Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA353100 | ENA |
REPOSITORIES: ENA
Similar Datasets
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.
2016-12-15 | GSE89757 | GEO
Project description:Experience-dependent plasticity (EDP) is essential for anatomical and functional maturation of sensory circuits during development and can be readily studied is the rodent barrel cortex. Using this model we aimed to uncover changes on the transcriptome level and applied RNA sequencing upon altered sensory experience in juvenile mice in a cortical column and layer specific manner. From column- and layer-specific barrel cortical tissue, high quality RNA was purified and sequenced. The current dataset entails an average of 50 million paired-end reads per sample, 75 base pairs in length.
2017-08-17 | GSE90929 | GEO
Project description:Visual cortical circuits show profound plasticity during early life and are later stabilized by molecular "brakes" limiting excessive circuit rewiring beyond a critical period. How the appearance of these factors is coordinated during the transition from development to adulthood remains unknown. We analyzed the role of miR-29a, a miRNA targeting factors involved in several important pathways for plasticity such as extracellular matrix and chromatin regulation. We found that visual cortical miR-29a expression in the visual cortex dramatically increases with age, but it is not experience-dependent. Precocious high levels of miR-29a induced by targeted intracortical injections of a miR-29a mimic 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 net intensity and number, and changed their chemical composition restoring permissive low chondroitin 4-O-sulfation levels characteristic of juvenile mice. Activated adult plasticity had the typical functional and proteomic signature of juvenile plasticity. Transcriptomic and proteomic studies indicated that miR-29a manipulation regulates the expression of plasticity factors acting at different cellular levels, from chromatin regulation to synaptic organization and extracellular matrix remodeling. Intriguingly, the projection of miR-29a regulated gene dataset onto cell-specific transcriptomes revealed that parvalbumin-positive interneurons and oligodendrocytes were the most affected cells. Overall, miR29a is a master regulator of the age-dependent plasticity brakes promoting stability of visual cortical circuits.
2020-11-04 | PXD016430 | Pride
Project description:Visual cortical circuits show profound plasticity during early life and are later stabilized by molecular "brakes" limiting excessive circuit rewiring beyond a critical period. How the appearance of these factors is coordinated during the transition from development to adulthood remains unknown. We analyzed the role of miR-29a, a miRNA targeting factors involved in several important pathways for plasticity such as extracellular matrix and chromatin regulation. We found that visual cortical miR-29a expression in the visual cortex dramatically increases with age, but it is not experience-dependent. Precocious high levels of miR-29a induced by targeted intracortical injections of a miR-29a mimic 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 net intensity and number, and changed their chemical composition restoring permissive low chondroitin 4-O-sulfation levels characteristic of juvenile mice. Activated adult plasticity had the typical functional and proteomic signature of juvenile plasticity. Transcriptomic and proteomic studies indicated that miR-29a manipulation regulates the expression of plasticity factors acting at different cellular levels, from chromatin regulation to synaptic organization and extracellular matrix remodeling. Intriguingly, the projection of miR-29a regulated gene dataset onto cell-specific transcriptomes revealed that parvalbumin-positive interneurons and oligodendrocytes were the most affected cells. Overall, miR29a is a master regulator of the age-dependent plasticity brakes promoting stability of visual cortical circuits.
2020-11-04 | PXD016358 | Pride
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.
2020-11-03 | GSE141734 | GEO
Project description:Experience-dependent plasticity of synapses modulates information processing in neural circuits and is essential for cognitive functions. Genomic enhancers are thought to modulate specific sets of synapses by regulating experience-induced transcription to thereby promote neural circuit plasticity. However, this idea remains untested. Thus, here we analyze the cellular and circuit functions of the genomic mechanisms that control the experience-induced transcription of Igf1 (Insulin-like growth factor 1) in disinhibitory VIP interneurons in the adult visual cortex. We find that two sensory-induced enhancers selectively and cooperatively drive sensory-induced Igf1 transcription and that these enhancers homeostatically control the ratio between excitation and inhibition (E/I-ratio) and neural activity in VIP interneurons to thereby restrict visual acuity. Thus, single experience-regulated enhancers are essential for maintaining sensory processing. Since cortical plasticity scales with neural activity in VIP interneurons, this also suggests that experience-induced transcription restricts plasticity in adult neural circuits to preserve the brain’s functional integrity.
2023-06-27 | GSE227342 | GEO
Project description:Experience-dependent synaptic plasticity refines brain circuits during development. To uncover protein synthesis-dependent mechanisms contributing to experience-dependent plasticity, we performed quantitative proteomic analysis of the nascent proteome using improved bio-orthogonal metabolic labeling (BONCAT) to identify candidate plasticity proteins (CPPs) that undergo differential protein synthesis in response to visual conditioning (VC) in Xenopus optic tectum. We identified 83 CPPs that formed strongly connected networks and were annotated to a variety of biological functions, including RNA splicing, protein translation, and chromatin remodeling. Functional analysis of select CPPs using translation blocking morpholinos revealed the requirement of eukaryotic initiation factor 3 subunit A (eIF3A), fused in sarcoma (FUS), and ribosomal protein s17 (RPS17) in experience-dependent structural plasticity of tectal neurons. These results demonstrate that the nascent proteome is dynamic in response to VC and that de novo synthesis of the machinery that regulates gene expression and protein translation is required for experience-dependent structural plasticity.
2017-11-21 | MSV000081728 | MassIVE
Project description:Sensory experience restricts cortical plasticity by inducing IGF-1 in VIP neurons
| PRJNA309869 | ENA
Project description:Experience-dependent gene transcription is required for nervous system development and function. However, the DNA regulatory elements that control this program of gene expression are not well defined. Here we characterize the enhancers that function across the genome to mediate activity-dependent transcription in neurons. While ~12,000 putative activity-regulated enhancer sequences have previously been identified that are enriched for H3K4me1 and the histone acetyltransferase CBP, we find that this chromatin signature is not sufficient to distinguish which of these regulatory sequences are actively engaged in promoting activity-dependent transcription. We show here that a subset of H3K4me1/CBP positive enhancers that is enriched for H3K27 acetylation (H3K27ac) in vivo, and shows increased H3K27ac upon membrane depolarization of cortical neurons, function to regulate activity-dependent transcription. The function of many of these activity-regulated enhancers appears to be dependent on the binding of FOS, a protein that had previously been thought to interact primarily with the promoters of activity-regulated genes. Furthermore, many of these target genes in cortical neurons encode neuron specific proteins that regulate synaptic development and function. These findings suggest that FOS functions at enhancers to control activity-dependent gene programs that are critical for nervous system function, and provide a resource of activity-dependent enhancers that may give insight into genetic variation that contributes to brain development and disease. Genome-wide maps of H3K27ac and AP1 transcription factors (CFOS, FOSB, JUNB) before and after neuronal activity in mouse cortical neurons.
2014-09-07 | E-GEOD-60192 | biostudies-arrayexpress
Project description:Microglial Rac1 is essential for experience-dependent brain plasticity and cognitive performance
| PRJNA1024533 | ENA