Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA320323 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In this study we hypothesize that early life stress perturbs the normal function of microglia in the developing hippocampus and that this effect is responsible for the ability of early life tress to disrupt normal synaptic maturation, myelination, and axonal growth in the developing hippocampus. To test this hypothesis we used the mouse immune panel from NanoString in order to identify immune-related genes whose expression is modified by BDS, a mouse model of early life stress, in microglia isolated from the hippocampus of 14-day old male pups. This project is part of a manuscript that is currently under preparation (Delpech J.C. et al. Early life stress perturbs the maturation of microglia in the developing hippocampus, Brain, Behavior and Immunity, 2016)
2016-05-03 | GSE81036 | GEO
Project description:In this study we hypothesize that early life stress perturbs the normal function of microglial in the developing hippocampus and that this effect is responsible for the ability of early life tress to disrupt normal synaptic maturation, myelination, and axonal growth in the developing hippocampus. To test this hypothesis we used the mouse immune panel from NanoString in order to identify immune-related genes whose expression is modified by BDS, a mouse model of early life stress, in microglia isolated from the hippocampus of 28-day old male pups. This project is part of a manuscript that is currently under preparation (Delpech J.C. et al. Early life stress perturbs the maturation of microglia in the developing hippocampus, Brain, Behavior and Immunity, 2016)
2016-05-03 | GSE81037 | GEO
Project description:Early life stress perturbs the maturation of microglia in the developing hippocampus [development]
| PRJNA320324 | ENA
Project description:Early life stress perturbs the maturation of microglia in the developing hippocampus
| PRJNA320321 | ENA
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
Project description:Early life stress perturbs the maturation of microglial in the developing hippocampus [P28]
| PRJNA320322 | ENA
Project description:The goal of this project was to assess the effects of two paradigms of early life stress on microglial gene expression in the developing hippocampus of 17-day old mice. Sixty thousands microglia were isolated from the hippocampus of 17-day old mice pups exposed to control (CTL), limited bedding (LB) or unpredictable postnatal stress (UPS) conditions and were processed to assess gene expression using the mouse Glia panel (Nanostring, Cat # XT-Mm Glial profiling CSO).
2022-09-28 | GSE190427 | GEO
Project description:Innate differences in human temperament strongly influence how individuals cope with stress and predispose for specific types of psychopathology. The present study examines the developing brain in an animal model of temperamental differences to understand how altered neurodevelopment may engender differences in emotional reactivity that are stable throughout the animal’s life. We utilize selectively-bred High Responder (bHR) and Low Responder (bLR) rats that exhibit dramatic emotional behavior differences, with bHRs exhibiting exaggerated novelty-exploration, aggression, impulsivity and drug self-administration, and bLRs showing marked behavioral inhibition, exaggerated anxiety- and depressive-like behavior. Using Affymetrix microarrays, we assessed bLR/bHR gene expression in the developing brain on postnatal days (P)7, 14, and 21, focusing on the hippocampus and nucleus accumbens, two regions related to emotionality and known to differ in adult bLR/bHR rats. We found dramatic bLR/bHR gene expression differences in the P7 and P14 hippocampus, with minimal differences in the nucleus accumbens. Some of the most profound differences involved genes critical for neurodevelopment and synaptogenesis. Stereological studies evaluated hippocampal structure in developing bHR/bLR pups, revealing enhanced hippocampal volume and cell proliferation in bLR animals. Finally, behavioral studies showed that the bHR/bLR behavioral phenotypes emerge very early in life, with exploratory differences apparent at P16 and anxiety differences present by P25. Together these data point to specific brain regions and critical periods when the bHR/bLR phenotypes begin to diverge, which may eventually allow us to test possible therapeutic interventions to normalize extreme phenotypes (e.g. the anxiety-prone nature of bLRs or drug addiction proclivity of bHRs). 2x2x3 factorial design with N=6 per group. Factors as follows: 1) Two selectively bred strains of rats (derived from an original Sprague Dawley population) termed High Responders (HR) and Low Responders (LR), 2) Two brain regions, Hippocampus (HPC) and Nucleus Accumbens (N.Acc), 3) Three developmental timepoints, specifically postnatal days 7 (P7), 14 (P14) and 21 (P21).
2011-12-31 | E-GEOD-29552 | biostudies-arrayexpress
Project description:Early life inflammation is known to promote the risk of depression in later life. Here, we demonstrate how early life inflammation causes adolescent depressive-like symptoms: by altering the long-term neuronal spine engulfment capacity of microglia. For mice exposed to lipopolysaccharide (LPS)-induced inflammation via the Toll-like receptor 4/NF-κB signaling pathway at postnatal day 14 (P14), ongoing longitudinal imaging of the living brain revealed that later stress (delivered during adolescence on P45) increases the extent of microglial engulfment around anterior cingulate cortex (ACC) glutamatergic neuronal (ACCGlu) spines. Through bluk RNA-seq of ACC tissue, we find that the fractalkine receptor CX3CR1 mediates stress-induced engulfment of ACCGlu neuronal spines.
2021-06-04 | GSE176140 | GEO
Project description:Innate differences in human temperament strongly influence how individuals cope with stress and predispose for specific types of psychopathology. The present study examines the developing brain in an animal model of temperamental differences to understand how altered neurodevelopment may engender differences in emotional reactivity that are stable throughout the animal’s life. We utilize selectively-bred High Responder (bHR) and Low Responder (bLR) rats that exhibit dramatic emotional behavior differences, with bHRs exhibiting exaggerated novelty-exploration, aggression, impulsivity and drug self-administration, and bLRs showing marked behavioral inhibition, exaggerated anxiety- and depressive-like behavior. Using Affymetrix microarrays, we assessed bLR/bHR gene expression in the developing brain on postnatal days (P)7, 14, and 21, focusing on the hippocampus and nucleus accumbens, two regions related to emotionality and known to differ in adult bLR/bHR rats. We found dramatic bLR/bHR gene expression differences in the P7 and P14 hippocampus, with minimal differences in the nucleus accumbens. Some of the most profound differences involved genes critical for neurodevelopment and synaptogenesis. Stereological studies evaluated hippocampal structure in developing bHR/bLR pups, revealing enhanced hippocampal volume and cell proliferation in bLR animals. Finally, behavioral studies showed that the bHR/bLR behavioral phenotypes emerge very early in life, with exploratory differences apparent at P16 and anxiety differences present by P25. Together these data point to specific brain regions and critical periods when the bHR/bLR phenotypes begin to diverge, which may eventually allow us to test possible therapeutic interventions to normalize extreme phenotypes (e.g. the anxiety-prone nature of bLRs or drug addiction proclivity of bHRs).
2011-12-31 | GSE29552 | GEO