Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA395044 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5839970_1.fastq.gz | Fastqsanger.gz | |||
| SRR5839970_2.fastq.gz | Fastqsanger.gz | |||
| SRR5839965_1.fastq.gz | Fastqsanger.gz | |||
| SRR5839965_2.fastq.gz | Fastqsanger.gz | |||
| SRR5839966_1.fastq.gz | Fastqsanger.gz |
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Project description:Binge drinking is rising among aged adults (>65 years of age). The distinct effects of binge ethanol exposure on neurodegeneration in the aged brain are not well described. Using our model of intermittent binge ethanol exposure in young and aged mice, we investigated how binge ethanol expoure may promote neurodegenerative diease development. Spatial transcriptomics revealed that binge ethanol exposure enriched neurodegenerative disease pathways in the aged hippocampus, including tau hyperphosphorylation and neuronal death. These data suggest binge drinking during advanced aging may promote neurodegenerative disease development.
2024-03-18 | GSE236787 | GEO
Project description:Hippocampal DNA methylation alterations following prenatal ethanol exposure and maternal separation stress in 70 day-old mice
| PRJNA574108 | ENA
Project description:Maternal alcohol consumption during pregnancy results in a spectrum of lifelong behavioral and cognitive deficits collectively known as Fetal Alcohol Spectrum Disorders (FASD). FASD is a major health burden in most societies, there is no cure, and the molecular mechanism involved in its development is poorly understood. Human neurodevelopment is a continuum that extends over two decades after birth, with the potential to influence outcomes both prenatally and postnatally. Here, we experimentally investigate if positive postnatal environment enrichment ameliorates behavioral deficits caused by ethanol exposure. Furthermore, we assessed if this modulation is associated with alterations in hippocampal gene expression. To accomplish this, we used a binge model of ethanol exposure followed by environmental enrichment in C57BL/6 mice to generate four groups of animals: (1) control mice raised in standard conditions, (2) mice raised in enriched environments, (3) ethanol-exposed mice raised in standard conditions, and (4) ethanol-exposed mice raised in enriched environments. The environmental enrichment includes larger home cages with more individuals for social interaction, regular exposure to novel items, and access to running wheels. Ethanol exposure results in anxiety-like behavior (light-dark box) as well as learning and memory deficits (Barnes maze) that are at least partially ameliorated by enrichment. Environmental enrichment also improves performance for individuals not exposed to ethanol. Ethanol exposure induces changes in adult hippocampal gene expression (RNA-Seq). Some of the changes in adult hippocampal gene expression following ethanol exposure are reversed by environmental enrichment. The results offer a potential mechanism of behavioral deficits caused by ethanol exposure, including the potential for amelioration after an FASD diagnosis.
2021-09-24 | GSE184615 | GEO
Project description:Prenatal alcohol exposure can cause long-lasting changes in functional and genetic programs of the brain, which may underlie behavioral alterations found in FASD. Here, we demonstrated that maternal binge alcohol consumption alters the expression of genes involved in nervous system development. Maternal binge alcohol consumption alters several important genes that are involved in nervous system development in the mouse hippocampus at embryonic day 18 (ED18)
2014-09-04 | E-GEOD-61049 | biostudies-arrayexpress
Project description:Adolescence is a critical period in cognitive and emotional development, characterized by high levels of social interaction and increases in risk-taking behavior including binge drinking. Adolescent exposure to social stress and binge ethanol have individually been associated with the development of social, emotional, and cognitive deficits, as well as increased risk for alcohol use disorder. Disruption of cortical development by early life social stress and/or binge drinking may partly underlie these enduring emotional, cognitive, and behavioral effects. The study goal is to implement a novel neighbor housing environment to identify the effects of adolescent neighbor housing and/or binge ethanol drinking on (1) a battery of emotional and cognitive tasks (2) adult ethanol drinking behavior, and (3) the nucleus accumbens and prefrontal cortex transcriptome. Adolescent male and female C57BL/6J mice were single or neighbor housed with or without access to intermittent ethanol. One cohort underwent behavioral testing during adulthood to determine social preference, expression of anxiety-like behavior, cognitive performance, and patterns of ethanol intake. The second cohort was sacrificed in late adolescence and brain tissue was used for transcriptomics analysis. As adults, single housed mice displayed decreased social interaction, deficits in the novel object recognition task, and increased anxiety-like behavior, relative to neighbor-housed mice. There was no effect of housing condition on adolescent or adult ethanol consumption. Adolescent ethanol exposure did not alter adult ethanol intake. Transcriptomics analysis revealed that adolescent housing condition and ethanol exposure resulted in differential expression of genes related to synaptic plasticity in the nucleus accumbens and genes related to methylation, the extracellular matrix and inflammation in the prefrontal cortex. The behavioral results indicate that social interaction during adolescence via the neighbor housing model may protect against emotional, social, and cognitive deficits. In addition, the transcriptomics results suggest that these behavioral alterations may be mediated in part by dysregulation of transcription in the frontal cortex or the nucleus accumbens
2023-09-18 | GSE242910 | GEO
Project description:We altered the NIAAA (Gao Binge Model) of 8 week chronic plus binge ethanol (E8G1) to have 3 total ethanol gavages (5 g/kg; 1 every 24h) of ethanol after 8 weeks of chronic ethanol feeding (E8G3) to determine how the liver responds to chronic plus consecutive binge ethanol. Surprisingly, E8G3 treatment induced lower levels of liver injury, steatosis, inflammation, and fibrosis as compared to mice after E8G1 treatment. Microarray analyses were performed, identifying several pathways that may contribute to the observed liver adaptation to binge ethanol. In addition, cytochrome P450 2B10 (Cyp2b10) was a top upregulated gene in the E8G1 group and further upregulated in the E8G3 group, but only moderately induced after chronic ethanol consumption, which was confirmed by RT-qPCR and western blot analyses. Genetic disruption of the Cyp2b10 gene worsened liver injury in E8G1 and E8G3 mice with higher blood ethanol levels compared to wild-type control mice, while in vitro experimentation revealed that CYP2b10 did not directly promote ethanol metabolism. Metabolomic analyses revealed significant differences in hepatic metabolites from E8G1-treated Cyp2b10 KO and WT mice, and these metabolic alterations may contribute to the reduced liver injury in Cyp2b10 KO mice.
