Similar Datasets
Project description:RNA-sequencing of adult rat amygdala tissue following acute ethanol treatment, compared to saline-treated controls.
2022-09-22 | GSE171400 | GEO
Project description:MicroRNA profiling of adult rat amygdala following acute ethanol (1g/kg IP) exposure
2016-11-29 | GSE68278 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-09-22 | GSE171412 | GEO
Project description:The objective of this study was to determine changes in gene expression within the extended amygdala following binge-like alcohol drinking by adolescent alcohol-preferring (P) rats. Starting at 28 days of age, P rats were given concurrent access to 15 and 30 % ethanol for 3 one-h sessions for 5 consecutive days each week until they were 49 days old. Rats were killed by decapitation 3 h after the first ethanol access session on the 15th day of drinking. RNA was prepared from micropunch samples of the nucleus accumbens shell (Acb-sh) and central nucleus of the amygdala (CeA). Ethanol intakes were 2.5 to 3.0 g/kg/session. There were 154 and 182 unique named genes that significantly differed (FDR = 0.2) between the water and ethanol group in the Acb-sh and CeA, respectively. Gene Ontology (GO) analyses indicated that adolescent binge drinking produced changes in the in biological processes involved in cell proliferation and regulation of cellular structure in the Acb-sh, and in neuron projection and positive regulation of cellular organization in the CeA. Ingenuity Pathway Analysis indicated that, in the Acb-sh, there were several major intracellular signaling pathways (e.g., cAMP-mediated and protein kinase A signaling pathways) altered by adolescent drinking, with 3-fold more genes up-regulated than down-regulated in the alcohol group. The cAMP-mediated signaling system was also up-regulated in the CeA of the alcohol group. Weighted gene co-expression network analysis (WGCNA) indicated significant G-protein coupled receptor signaling and transmembrane receptor protein kinase signaling categories in the Acb-sh and CeA, respectively. Overall, the results of this study indicated that binge-like alcohol drinking by adolescent P rats is differentially altering the expression of genes in the Acb-sh and CeA, some of which are involved in intracellular signaling pathways and may produce long-term changes in neuronal function. Differences in gene expression in the central nucleus of the amygdala (CeA) were compared in two groups of alcohol-preferring (P) rats, one given water only and the other given access to 15 & 30% ethanol during adolescence.
2013-07-20 | E-GEOD-49040 | biostudies-arrayexpress
Project description:Behavioral transitions Young infant rats paradoxically prefer odors paired with shock but older pups learn aversions. This transition is amygdala- and corticosterone-dependent. Microarray results showed downregulated dopaminergic presynaptic function in the amygdala with preference learning. Corticosterone injected 8-day-old pups and untreated 12-day-old pups learn aversions and had dopaminergic upregulation in the amygdala. 8 day saline or corticosterone treated- or 12 day old untreated rat pups were trained with odor-shock pairings. Immediately after training pups were sacrificed and the amygdala dissected out. Controls were unpaired shock-odor groups.Paired and unpaired groups were processed together for each experimental condition. Paired and unpaired data were compared by ranked products.
2009-09-27 | E-GEOD-17651 | biostudies-arrayexpress
Project description:The objective of this study was to determine changes in gene expression within the extended amygdala following binge-like alcohol drinking by adolescent alcohol-preferring (P) rats. Starting at 28 days of age, P rats were given concurrent access to 15 and 30 % ethanol for 3 one-h sessions for 5 consecutive days each week until they were 49 days old. Rats were killed by decapitation 3 h after the first ethanol access session on the 15th day of drinking. RNA was prepared from micropunch samples of the nucleus accumbens shell (Acb-sh) and central nucleus of the amygdala (CeA). Ethanol intakes were 2.5 – 3.0 g/kg/session. There were 154 and 182 unique named genes that significantly differed (FDR = 0.2) between the water and ethanol group in the Acb-sh and CeA, respectively. Gene Ontology (GO) analyses indicated that adolescent binge drinking produced changes in the in biological processes involved in cell proliferation and regulation of cellular structure in the Acb-sh, and in neuron projection and positive regulation of cellular organization in the CeA. Ingenuity Pathway Analysis indicated that, in the Acb-sh, there were several major intracellular signaling pathways (e.g., cAMP-mediated and protein kinase A signaling pathways) altered by adolescent drinking, with 3-fold more genes up-regulated than down-regulated in the alcohol group. The cAMP-mediated signaling system was also up-regulated in the CeA of the alcohol group. Weighted gene co-expression network analysis (WGCNA) indicated significant G-protein coupled receptor signaling and transmembrane receptor protein kinase signaling categories in the Acb-sh and CeA, respectively. Overall, the results of this study indicated that binge-like alcohol drinking by adolescent P rats is differentially altering the expression of genes in the Acb-sh and CeA, some of which are involved in intracellular signaling pathways and may produce long-term changes in neuronal function.
