranscriptional consequences of REST action maximize the contrast between neuronal and nonneuronal cell phenotypes.
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The bifunctional microRNA miR-9/miR-9* regulates REST and CoREST and is downregulated in Huntington's disease.

TL;DR: It is found that levels of several microRNAs (miRNAs) with upstream RE1 sites are decreased in HD patient cortices relative to healthy controls, providing evidence for a double negative feedback loop between the REST silencing complex and the miRNAs it regulates.
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Modification of seizure activity by electrical stimulation: Cortical areas

TL;DR: Three different cortical areas were found with respect to the development, by repeated electrical stimulation, of electrographic and motor seizures in rats, and all areas showed similar reductions in AD thresholds when repeatedly stimulated.
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DICER1 deficit induces Alu RNA toxicity in age-related macular degeneration

TL;DR: Findings reveal a miRNA-independent cell survival function for DICER1 involving retrotransposon transcript degradation, show that Alu RNA can directly cause human pathology, and identify new targets for a major cause of blindness.
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Altered brain microRNA biogenesis contributes to phenotypic deficits in a 22q11-deletion mouse model

TL;DR: Evidence is provided that the abnormal miRNA biogenesis emerges because of haploinsufficiency of the Dgcr8 gene, which encodes an RNA-binding moiety of the 'microprocessor' complex and contributes to the behavioral and neuronal deficits associated with the 22q11.2 microdeletion.
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