Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA287327 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2069440.fastq.gz | Fastqsanger.gz | |||
| SRR2069450.fastq.gz | Fastqsanger.gz | |||
| SRR2069441.fastq.gz | Fastqsanger.gz | |||
| SRR2069451.fastq.gz | Fastqsanger.gz | |||
| SRR2069461.fastq.gz | Fastqsanger.gz |
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Project description:Drug exposure during critical periods of development is known to have lasting effects, increasing one’s risk for developing mental health disorders. Emerging evidence has also indicated the possibility for drug exposure to even impact subsequent generations. Our previous work demonstrated that adolescent exposure to Δ9-tetrahydrocannabinol (THC), the main psychoactive component of marijuana (Cannabis sativa), in a Long-Evans rat model affects reward-related behavior and gene regulation in the subsequent (F1) generation unexposed to the drug. Questions, however, remained regarding potential epigenetic consequences. In the current study, using the same rat model, we employed Enhanced Reduced Representation Bisulfite Sequencing to interrogate the epigenome of the nucleus accumbens, a key brain area involved in reward processing. This analysis compared 16 animals with parental-THC exposure and 16 without to characterize relevant systems-level changes in DNA methylation. We identified 1,027 differentially methylated regions (DMRs) associated with parental THC exposure in F1 adults, each represented by multiple CpGs. These DMRs fell predominantly within introns, exons, and intergenic intervals, while showing a significant depletion in gene promoters. From these, we identified a network of DMR-associated genes involved in glutamatergic synaptic regulation, which also exhibited altered mRNA expression in the nucleus accumbens. These data provide novel insight into drug-related cross-generational epigenetic effects, and serve as a useful resource for investigators to explore novel neurobiological systems underlying drug abuse vulnerability. Study consisted of a total of 32 F1 individuals (Long-Evan rats); 16 animals (8 female, 8 male) were offspring from THC-exposed parents, and the remaining 16 animals (8 female, 8 male) were offspring from saline-exposed parents ("controls"; "VEH-exposed").
2015-06-19 | E-GEOD-69984 | biostudies-arrayexpress
Project description:Drug exposure during critical periods of development is known to have lasting effects, increasing one’s risk for developing mental health disorders. Emerging evidence has also indicated the possibility for drug exposure to even impact subsequent generations. Our previous work demonstrated that adolescent exposure to Δ9-tetrahydrocannabinol (THC), the main psychoactive component of marijuana (Cannabis sativa), in a Long-Evans rat model affects reward-related behavior and gene regulation in the subsequent (F1) generation unexposed to the drug. Questions, however, remained regarding potential epigenetic consequences. In the current study, using the same rat model, we employed Enhanced Reduced Representation Bisulfite Sequencing to interrogate the epigenome of the nucleus accumbens, a key brain area involved in reward processing. This analysis compared 16 animals with parental-THC exposure and 16 without to characterize relevant systems-level changes in DNA methylation. We identified 1,027 differentially methylated regions (DMRs) associated with parental THC exposure in F1 adults, each represented by multiple CpGs. These DMRs fell predominantly within introns, exons, and intergenic intervals, while showing a significant depletion in gene promoters. From these, we identified a network of DMR-associated genes involved in glutamatergic synaptic regulation, which also exhibited altered mRNA expression in the nucleus accumbens. These data provide novel insight into drug-related cross-generational epigenetic effects, and serve as a useful resource for investigators to explore novel neurobiological systems underlying drug abuse vulnerability.
2015-06-19 | GSE69984 | GEO
Project description:Canabinoid exposure during adolescence alters the rewarding properties of drugs of abuse by mechanisms that are not fully understood. The nucleus accumbens is a key node of the circuit mediating the rewarding effects of most drugs. Here, we present data on the differential gene expression in the nucleus accumbens shell in male and female Wistar rats (postnatal day 90) after exposure to THC (3 mg/kg i.p.) or vehicle (ethanol:cremophor:saline; 1:1:18; 2 mL/kg i.p.) during adolescence (postnatal day 28 to postnatal day 44; injections on alternate days). There were 96 DEGs in THC-males compared to VEH-males and 87 DEGs in the females’ comparison. Only nine of these DEGs were present in both the THC vs. VEH comparison in both sexes. Our results suggest that THC exposure during adolescence affects several families of genes that have important functions for brain development, behavior and synaptic plasticity and could explain, at least in part, the complex behavioral phenotype observed in adult individuals with exposure to cannabinoids during adolescence.