2013-07-20 | GSE49040 | GEO
Project description:In this study, we tested if miRNAs are altered in amygdala and ventral striatum as a consequence of prenatal ethanol exposure and/or social enrichment. miRNA samples from 72 male and female adolescent rats were analyzed by RNA-Seq analysis and Affymetrix miRNA arrays. Several miRNAs showed significant changes due to prenatal ethanol exposure or social enrichment in one or both brain regions. Some of the miRNA changes caused by ethanol were reversed by social enrichment. The top predicted gene targets of these miRNAs were mapped and subjected to pathway enrichment analysis. We also directly examined the evidence for modulation of target mRNAs in whole transcriptome microarray data from the same rats. Among the pathways most strongly affected were p53, CREB, Glutamate and GABA signaling. Together, our data suggest a number of novel epigenetic mechanisms for social enrichment to reverse the effects of ethanol exposure. A total of 48 Rat ST Gene 1.0 GeneChips and 48 miRNA 2.0 GeneChips were run on RNA purified from 2 brain regions (amygdala and ventral striatum) of postnatal day 42 Long Evans rats. 3 replicate arrays were run for each gender within 4 different treatment groups (prenatal ethanol or prenatal saline exposed; postnatal socially-enriched or non-enriched environment)
2014-08-28 | E-GEOD-60819 | biostudies-arrayexpress
Project description:Repeated excessive alcohol consumption is a risk factor for alcohol use disorder (AUD). Although AUD has been more common in men than women, women develop more severe behavioral and physical impairments. However, relatively few new therapeutics targeting development of AUD have been validated. Here, to gain a better understanding of molecular mechanisms underlying alcohol intake, we conducted a genome-wide RNA-sequencing analysis in female mice exposed to different modes (acute vs chronic) of ethanol drinking. We focused on transcriptional profiles in amygdala including the central and basolateral subnuclei, brain areas previously implicated in alcohol drinking and seeking. We found distinct gene expression patterns and canonical pathways induced by both acute and chronic intake. Surprisingly, both drinking modes triggered similar transcriptional changes, including up-regulation of ribosome-related/translational pathways and myelination pathways, and down-regulation of chromatin binding and histone modification. Notably, multiple genes that were significantly altered with alcohol drinking, including Atp2b1, Hspa4, Slc4a7, Sbno1, Ubxn2b, Nfkb1, Nts, and Hdac2, had previously been associated with human AUD via GWAS or other genomic studies. In addition, subsequent analyses of hub genes and upstream regulatory pathways predicted that voluntary ethanol consumption affects epigenetic changes via histone deacetylation pathways, oligodendrocyte and myelin function, and the oligodendrocyte-related transcription factor, Sox17. Overall, our results suggest that the expression of oligodendrocyte-related genes in the central and basolateral subnuclei of the amygdala is sensitive to voluntary alcohol drinking. These findings suggest potential molecular targets for future therapeutic approaches to prevent the development of AUD, particularly in women, due to repeated excessive alcohol consumption
2022-11-28 | GSE208014 | GEO
Project description:The amygdala controls socioemotional behavior and has consistently been implicated in the etiology of Autism Spectrum Disorder (ASD). Precocious amygdala development is commonly reported in ASD youth with the degree of overgrowth positively correlated to the severity of ASD symptoms. However, surprisingly little is known about the cellular, molecular, or genetic changes that occur in the amygdala over development in ASD individuals or rodent models. We examined abnormalities in gene expression in the amygdala and socioemotional behavior across development in the valproic acid (VPA) rat model of ASD.
2017-07-03 | GSE98777 | GEO
Project description:Amygdala gene regulation during escalation of alcohol intake in mice
2011-12-31 | E-TABM-956 | biostudies-arrayexpress