Cocaine-regulated expression of striatal microRNAs
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Brenton Graveley
PROVIDER: E-GEOD-29261 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Publications
microRNA-Seq reveals cocaine-regulated expression of striatal microRNAs.
Eipper-Mains Jodi E JE Kiraly Drew D DD Palakodeti Dasaradhi D Mains Richard E RE Eipper Betty A BA Graveley Brenton R BR
RNA (New York, N.Y.) 20110627 8
MicroRNAs (miRNAs) are small RNAs that modulate gene expression by binding target mRNAs. The hundreds of miRNAs expressed in the brain are critical for synaptic development and plasticity. Drugs of abuse cause lasting changes in the limbic regions of the brain that process reward, and addiction is viewed as a form of aberrant neuroplasticity. Using next-generation sequencing, we cataloged miRNA expression in the nucleus accumbens and at striatal synapses in control and chronically cocaine-treate ...[more]
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Project description:Genetic association studies, pharmacological investigations and analysis of mice-lacking individual genes have made it clear that Cocaine administration and Withdrawal have a profound impact on multiple neurotransmitter systems. The GABAergic medium spiny neurons of the nucleus accumbens (NAc) exhibit changes in the expression of genes encoding receptors for glutamate and in the signaling pathways triggered by dopamine binding to G-protein-coupled dopamine receptors. Deep sequence analysis provides a sensitive, quantitative and global analysis of the effects of Cocaine on the NAc transcriptome. RNA prepared from the NAc of adult male mice receiving daily injections of Saline or Cocaine, or Cocaine followed by a period of Withdrawal, was used for high-throughput sequence analysis. Changes were validated by quantitative polymerase chain reaction or Western blot. On the basis of pathway analysis, a preponderance of the genes affected by Cocaine and Withdrawal was involved in the cadherin, heterotrimeric G-protein and Wnt signaling pathways. Distinct subsets of cadherins and protocadherins exhibited a sustained increase or decrease in expression. Sustained down-regulation of several heterotrimeric G-protein β- and γ-subunits was observed. In addition to altered expression of receptors for small molecule neurotransmitters, neuropeptides and endocannabinoids, changes in the expression of plasma membrane transporters and vesicular neurotransmitter transporters were also observed. The effects of chronic Cocaine and Withdrawal on the expression of genes essential to cholinergic, glutamatergic, GABAergic, peptidergic and endocannabinoid signaling are as profound as their effects on dopaminergic transmission. Simultaneous targeting of multiple Withdrawal-specific changes in gene expression may facilitate development of new therapeutic approaches that are better able to prevent relapse. High-throughput sequence analysis of RNA prepared from the nucleus accumbens of adult male mice receiving daily injections of Saline or Cocaine, or Cocaine followed by a period of Withdrawal. Nucleus accumbens libraries were sequenced in nine lanes (three technical replicates per sample) on an Illumina GAIIx using a 37-cycle paired-end sequencing protocol. Replicates were analyzed for intra-sample disparity and read data from all three lanes were then merged into one composite data file per sample; intra-sample coefficient of determination, R2 ≥ 0.98. The composite file was used for subsequent analyses.
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Project description:Despite addiction being one of the most prevalent and debilitating disorders worldwide, effective treatments are lacking. Repeated cocaine exposure induces maladaptive transcriptional regulation within the brainâ??s reward circuitry, such as the nucleus accumbens (NAc), and epigenetic mechanisms, such as histone acetylation or methylation on Lys (K) residues, have been linked to these lasting actions of cocaine. However, in contrast to K methylation, the functional role of histone Arg (R) methylation remains unexplored in addiction models and poorly understood in brain in general. Here we show that protein-R-methyltransferase-6 (PRMT6) and its associated histone mark, asymmetric dimethylation of R2 on histone H3 (H3R2me2a), are decreased in the NAc of mice and rats after repeated cocaine exposure, as well as in the NAc of cocaine-addicted humans. PRMT6 downregulation occurs selectively in NAc medium spiny neurons expressing dopamine D2 receptors (D2-MSNs) and serves to protect against cocaine-induced addictive-like behavioral abnormalities. Using ChIP-seq, we demonstrate that reduced H3R2me2a binding at gene targets in NAc after repeated cocaine is strongly correlated with increased binding of H3K4me3, and identify Src kinase signaling inhibitor 1 (Srcin1 or p140Cap) as a key gene for these chromatin modifications. Cocaine induction of Srcin1 in NAc, which is associated with reduced Src signaling, decreases cocaine reward, the motivation to self administer cocaine, and cocaine-induced changes in NAc MSN dendritic spines. These results suggest that this suppression of Src signaling in NAc D2-MSNs, via PRMT6 and H3R2me2a downregulation, functions as a homeostatic brake to restrain cocaine action, and provide novel candidates for the development of new treatments for cocaine addiction. H3R2me2A ChIP-seq of mouse. Cocaine vs Saline, 3 biological replicates.
