Whole Genome array hippocampus_cocaine
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE6651 | GEO | 2007/01/09
SECONDARY ACCESSION(S): PRJNA98635
REPOSITORIES: GEO
Similar Datasets
Project description:We explored the hypothesis that maternal cocaine exposure could alter the fetal epigenetic machinery sufficiently to cause lasting neurochemical and functional changes in the offspring. These data were used as preliminary results for paper:; Maternal cocaine administration in mice alters DNA methylation and gene expression in hippocampal neurons of neonatal and prepubertal offspring. Svetlana I. Novikova, Fang He, Jie Bai, Nicholas J. Cutrufello, Ashiwel S. Undieh and Michael S. Lidow Experiment Overall Design: Pregnant CD1 mice were administered either saline or 20 mg/kg cocaine twice daily on gestational days 8-19. Male pups from each of ten litters of the cocaine and control groups were analyzed at 3 (P3) day postnatum. Pyramidal layer tissue from the right hemisphere of one of these brains (On every section, the pyramidal layer, encompassing the C1, C2 and C3 hippocampal regions, was carefully cut out)was used for analyzing gene expression. Laser microdissection was performed on a Leica ASLMD laser capture microdissection system (Leica Microsystems, Wetzlar, Germany).
2008-06-15 | E-GEOD-6651 | biostudies-arrayexpress
Project description:Substance abuse, particularly cocaine, has detrimental effects on global public health, as acute intoxication often results in adverse outcomes and current pharmacological treatments exhibit limited effectiveness. The intricate process of cocaine intoxication involves substantial alterations in the brain's neurochemical systems, including fluctuations in neuropeptide levels. To unravel these complexities, we devised an acute intoxication model in rats and undertook a comprehensive brain peptidome analysis using liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS).
2025-01-02 | PXD042363 | Pride
Project description:Early-life exposure to high-fat diet (HF) can program metabolic and cognitive alterations in adult offspring. Although the hippocampus plays a crucial role in memory and metabolic homeostasis, few studies reported the impact of maternal HF on this structure. We assessed the effects of maternal HF during lactation on physiological, metabolic and cognitive parameters in young adult offspring mice. To identify early-programming mechanisms in hippocampus, we developed a multi-omics strategy in male and female offspring. Maternal HF induced a transient increased body weight at weaning, a mild glucose intolerance only in 3-month-old male mice with no change in plasma metabolic parameters in adult male and female offspring. Behavioral alterations revealed by Barnes maze test were observed both in 6-month-old male and female mice. Multi-omics strategy unveiled sex-specific transcriptomic and proteomic modifications in the hippocampus of adult offspring. These studies, that were confirmed by regulon analysis, showing that, although genes whose expression was modified by maternal HF were different between sexes, the main pathways affected were similar with mitochondria and synapses as main hippocampal targets of maternal HF. The effects of maternal HF reported here may help to better characterize sex-dependent molecular pathways involved in cognitive disorders and neurodegenerative diseases.
2024-01-26 | PXD045639 | Pride
Project description:“Dysbiosis" of the maternal gut microbiome, in response to environmental challenges such as infection, altered diet and stress during pregnancy, has been increasingly associated with abnormalities in offspring brain function and behavior. However, whether the maternal gut microbiome regulates neurodevelopment in the absence of environmental challenge remains unclear. In addition, whether the maternal microbiome exerts such influences during critical periods of embryonic brain development is poorly understood. Here we investigate how depletion, and selective reconstitution, of the maternal gut microbiome influences fetal neurodevelopment in mice. Embryos from antibiotic-treated and germ-free dams exhibit widespread transcriptomic alterations in the fetal brain relative to conventionally-colonized controls, with reduced expression of several genes involved in axonogenesis. In addition, embryos from microbiome-depleted mothers exhibit deficient thalamocortical axons and impaired thalamic axon outgrowth in response to cell-extrinsic guidance cues and growth factors. Consistent with the importance of fetal thalamocortical axonogenesis for shaping neural circuits for sensory processing, restricted depletion of the maternal microbiome from pre-conception through mid-gestation yields offspring that exhibit tactile hyposensitivity in select sensorimotor behavioral tasks. Gnotobiotic colonization of antibiotic-treated dams with a limited consortium of spore-forming bacteria indigenous to the gut microbiome prevents abnormalities in fetal brain gene expression, fetal thalamocortical axonogenesis and adult tactile sensory behavior associated with maternal microbiome depletion. Metabolomic profiling reveals that the maternal microbiota regulates levels of numerous small molecules in the maternal serum as well as the brains of fetal offspring. Select microbiota-dependent metabolites – trimethylamine N-oxide, 5-aminovalerate, imidazole propionate, and hippurate – sufficiently promote axon outgrowth from fetal thalamic explants. Moreover, maternal supplementation with the metabolites during early gestation abrogates deficiencies in fetal thalamocortical axons and prevents abnormalities in tactile sensory behavior in offspring from microbiome-depleted dams. Altogether, these findings reveal that the maternal gut microbiome promotes fetal thalamocortical axonogenesis and select tactile sensory behaviors in mice, likely by signaling of microbially modulated metabolites to neurons in the developing brain.