2022-09-07 | GSE212755 | GEO
Project description:Background: Fetal Alcohol Spectrum Disorders (FASD) cause life-long cognitive and behavioral impairment and are highly prevalent across the world. The effects of developmental ethanol exposure on astrocyte functions in vivo are poorly understood. To fill this gap, we assessed changes in the astrocyte translatome following in vivo developmental ethanol exposure and mechanistically linked some of these changes to altered neuronal development. Methods: The translating RNA from hippocampal astrocytes of neonatal Aldh1l1-EGFP-Rpl10a mice exposed to ethanol was isolated by Translating Ribosomal Affinity Purification and sequenced; neuronal dendritic morphology was assessed by Golgi-Cox staining and morphometric analysis; chondroitin sulfate glycosaminoglycan (CS-GAG) disaccharides were measured by Liquid Chromatography/Mass Spectrometry; neurite outgrowth was assessed in in vitro hippocampal neurons incubated in the presence of astrocyte-conditioned medium prepared from control and Chpf2-silenced astrocytes. Results: Translatome results suggested that ethanol alters mechanisms of astrocyte-neuron interactions involved in neuronal development. Moreover, ethanol increased dendritic arborization in hippocampal pyramidal neurons, inhibited the astrocyte translation of enzymes involved in the biosynthesis of inhibitory CS-GAGs, and decreased the levels of disaccharides forming CS-GAGs in vivo. Lastly, the silencing of CS-GAG biosynthetic enzyme Chpf2 in astrocyte cultures increased neurite branching of hippocampal neuron in vitro. Conclusions: Translatome analysis revealed novel effects of developmental ethanol exposure on astrocytes and provided mechanistic insights into altered brain development possibly relevant to the pathophysiology of FASD. We also identified a novel mechanism by which ethanol-induced reduction of astrocyte-produced inhibitory extracellular matrix components CS-GAGs increases dendritic arborization.
2024-09-30 | GSE272272 | GEO
Project description:Adolescent binge alcohol exposure has been previously shown to have long-lasting effects on the expression of hypothalamic genes that regulate the stress response, even in the absence of subsequent adult alcohol exposure. Those data suggested that alcohol can induce permanent gene expression changes, potentially through epigenetic modifications. Importantly, epigenetic modifications can be transmitted to future generations therefore, in these studies we investigated the effects of adolescent binge alcohol exposure on hypothalamic gene expression patterns in the F1 generation offspring. It has been well documented that maternal alcohol exposure during fetal development can have devastating neurological consequences. However, less is known about the consequences of maternal and/or paternal alcohol exposure outside of the gestational time frame. Here, we exposed adolescent male and female rats to a repeated binge EtOH exposure paradigm and then mated them in adulthood. Hypothalamic samples were taken from the offspring of these animals at postnatal day (PND) 7 and subjected to a genome-wide microarray analysis followed by qRT-PCR for selected genes. Importantly, the parents were not intoxicated at the time of mating and were not exposed to EtOH at any time during gestation therefore, the offspring were never directly exposed to EtOH. Our results showed that the offspring of alcohol-exposed parents had significant differences in the expression of hypothalamic genes that mediate neurogenesis and synaptic plasticity during neurodevelopment, genes important for directing chromatin remodeling, posttranslational modifications or transcription regulation, as well as genes involved in regulation of obesity and reproductive function. These data demonstrate that repeated binge alcohol exposure during pubertal development can potentially have detrimental effects on future offspring even in the absence of direct fetal alcohol exposure. Male and female Wistar rats were purchased from Charles River Laboratories (Wilmington, MA) at weaning (postnatal day (PND) 23) and allowed to acclimate for 7 days after arrival. Animals were handled for 5 min./once/day beginning at PND 30. Pubertal EtOH exposure began on PND 37, which is defined as peri-puberty. Animals were undisturbed following the first exposure of our binge EtOH exposure paradigm until PND 68 (late puberty/early adult) at which time they received a second exposure to the same treatment paradigm. During the duration of the experiment, males and females were separately housed in pairs on a 12:12 light/dark cycle with lights on at 0700 h with food and water available ad libitum. Binge Exposure Paradigm and Treatment Design. Rats were handled 5min./once/day for 7 d prior to treatment to control for nonspecific stress responses. At 37 d, animals were given 3 g/kg EtOH (20% v/v in tap water; N = 3/sex), or tap water