2016-08-08 | E-GEOD-85310 | biostudies-arrayexpress
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2011-01-18 | E-GEOD-24850 | biostudies-arrayexpress
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2016-07-30 | E-GEOD-85005 | biostudies-arrayexpress
Project description:The aim of the study was to investigate whether environmental factors like S-adenosylmethionine (SAM) via affecting epigenome could alter cocaine-induced gene expression and locomotor sensitization in mice. Using mouse nucleus accumbens (NAc) tissue, whole-genome gene expression profiling revealed that repeated SAM treatment affected a limited number of genes, but significantly modified cocaine-induced gene expression by blunting nonspecifically the cocaine response. At the gene level, we discovered that SAM modulated cocaine-induced DNA methylation by inhibiting both promoter-associated CpG-island hyper- and hypomethylation in the NAc but not in the reference tissue cerebellum. Total RNA was extracted from the mouse nucleus accumbens (NAc) tissue. Two tissues were combined to a sample, 4 samples per group used. RNA quality and quantity were assessed using the Nano-Drop -1000 spectrophotometer and the Agilent 2100 Bioanalyzer.
2013-06-27 | E-GEOD-48365 | biostudies-arrayexpress
Project description:Many of the long-term effects of cocaine on the brain's reward circuitry have been shown to be mediated by alterations in gene expression. Several chromatin modifications, including histone acetylation and methylation, have been implicated in this regulation, but the effect of other histone modifications remains poorly understood. Poly(ADP-ribose) polymerase-1 (PARP-1), a ubiquitous and abundant nuclear protein, catalyzes the synthesis of a negatively charged polymer called poly(ADP-ribose) or PAR on histones and other substrate proteins and forms transcriptional regulatory complexes with several other chromatin proteins. Here, we identify an essential role for PARP-1 in cocaine-induced molecular, neural, and behavioral plasticity. Repeated cocaine administration, including self-administration, increased global levels of PARP-1 and its mark PAR in mouse nucleus accumbens (NAc), a key brain reward region. Using PARP-1 inhibitors and viral-mediated gene transfer, we established that PARP-1induction in NAc mediates enhanced behavioral responses to cocaine, including increased self-administration of the drug. Using chromatin immunoprecipitation sequencing, we demonstrated a global, genome-wide enrichment of PARP-1 in NAc of cocaine-exposed mice and identified several PARP-1 target genes that could contribute to the lasting effects of cocaine. Specifically, we identified sidekick-1-important for synaptic connections during development-as a critical PARP-1 target gene involved in cocaine's behavioral effects as well as in its ability to induce dendritic spines on NAc neurons. These findings establish the involvement of PARP-1 and PARylation in the long-term actions of cocaine. c57bl/6 mice were given IP injections of chronic cocaine 20mg/kg once per day for 7 days and sacrificed 30 minutes after the final dose of cocaine. Control animals were given saline for 7 days and sacrificed 30 minutes after the final dose of saline. Nucleus accumbens (NAc) tissue was collected and then PARP-1 ChIP-seq was performed. Three sequencing replicates were performed on each group.