2020-04-17 | GSE147183 | GEO
Project description:Evaluate differences in gene methylation levels between offspring born after maternal bariatric surgery and their siblings born before surgery Offspring born after maternal bariatric surgery (AMS, N=25) vs. offspring born before maternal surgery (BMS, N=25)
2013-05-16 | E-GEOD-44798 | biostudies-arrayexpress
Project description:Evaluate differences in gene expression levels between offspring born after maternal bariatric surgery and their siblings born before surgery Offspring born after maternal bariatric surgery (AMS, N=23) vs. offspring born before maternal surgery (BMS, N=23)
2013-05-16 | E-GEOD-44407 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE40471: Maternal slimming reprograms metabolic gene expression in mice offspring (NimbleGen expression) GSE40477: Maternal slimming reprograms metabolic gene expression in mice offspring (NimbleGen methylation) GSE40478: Maternal slimming reprograms metabolic gene expression in mice offspring (mRNA-Seq) Refer to individual Series
2012-08-30 | E-GEOD-40479 | biostudies-arrayexpress
Project description:Background: Environmental insults that activate the maternal immune system are potent primers of developmental neuropathology and maternal immune activation (MIA) has emerged as a risk factor for neurodevelopmental and psychiatric disorders. Animal models of MIA provide an opportunity to identify molecular pathways that initiate disease processes and lead to neuropathology and behavioral deficits in offspring. MIA-induced behaviors are accompanied by anatomical and neurochemical alterations in adult offspring that parallel those seen in affected human populations. Methods: We performed transcriptional profiling and neuroanatomical characterization in a time course across mouse embryonic cortical development, following MIA via single injection of the viral mimic polyinosinic:polycytidylic acid (polyI:C) at E12.5. Transcriptional changes identified in the cortex of MIA offspring at E17.5 were validated and mapped to cortical neuroanatomy and cell types via protein analysis and immunohistochemistry. Results: MIA induced strong transcriptomic signatures, including induction of genes associated with hypoxia, immune signaling, and angiogenesis. The acute response identified 6h after the MIA insult was followed by changes in proliferation, neuronal and glial differentiation, and cortical lamination that emerged at E14.5 and peaked at E17.5. Decreased numbers of proliferative cell types in germinal zones and alterations in neuronal and glial cell types across cortical lamina were identified in the MIA-exposed cortex. Conclusions: MIA-induced transcriptomic signatures in fetal offspring overlap significantly with perturbations identified in neurodevelopmental disorders (NDDs), and provide novel insights into alterations in molecular and developmental timing processes linking MIA and neuropathology, potentially revealing new targets for development of novel approaches for earlier diagnosis and treatment of these disorders.
2021-02-09 | GSE166376 | GEO
Project description:Substance use disorders are more prevalent in schizophrenia, but the causal links between both conditions remain unclear. Maternal immune activation (MIA) is associated with schizophrenia which may be triggered by stressful experiences during adolescence. Therefore, we used a double-hit rat model, combining MIA and peripubertal stress (PUS), to study cocaine addiction and the underlying neurobehavioural alterations. We injected lipopolysaccharide or saline on gestational days 15 and 16 to Sprague-Dawley dams. Their male offspring underwent five episodes of unpredictable stress every other day from postnatal day 28 to 38. When animals reached adulthood, we studied cocaine addiction-like behaviour, impulsivity, Pavlovian and instrumental conditioning, and several aspects of brain structure and function by MRI, PET and RNAseq. MIA facilitated the acquisition of cocaine self-administration and increased the motivation for the drug; however, PUS reduced cocaine intake, an effect that was reversed in MIA + PUS rats. We found concomitant brain alterations: MIA + PUS altered the structure and function of the dorsal striatum, increasing its volume and interfering with glutamatergic dynamics (PUS decreased the levels of NAA + NAAG but only in LPS animals) and modulated specific genes that could account for the restoration of cocaine intake such as the pentraxin family. On its own, PUS reduced hippocampal volume and hyperactivated the dorsal subiculum, also having a profound effect on the dorsal striatal transcriptome. However, these effects were obliterated when PUS occurred in animals with MIA experience. Our results describe an unprecedented interplay between MIA and stress on neurodevelopment and the susceptibility to cocaine addiction.
2021-10-04 | GSE185195 | GEO
Project description:Whole genome trancription study of Citrobacter rodentium grown in rich media. Publication Title: Citrobacter rodentium is an Unstable Pathogen Showing Evidence of Significant Genomic Flux Publication Author List: Nicola K. Petty, Theresa Feltwell, Derek Pickard, Simon Clare, Ana L. Toribio, Maria Fookes, Kevin Roberts, Rita Monson, Satheesh Nair, Robert A. Kingsley, Richard Bulgin, Siouxsie Wiles, David Goulding, Craig Corton, Nicola Lennard, David Harris, David Willey, Richard Rance, Lu Yu, Jyoti S. Choudhary, Carol Churcher, Michael A. Quail, Julian Parkhill, Gad Frankel, Gordon Dougan, George P.C. Salmond, Nicholas R. Thomson ArrayExpress Release Date: 2011-02-12 Person Roles: investigator Person Last Name: Thomson Person First Name: Nicholas Person Mid Initials: Person Email: nrt@sanger.ac.uk Person Phone: Person Address: Wellcome Trust Genome Campus, Hinxton, Cambridge, UK Person Affiliation: Wellcome Trust Sanger Institute Person Roles: submitter Person Last Name: Service Person First Name: Submission Person Mid Initials: Person Email: datahose@sanger.ac.uk Person Phone: Person Address: The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, CB10 1SA, United Kingdom Person Affiliation: Wellcome Trust Sanger Institute
2011-07-14 | GSE30610 | GEO