Expression data from postnatal day (P) 14, 28, 60 mouse visual cortex (V1)
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE11764 | GEO | 2008/06/12
SECONDARY ACCESSION(S): PRJNA105945
REPOSITORIES: GEO
Similar Datasets
Project description:Analysis of gene expression before (P14), during (P28), and after (P60) the critical period for ocular dominance plasticity. Experiment Overall Design: V1 from litters of mice were microdissected and processed for RNA extraction.
2008-10-21 | E-GEOD-11764 | biostudies-arrayexpress
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:Visual deprivation, either in the form of dark rearing (DR) or monocular deprivation (MD) are established paradigms for studying cortical plasticity. We have used miRNA microarray to uncover miRNAs whose expression is altered in primary visual cortex following DR and/or MD. C57BL6 mice were reared in normal light and dark conditions (control) till P28, in complete darkness since birth (DR) till P28, or were grown in normal light/dark conditions from birth till P24 and then subjected to lid suturing of one eye till P28. Mice were euthanized at P28 and their primary visual cortex areas were excised and subjected to RNA isolation. In the case of MD mice only the contralateral to lid suture primary visual cortex was extracted. 100ng of total RNA (tested and quantified using the Agilent Bioanalyzer 2100) were labeled using the Agilent miRNA labeling system and hybridized to Agilent murine miRNA arrays. Microarrays were hybridized overnight at 64 ºC, scanned using an Agilent scanner and extracted with Agilent feature extractor 10.1.
2011-09-03 | E-GEOD-31536 | biostudies-arrayexpress
Project description:Chrdl1, a BMP antagonist, is an astrocyte-secreted factor that promotes synapse maturation in the upper layers of the visual cortex at P14. We analyzed the transcriptome of the visual cortex of WT and Chrdl1 KO mice at P14 in order to determine if genes related to BMP signaling, astrocyte development or synapse formation were altered.
2018-10-29 | GSE108483 | 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:RNA sequencing of peripheral nerve lysates covering various developmental stages in mice (E13.5, E17.5, P1, P5, P14, P24, P60)
2021-04-22 | GSE137868 | GEO
Project description:To profile gene expression differences in astrocytes in postnatal cerebellar astrocytes . Comparing cerebellar astrocyte transcriptomes at postnatal days 1, 7, 14, and 28 (P1, P7, P14, and P28),
2024-02-09 | GSE252519 | GEO
Project description:The goal of this project was to identify genes whose expression is modified by age in microglia isolated from the hippocampus of 14 and 28-day old control mice (i.e. normally developing mice). To accomplish this we used two independent cohorts of control mice and identified a list of 76 genes that were significantly regulated by age (p< 0.05) in both cohorts. Data for cohort 1 were extracted from gene expression of P14 and P28 control mice available in the BDS-P14-male series (GSE81036) and BDS-P28-male series (GSE81037). Data for cohort 2 are available in this series. These data are summarized also in Table S3 in Delpech J.C. et al. Early life stress perturbs the maturation of microglial cells in the developing hippocampus, Brain, Behavior and Immunity, 2016 (in preparation).
2016-05-03 | GSE81035 | GEO