alone (N = 3/sex), once/day via oral gavage at 10:00 AM to avoid disrupting normal feeding patterns. This process was repeated according to the following schedule for a total duration of 8 consecutive days: 3 d EtOH, 2 d tap water, 3 d EtOH. Control animals were given tap water alone once/day for 8 consecutive days. Our previous studies showed that this repeated binge-pattern EtOH paradigm does not affect body weight/growth curves and consistently results in blood alcohol concentrations (BAC) of 150-180 mg/dl in males and 210-240 mg/dl in females. We and others have previously used this paradigm as a model for the pattern of binge alcohol consumption observed in adolescents and BAC achieved are similar to those observed in humans following a binge drinking episode . After peri-pubertal treatments, animals were left undisturbed in their home cage until PND 68 when each group was again exposed to their respective treatment (i.e. control or binge EtOH. We waited 24 hours after the last dose of EtOH to ensure that blood alcohol concentrations in the parents were undetectable at the time of mating (data not shown). Animals were grouped into mating pairs: binge male + binge female (N = 3 pairs); water male + water female (N = 3 pairs). All of the females gave birth to 12-16 pups approximately 28 d after being housed with a male, indicating that conception took place approximately 6 d after pairing; therefore, the pups were never directly exposed to alcohol at any time. At PND 7 pups were deeply anesthetized on ice and sacrificed. Brains were rapidly removed, the hypothalamus microdissected on ice, and then stored in -80ºC until further processing for a genome-wide analysis on hypothalamic total RNA samples using a chip-based microarray (Southern California Genotyping Consortium, SCGC, Illumina Rat Ref-12). The PND 7 time point was chosen because the extent of rat neurodevelopment at PND 7 is roughly equivalent to that of a human infant at birth
2014-03-19 | E-GEOD-53028 | biostudies-arrayexpress
Project description:Acute ethanol exposure produces rapid alterations in neuroimmune gene expression that are both time- and cytokine-dependent. Interestingly, adolescent rats, who often consume binge-like quantities of alcohol, displayed reduced neuroimmune responses to acute ethanol challenge. However, it is not known whether growth factors, a related group of signaling factors, respond to ethanol similarly in adults and adolescents. To test this, adolescent and adult Sprague Dawley rats of both sexes were injected with either ethanol or saline, and brains were harvested 3 hr post-injection for assessment of growth factor, cytokine, or miRNA expression. RNASeq revealed a rapid suppression of 12 miRNA species. Of the miRNA affected by ethanol, the majority were related to inflammation or cell survival and proliferation factors, including FGF2, MAPK, NFκB, and VEGF.
2022-04-03 | GSE199848 | GEO
Project description:Preimplantation alcohol exposure can negatively impact embryonic development through disruption of molecular profiles and lead to fetal alcohol spectrum disorder (FASD). Despite the central role of the placenta in proper embryonic development and successful pregnancy, studies on the placenta in a FASD context are markedly lacking. Here, preimplantation binge-like alcohol exposure was implemented on pregnant C57BL/6 female mice through subcutaneous injection with two doses of either 2.5 g/kg 50% ethanol or an equivalent volume of saline at 2-h intervals on embryonic day 2.5 corresponding to the 8-cell stage. The placental morphology, DNA methylation and gene expression patterns in male and female late-gestation (E18.5) placentas were assessed. While overall placental morphology was not affected, we found a significant decrease in male ethanol-exposed embryo weights. When looking at molecular profiles, we uncovered numerous differentially methylated regions (DMRs ≥10% difference; 991 in males; 1309 in females) and differentially expressed genes (DEGs; 1046 in males; 340 in females) in the placentas. Remarkably, only 21 DMRs and 54 DEGs were common to both sexes, which were enriched for genes involved in growth factor response pathways. Preimplantation alcohol exposure had a greater impact on imprinted genes expression in male placentas (imprinted DEGs: 18 in males; 1 in females). Finally, by using L1-regularized linear regression, we were able to precisely discriminate control and ethanol-exposed placentas based on their specific DNA methylation patterns. This is the first study demonstrating that preimplantation alcohol exposure alters the DNA methylation and transcriptomic profiles of late-gestation placentas in a sex-specific manner. Importantly, it reveals a placental DNA methylation signature that can detect prenatal alcohol exposure in early life in order to provide appropriate support to attenuate and prevent eventual impact.
2024-02-07 | GSE254846 | GEO