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2015-02-27 | E-GEOD-66349 | biostudies-arrayexpress
Project description:Several recent reports show that the cerebral cortex in humans and animals with altered expressions of Wnt/cadherin network-associate molecules display cytoarchitectural abnormalities reminiscent of cortical dysplasias seen in some (mouse-, rat-, and monkey-based) animal models of prenatal cocaine exposure. Therefore, we employed oligo microarrays followed by real-time RT-PCR to compare expressions of genes involved in Wnt and cadherin systems in the cerebral wall of 18-day-old (E18) fetuses from cocaine-treated (20 mg/kg cocaine, s.c., b.i.d., E8-18) and drug-naive (saline, s.c.) mice. The pregnant mice chronically treated with cocaine in the above-described manner represent one of the animal models producing offspring with widespread cortical dysplasias. Out of more than 150 relevant genes in the arrays, 32 were upregulated and 9 were downregulated in cocaine-exposed fetuses. The majority of these genes (30 out of 41) were similarly affected in the frontal and occipital regions of the cerebral wall. We also used Western immunoblotting to examine the ability of cocaine to regulate the protein levels of beta-catenin, the key functional component of both Wnt and cadherin systems. While the total cell levels of beta-catenin were increased throughout the cerebral wall of cocaine-exposed fetuses, its nuclear (gene-transcription driving) levels remained unaltered. This suggests a transcription-unrelated role for cocaine-induced upregulation of this protein. Overall, our findings point to an intriguing possibility that that cerebral cortical dysplasias observed in several animal models of prenatal cocaine exposure may be at least in part related to alterations in the Wnt/cadherin molecular network. It has been demonstrated that exposure to cocaine increases cell death in the fetal CNS. To examine the molecular mechanisms of this effect, we employed mouse oligo microarrays followed by real-time reverse transcriptase-polymerase chain reaction (real-time RT-PCR) to compare expressions of apoptosis-related genes in the cerebral wall of 18-day-old (E18) fetuses from cocaine-treated (20 mg/kg cocaine, s.c., b.i.d., E8th-E18th) and drug-naive (saline, s.c.) mice. Out of approximately 400 relevant genes in the arrays, 53 showed alterations in expression in cocaine-exposed fetuses. Upregulation was observed in 35 proapoptotic and 8 antiapoptotic genes; 4 proapoptotic and 6 antiapoptotic genes were down-regulated. The affected genes encode a wide range of apoptosis-related proteins, including death receptors (NTF-R1, NTF-R2, DR3, DR5, LTbeta-R, GITR, P57 TR-1) and their adaptor and regulatory proteins (MASGE-D1, TRAF-2, SIVA, MET, FLIP, FAIM, IAP1, ATFA), members of transcription regulatory pathways (JNK, NF-kappaB, P53), members of BCL-2 family of proteins (BID, BAD, BAX, BIK, NIP21, NIP3, NIX, BCL-2), DNA damage sensor (PARP-1), caspases and their substrates and regulatory proteins (caspases 8, 4, 9, and 3, ACINUS, CIDE-A, CIDE-B, GAS2), mitochondrially released factors (cytochrome c, AIF, PRG3), specific endoplasmic reticulum- and oxidative stress-associated factors (BACH2, ABL1, ALG2, CHOP), members of cell survival AKT and HSP70 pathways (PIK3GA, PTEN, HSP70, BAG1, BAG2), and others. This suggests that cocaine affects survival of developing cerebral cells via multiple apoptosis-regulating mechanisms. Experiment Overall Design: Animals Experiment Overall Design: Timed pregnant Swiss Webster (CFW; Charles River Experiment Overall Design: Lab. Wilmington, MA) dams were maintained in individual Experiment Overall Design: cages in a climate-controlled room on a 12/12-h light/ Experiment Overall Design: dark cycle. They were divided into two groups. The first Experiment Overall Design: (experimental) group received subcutaneous (at the dorsum Experiment Overall Design: of the neck) injections of 20 mg/kg cocaine hydrochloride Experiment Overall Design: (Research Technology Branch, National Institute Experiment Overall Design: of Drug Abuse, Rockville, MD) dissolved in 200 mkl of Experiment Overall Design: 0.9% saline, twice a day (at 8:00 AM and 8:00 PM) from Experiment Overall Design: 8th through 18th day of pregnancy (E8âE18). The second Experiment Overall Design: (control) group was subjected to the same schedule of Experiment Overall Design: 0.9% saline only injections. The cocaine treatment was Experiment