2020-09-19 | GSE158188 | GEO
Project description:DNA methylation changes in rat sperm following exposure to THC
| PRJNA633085 | ENA
Project description:Background: Adolescent cannabis use leads to long-lasting behavioral changes involving cognitive and reward processes. However, the underlying molecular mechanisms are not well understood. To address this limitation, we performed gene network analyses using transcriptomic data from mice exposed during adolescence to Δ-9-tetrahydrocannabinol (THC), the major psychoactive component of cannabis. Methods: We injected vehicle or THC in female and male mice during the entire adolescence period. Two weeks following the last exposure, we measured recognition memory, social interaction and anxiety-related behaviors. We generated 120 RNA-seq datasets from 5 brain regions for each mouse. We performed differential gene expression analysis and constructed co-expression networks to identify THC-induced transcriptional alterations at the level of individual genes, gene networks, biological pathways, and cellular specificity. Further, we integrated THC-correlated gene networks with human traits from genome-wide association studies and performed key driver analysis to identify potential regulators of disorder-associated networks. Results: THC impaired cognitive behaviors of mice, with memory being more impacted in females, which coincided with larger transcriptional alterations in the female brain. Gene network analyses identified brain region-, cell type- and sex- specific co-expressed genes (“modules”) dysregulated by THC. THC-induced memory deficits in females were correlated with disruption of gene networks involved in endocannabinoid signaling and inflammation. Additional THC-correlated modules in both sexes involved converging pathways related to dopamine signaling and addiction processes. Moreover, the connectivity map of THC-correlated modules uncovered intra- and inter-region molecular circuitries influenced by THC. Further, modules altered by THC treatment were enriched in genes relevant for human cognition and schizophrenia. Conclusions: These findings provide novel insights concerning the genes, cell types, and pathways underlying persistent behavioral deficits induced by adolescent exposure to THC in a sex-specific manner, and highlight the connection between adolescent cannabis use and neuropsychiatric disorders in humans.
2021-12-06 | GSE189821 | GEO
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:Adolescence is a time of experimentation with cannabis. We evaluated whether adolescent exposure to the drug's psychotropic consituent, delta-9-tetrahydrocannabidiol (THC), might persistently alter microglia function and brain immune responses to lipopolysaccaride administration.
2022-09-22 | GSE213734 | GEO
Project description:Adolescent cannabis use has been associated with long-term cognitive dysfunction attributed to action of the main cannabis ingredient, delta-9-tetrahydrocannabinol (Δ9-THC), on the cannabinoid receptor 1 (CNR1). However, not all marijuana users develop cognitive impairment, suggesting a genetic vulnerability to adverse effects of cannabis. As both neurons and glial cells express CNR1, genetic vulnerability could influence Δ9-THC-induced signaling in a cell type-specific manner. Here we use an animal model of inducible expression of dominant-negative Disrupted-In-Schizophrenia-1 (DN-DISC1) selectively in astrocytes to evaluate the molecular mechanisms whereby an astrocyte genetic vulnerability could synergistically interact with adolescent Δ9-THC exposure to impair recognition memory in adulthood. We report that selective expression of DN-DISC1 in astrocytes and adolescent treatment with Δ9-THC synergistically affected recognition memory in adult mice. Similar deficits in recognition memory were observed following knockdown of endogenous Disc1 in hippocampal astrocytes in mice treated with Δ9-THC during adolescence. At the molecular level, DN-DISC1 and Δ9-THC synergistically activated the NF-kB-COX-2 (encoded by Ptgs2 gene) pathway in astrocytes and decreased immunoreactivity of parvalbumin-positive pre-synaptic inhibitory boutons around pyramidal neurons of the CA3 area of the hippocampus. The cognitive abnormalities were prevented in DN-DISC1 mice exposed to Δ9-THC by simultaneous adolescent treatment with the COX-2 inhibitor, NS389. Our data demonstrate that individual vulnerability to cannabis can be exclusively mediated by astrocytes. Results of this work suggest that genetic predisposition within astrocytes can exaggerate Δ9-THC-produced cognitive impairments via convergent inflammatory signaling, suggesting possible targets for preventing adverse effects of cannabis within susceptible individuals.
2018-12-31 | GSE116813 | GEO
Project description:Rat DNA methylation in the Nucleus Accumbens in Incubation of Cocaine Craving
| PRJNA276582 | ENA
Project description:Rat gene expression in the Nucleus Accumbens in Incubation of Cocaine Craving
| PRJNA276584 | ENA