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SnRNA-seq dataset for "Reelin marks cocaine-activated striatal ensembles, promotes neuronal excitability, and regulates cocaine reward"

ABSTRACT: snRNA-seq dataset for "Reelin marks cocaine-activated striatal ensembles, promotes neuronal excitability, and regulates cocaine reward"

PROVIDER: PRJNA1122135 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29342758_1.fastq.gz	Fastqsanger.gz
	SRR29342758_2.fastq.gz	Fastqsanger.gz
	SRR29342759_1.fastq.gz	Fastqsanger.gz
	SRR29342759_2.fastq.gz	Fastqsanger.gz
	SRR29342760_1.fastq.gz	Fastqsanger.gz

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RNA-seq dataset for "Reelin marks cocaine-activated striatal ensembles, promotes neuronal excitability, and regulates cocaine reward"

Project description:RNA-seq dataset for "Reelin marks cocaine-activated striatal ensembles, promotes neuronal excitability, and regulates cocaine reward"

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Differential genetic expression within reward-specific ensembles in mice

Project description:Maladaptive reward seeking is a hallmark of cocaine use disorder. To develop therapeutic targets, it is critical to understand the neurobiological changes specific to cocaine-seeking without altering the seeking of natural rewards, e.g., sucrose. The prefrontal cortex (PFC) and the nucleus accumbens core (NAcore) are known regions associated with cocaine- and sucrose-seeking ensembles, i.e., a sparse population of co-activated neurons. Within ensembles, transcriptomic alterations in the PFC and NAcore underlie the learning and persistence of cocaine- and sucrose-seeking behavior. However, transcriptomes exclusively driving cocaine seeking independent from sucrose seeking have not yet been defined using a within-subject approach. Using Ai14:cFos-TRAP2 transgenic mice in a dual cocaine and sucrose self-administration model, we fluorescently sorted (FACS) and characterized (RNAseq) the transcriptomes defining cocaine- and sucrose-seeking ensembles. We found reward- and region-specific transcriptomic changes that will help develop clinically relevant genetic approaches to decrease cocaine-seeking behavior without altering non-drug reward-based positive reinforcement.

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snRNA-seq dataset for "Reelin marks cocaine-activated striatal ensembles, promotes neuronal excitability, and regulates cocaine reward"

Project description:This dataset contains single-nucleus RNA-seq results from rat adult nucleus accumbens tissue treated with CRISPRi machinery (hSyn-driven dCas9-KRAB-MeCP2 fusion) with a CRISPR sgRNA targeting lacZ (a bacterial gene not found in the mammalian genome; used as a non-targeting control) or Reln.

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RNA-seq dataset for "Reelin marks cocaine-activated striatal ensembles, promotes neuronal excitability, and regulates cocaine reward"

Project description:This dataset contains RNA-seq results from rat embryonic striatal neuronal cultures treated with CRISPRi machinery (dCas9-KRAB-MeCP2 fusion) with a CRISPR sgRNA targeting lacZ (a bacterial gene not found in the mammalian genome; used as a non-targeting control) or Reln.

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Differential genetic expression within reward-specific ensembles in mice

Project description:Differential genetic expression within reward-specific ensembles in mice

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Cocaine self-administration alters transcriptome-wide responses in the brain's reward circuitry

Project description:Global changes in gene expression that underlie the circuit and behavioral dysregulation associated with cocaine addiction remain incompletely understood. Here, we determined how a history of cocaine self-administration (SA) “re-programs” transcriptome-wide responses at baseline and in response to cocaine re-exposure after prolonged withdrawal (WD). We assigned male mice to one of six groups: saline or cocaine SA + 24 hr WD; or saline/cocaine SA + 30 d WD + an acute saline/cocaine challenge within the previous drug-paired context. RNA-seq was then conducted on six interconnected brain reward regions. We focused on patterns of gene expression that were altered by cocaine SA, in particular, molecular targets that show priming or desensitization upon re-exposure to cocaine. Genes that were affected uniquely by acute cocaine after cocaine SA+WD displayed region-specific regulation. The greatest number of regulated genes were seen in nucleus accumbens, dorsal striatum, and basolateral amygdala. Further analysis revealed several transcription factors as key upstream regulators in these three regions, including several not previously implicated in cocaine action. Regulation of subsets of these primed and desensitized genes correlated robustly with SA behavior displayed by individual mice. For example, analysis of transcriptome-wide expression changes revealed that genes associated with cocaine intake respond to contextual information in a region-specific manner. This comprehensive picture of transcriptome-wide regulation by cocaine SA and WD throughout the brain’s reward circuitry provides new insight into the molecular basis of cocaine addiction, which will guide future studies of the key molecular pathways involved.

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Chromatin-mediated alternative splicing regulates cocaine reward behavior

Project description:Chromatin-mediated alternative splicing regulates cocaine reward behavior

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Project description:ATP-dependent chromatin remodeling proteins are being implicated increasingly in the regulation of complex behaviors, including models of several psychiatric disorders. Here, we demonstrate that Baz1b, an accessory subunit of the ISWI family of chromatin remodeling complexes, is upregulated in the nucleus accumbens (NAc), a key brain reward region, in both chronic cocaine-treated mice and mice that are resilient to chronic social defeat stress. In contrast, no regulation is seen in mice that are susceptible to this chronic stress. Viral-mediated overexpression of Baz1b, along with its associated subunit Smarca5, in mouse NAc is sufficient to potentiate both rewarding responses to cocaine, including cocaine self-administration, and resilience to chronic social defeat stress. However, despite these similar, proreward behavioral effects, genome-wide mapping of BAZ1B in NAc revealed mostly distinct subsets of genes regulated by these chromatin remodeling proteins after chronic exposure to either cocaine or social stress. Together, these findings suggest important roles for BAZ1B and its associated chromatin remodeling complexes in NAc in the regulation of reward behaviors to distinct emotional stimuli and highlight the stimulus-specific nature of the actions of these regulatory proteins. BAZ1B (WSTF) ChIP-seq of mouse. Cocaine vs Saline, 3 biological replicates. In social defeat model: Normal control vs Susceptible vs Resilient, 3 biological replicates.

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Genome-Wide Promoter Analysis of Epigenetic Regulation by Cocaine (MM5 data)

Project description:Changes in gene expression contribute to the long-lasting regulation of the brain's reward circuitry seen in drug addiction, however, the specific genes regulated and the transcriptional mechanisms underlying such regulation remain poorly understood. Here, we used chromatin immunoprecipitation coupled with promoter microarray analysis to characterize genome-wide epigenetic changes in the mouse nucleus accumbens, a crucial brain reward region, after repeated cocaine administration. Our findings reveal several interesting principles of gene regulation by cocaine and of the role of Î?FosB and CREB, two prominent cocaine-induced transcription factors, in this brain region. Mice were treated with cocaine or saline. Chromatin immunoprecipitation was performed for acetylated histone H3 and H4 as described previously (Kumar et al., 2005) with minor modifications. Immunoprecipitated DNA was amplified via ligation-mediated PCR and hybridized to Nimblgen mouse MM5 promoter arrays. 2 biological replicates per condition.

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