Overall Design: designed to replicate the one capable of reducing cerebral Experiment Overall Design: cortical mass in mouse offspring. Also, the Experiment Overall Design: relatively protracted period the chronic treatment was Experiment Overall Design: chosen to maximize the changes in the tissue expression Experiment Overall Design: of cocaine-regulated genes of interest. Throughout the Experiment Overall Design: treatment, all mice were weighed daily, and, from E8, the Experiment Overall Design: control and experimental animals were pair-fed, with the Experiment Overall Design: daily amount of food (Mouse Chow; Ralston Purina Saint Experiment Overall Design: Louis, MO) provided to each control dam being matched Experiment Overall Design: to that consumed by the paired experimental dam. Water Experiment Overall Design: was available ad libitum. We found that this feeding Experiment Overall Design: regiment resulted in similar weight gains from E8 to E18 Experiment Overall Design: in both experimental and control animal groups Experiment Overall Design: (46.41F0.45% and 44.99F0.59% respectively). On E18, Experiment Overall Design: 1 h after the morning treatment, the animals were Experiment Overall Design: anesthetized by peritoneal injection of 50 mg/kg sodium Experiment Overall Design: pentobarbital (Abbott Lab., Abbott Park, IL) and their Experiment Overall Design: uteri were removed. The frontal cerebral wall (containing Experiment Overall Design: cerebral cortex and underlying transient cortical zones Experiment Overall Design: anterior to the striatal level) and the occipital cerebral wall Experiment Overall Design: (containing cerebral cortex and underlying transient Experiment Overall Design: cortical zones posterior to the level of the hippocampus) Experiment Overall Design: were dissected from the fetuses and stored in liquid Experiment Overall Design: nitrogen prior to analysis. The animal experimentations Experiment Overall Design: used in this study were approved by the University of Experiment Overall Design: Maryland Animal Care and Use Committee. Experiment Overall Design: Microarray Experiment Overall Design: Tissue from two control and two experimental fetuses Experiment Overall Design: were used in the processing of a single microarray slide Experiment Overall Design: (Part G4121A, Agilent Technol). Five slides were processed Experiment Overall Design: per region of the fetal cerebral wall. For a given region, the Experiment Overall Design: tissue for each microarray slide was obtained from a Experiment Overall Design: separate set of control and experimental litters. Total RNA Experiment Overall Design: was isolated using TRIzol Reagent (Invitrogen, Carlsbad, Experiment Overall Design: CA). The yield of total RNA was determined by absorbance Experiment Overall Design: at 260 nm on a DU 640 Spectrophotometer (Beckman Experiment Overall Design: Coulter, Fullerton, CA). The 260/280 nm ratios of the Experiment Overall Design: samples were >1.8. For each assay, 5 mkg of RNA from Experiment Overall Design: control tissue and 5 mkg of RNA from experimental tissue Experiment Overall Design: were reverse transcribed using 3DNA Array Detection Kit Experiment Overall Design: (Genesphere, Hatfield, PA) with primers containing different Experiment Overall Design: dcaptureT sequences for control and experimental Experiment Overall Design: samples. SuperScript II Reverse Transcriptase for these Experiment Overall Design: reactions was purchased from Gibco BRL (Gaithersburg, Experiment Overall Design: MD). The resultant cDNAs were hybridized to microarray Experiment Overall Design: slides for 16 h in Agilent Hybridization Buffer (Agilent Experiment Overall Design: Technol) at 60 8C. Upon completion of the hybridization, Experiment Overall Design: the slides were washed for 10 min with 0.005% Triton in Experiment Overall Design: 6xsodium chloride/sodium citrate buffer (pH 7; SSC) at Experiment Overall Design: room temperature and then for five more min with 0.005% Experiment Overall Design: Triton in 0.1xSSC and 1 more minute in 0.1xSSC (pH 7), Experiment Overall Design: both at 4 8C. Washed slides were air-dried for 30 s. For Experiment Overall Design: fluorescent labeling of microarray-bound cDNA, the slides Experiment Overall Design: were incubated for 3 h at 65 8C with Capture Reagent Experiment Overall Design: Hybridization Mixture from 3DNA Array Detection Kit Experiment Overall Design: (Genesphere). In this