Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA384021 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5470480_1.fastq.gz | Fastqsanger.gz | |||
| SRR5470480_2.fastq.gz | Fastqsanger.gz | |||
| SRR5470471_1.fastq.gz | Fastqsanger.gz | |||
| SRR5470471_2.fastq.gz | Fastqsanger.gz | |||
| SRR5470481_1.fastq.gz | Fastqsanger.gz |
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Project description:Throughout childhood and adolescence, periods of heightened neuroplasticity are critical for the development of healthy brain function and behavior. Given the high prevalence of neurodevelopmental disorders such as autism, identifying disruptors of developmental plasticity represents an essential step for developing strategies for prevention and intervention. Applying a novel computational approach that systematically assessed connections between 436 transcriptional signatures of disease and multiple signatures of neuroplasticity, we identified inflammation as a common pathological process central to a diverse set of diseases predicted to dysregulate plasticity signatures. We tested the hypothesis that inflammation disrupts developmental cortical plasticity in vivo using the mouse ocular dominance model of experience-dependent plasticity in primary visual cortex. We found administration of systemic lipopolysaccharide suppressed plasticity during juvenile critical period with accompanying transcriptional changes in a particular set of molecular regulators within primary visual cortex. These findings suggest inflammation may have unrecognized adverse consequences on the postnatal developmental trajectory and indicates that treating inflammation may reduce the burden of neurodevelopmental disorders.
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Project description:Autism spectrum disorders such as Rett syndrome (RTT) have been hypothesized to arise from defects in experience-dependent synapse maturation. RTT is caused by mutations in MECP2, a nuclear protein that becomes phosphorylated at S421 in response to neuronal activation. We show here that disruption of MeCP2 S421 phosphorylation in vivo results in defects in synapse development and behavior, implicating activity-dependent regulation of MeCP2 in brain development and RTT. We investigated the mechanism by which S421 phosphorylation regulates MeCP2 function and show by chromatin immunoprecipitation-sequencing that this modification occurs on MeCP2 bound across the genome. The phosphorylation of MeCP2 S421 appears not to regulate the expression of specific genes; rather, MeCP2 functions as a histone-like factor whose phosphorylation may facilitate a genome-wide response of chromatin to neuronal activity during nervous system development. We propose that RTT results in part from a loss of this experience-dependent chromatin remodeling. Gene expression analysis of RNA isolated from P17 mouse visual cortex was performed comparing global gene expression between Wild-Type and MeCP2 S421A knock-in mice. We isolated RNA from the visual cortex of 4 wild-type and 4 MeCP2 S421A littermate P17 Mice, and analyzed mRNA expression using the Affymetrix Mouse Gene 1.0 ST microarray platform.
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Project description:Visual cortical circuits show profound plasticity during early life and are later stabilized by molecular "brakes" limiting excessive rewiring beyond a critical period. The mechanisms coordinating the expression of these factors during the transition from development to adulthood remain unknown. We found that miR-29a expression in the visual cortex dramatically increases with age, but it is not experience-dependent. Precocious high levels of miR-29a blocked ocular dominance plasticity and caused an early appearance of perineuronal nets. Conversely, inhibition of miR-29a in adult mice using LNA antagomirs activated ocular dominance plasticity, reduced perineuronal nets and restored their juvenile chemical composition. Activated adult plasticity had the typical functional and proteomic signature of critical period plasticity. Transcriptomic and proteomic studies indicated that miR-29a manipulation regulates the expression of plasticity brakes mainly affecting parvalbumin-positive interneurons. These data indicate that miR29a is a master regulator of the plasticity brakes promoting age-dependent stabilization of visual cortical circuits.
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