mixture, Alexa 546 fluorochromeincorporating Experiment Overall Design: dendrimers contained single-stranded arms Experiment Overall Design: complimentary to the dcaptureT sequences used in the Experiment Overall Design: reverse transcription of RNA from control tissue, while Experiment Overall Design: Alexa 647 fluorochrome-incorporating dendrimers contained Experiment Overall Design: arms complimentary to the capture sequences used Experiment Overall Design: in reverse transcription of RNA from experimental tissue. Experiment Overall Design: The labeling reaction was terminated by washing of the Experiment Overall Design: microarray slides at room temperature for 10 min with Experiment Overall Design: 0.005% Triton in 2xSSC and for another 10 min with in Experiment Overall Design: 0.2xSSC. After that, the slides were air-dried for 30 s. The Experiment Overall Design: processed microarray slides were scanned at 10 Am Experiment Overall Design: resolution on a GenePix 4100A scanner (Axon Instr., Union Experiment Overall Design: City, CA) with the laser excitation at 532 nm [emission filter Experiment Overall Design: 575DF35 (green); photomultiplier voltage 550] for Alexa Experiment Overall Design: 546 (control samples) and the laser excitation at 635 nm Experiment Overall Design: [emission filter 670DF40 (red); photomultiplier voltage Experiment Overall Design: 695] for Alexa 647 (experimental samples). The signals Experiment Overall Design: were converted into 16-bits-per pixel resolution images, Experiment Overall Design: providing color depth of 65,536 levels. The densitometry Experiment Overall Design: was performed with GenePix Pro 4.1 software (Axon Instr.). Experiment Overall Design: Background was subtracted using the dlocal background Experiment Overall Design: correctionT procedure available in the software. Quality control utilized 255 positive controls, 161 negative controls Experiment Overall Design: and 646 QC-spots present on Agilentâs arrays. For Experiment Overall Design: replicates within a slide, median signal values were Experiment Overall Design: calculated. For each array, the data were normalized in Experiment Overall Design: Acuity 3.1 software (Axon Instr.) by applying locally Experiment Overall Design: weighted scatterplot smoothing (LOWESS) transformation. Experiment Overall Design: The between array scale normalization Experiment Overall Design: was done using intensity log10 ratio distribution box plots (GeneSight Experiment Overall Design: software, BioDiscovery, El Segundo, CA) for verification. Experiment Overall Design: Statistical analysis of the normalized data was conducted Experiment Overall Design: by the Significant Analyses for Microarray Algorithm Experiment Overall Design: (SAM) using Excel macros available at the Stanford SAM website. Experiment Overall Design: In the analyses of both frontal and occipital regions of the fetal cerebral wall, Experiment Overall Design: the cut-off thresholds were set to identify the maximum Experiment Overall Design: number of cocaine exposure-regulated genes at the minimal Experiment Overall Design: false discovery rate (FDR) allowed by SAM for a given set Experiment Overall Design: of microarray data. For both regions, the FDR rates were Experiment Overall Design: <0.5%. The apoptosis and Wnt pathway-related genes were identified with Pathway Assist 2.0 software (Stratagene, La Jolla, CA). Experiment Overall Design: This was followed by manual review of literature for each Experiment Overall Design: identified gene.
2008-06-15 | E-GEOD-6628 | biostudies-arrayexpress
Project description:DNA methylation profiling of nucleus Accumbens of rats that self administered cocaine and were subjected to 1 or 30 withdrawal days with or without extinction tests. The groups consist of 1. Saline rats (Sal.) 2. Rats that self-administered cocaine for 10 days and that were subjected to a withdrawal period of 1 day (1W) 3. Rats that self-administered cocaine for 10 days and that were subjected to a withdrawal period of 1 day and to an extinction test for assessment of cue-induced cocaine-seeking behavior (1C) 4. Rats that self-administered cocaine for 10 days and that were subjected to a withdrawal period of 30 days (30W) 5. Rats that self-administered cocaine for 10 days and that were subjected to a withdrawal period of 30 days and to an extinction test for assessment of cue-induced cocaine-seeking behavior (30C)
2015-02-27 | E-GEOD-66348 | biostudies-arrayexpress