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Claustral cell identity is determined by Nurr1 and regulates hallucinogenic-like states

ABSTRACT: Claustral cell identity is determined by Nurr1 and regulates hallucinogenic-like states

PROVIDER: PRJNA955719 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24171537_1.fastq.gz	Fastqsanger.gz
	SRR24171537_2.fastq.gz	Fastqsanger.gz
	SRR24171538_1.fastq.gz	Fastqsanger.gz
	SRR24171538_2.fastq.gz	Fastqsanger.gz
	SRR24171539_1.fastq.gz	Fastqsanger.gz

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Claustral cell identity is determined by Nurr1 and regulates hallucinogenic-like states

Project description:Nurr1 is a transcription factor, which is highly enriched in the claustrum (CLA), an enigmatic brain region that has been hypothesized to control hallucinations. Here, by using virus mediated deletion in conditional gene-targeted mice, we investigated the role of Nurr1 in CLA. These mice exhibited loss of the CLA transcriptional identity. To further study the role of Nurr1 in CLA we designed conditional Nurr1 knock out mice under D1 receptor promoter (D1R-Nurr1cKO). Accordingly, these mice showed similar results in CLA marker gene expression with the viral-targeted strategy. Moreover, D1R-Nurr1cKO mice exhibited loss of hallucinogen receptor signaling in CLA. Functional ultrasound imaging showed that hallucinogenic serotoninergic and opioidergic receptor agonists increased functional connectivity between prefrontal cortex and somatomotor regions in control mice but not in D1R-Nurr1cKO. Conclusively, we demonstrate that Nurr1 loss ablates CLA cell identity, which may affect hallucinogenic-like states. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells at two time points.

2024-08-04 | GSE229732 | GEO

Claustrum/dorsal Endopiriform cortex complex cell identity is determined 1 by Nurr1 and regulates hallucinogenic-like states.

Project description:Claustrum/dorsal Endopiriform cortex complex cell identity is determined 1 by Nurr1 and regulates hallucinogenic-like states.

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Claustrum/dorsal Endopiriform cortex complex cell identity is determined 1 by Nurr1 and regulates hallucinogenic-like states.

Project description:The Claustrum/dorsal Endopiriform cortex complex (CLA) is an enigmatic brain region with 19 extensive glutamatergic projections to multiple cortical areas. The transcription factor Nurr1 is 20 highly expressed in the CLA, but its role in this region is not understood. By using conditional 21 gene-targeted mice, we show that Nurr1 is a crucial regulator of CLA neuron identity. Although 22 CLA neurons remain intact in the absence of Nurr1, the distinctive gene expression pattern in 23 the CLA is abolished. CLA has been hypothesized to control hallucinations, but little is known 24 of how the CLA responds to hallucinogens. After the deletion of Nurr1 in the CLA, both 25 hallucinogen receptor expression and signaling are lost. Furthermore, functional ultrasound 26 imaging and Neuropixel electrophysiological recordings revealed that the effects of 27 hallucinogenic receptor agonists on functional connectivity between the prefrontal and 28 sensorimotor cortices are altered in Nurr1-ablated mice. Our findings suggest that Nurr1-29 targeted strategies provide new avenues for functional studies of the CLA.

2024-08-05 | GSE229770 | GEO

Claustrum and dorsal endopiriform cortex complex cell-identity is determined by Nurr1 and regulates hallucinogenic-like states in mice.

Project description:The Claustrum/dorsal endopiriform cortex complex (CLA) is an enigmatic brain region with extensive glutamatergic projections to multiple cortical areas. The transcription factor Nurr1 is highly expressed in the CLA, but its role in this region is not understood. By using conditional gene-targeted mice, we show that Nurr1 is a crucial regulator of CLA neuron identity. Although CLA neurons remain intact in the absence of Nurr1, the distinctive gene expression pattern in the CLA is abolished. CLA has been hypothesized to control hallucinations, but little is known of how the CLA responds to hallucinogens. After the deletion of Nurr1 in the CLA, both hallucinogen receptor expression and signaling are lost. Furthermore, functional ultrasound and Neuropixel electrophysiological recordings revealed that the hallucinogenic-receptor agonists' effects on functional connectivity between prefrontal and sensorimotor cortices are altered in Nurr1-ablated mice. Our findings suggest that Nurr1-targeted strategies provide additional avenues for functional studies of the CLA.

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Nurr1 orchestrates claustrum development and functionality

Project description:Claustrum is the part of the forebrain known to be most widely interconnected tissue with almost all global regions. It is believed to be involved in coordinating multiple cognitive behaviors including consciousness formation. However, little is known about the molecular mechanisms underlying its development and involvement in behavioral control. Here we show that Nurr1 (Nr4a2) is the key transcription factor orchestrating claustral morphogenesis, functional connectivity and thus behaviors. Nurr1 deficient claustral cells aberrantly migrate into insular cortex, shaping claustrum into an abnormal wing-like structure, and ectopically turn on insular cortex genetic program. Accordingly, functional connectivity of the claustrum is not properly formed and relevant behaviors are dysregulated in Nurr1 deficient mice. We show that Nurr1 regulates claustral neuron positioning by suppressing G-protein signaling.

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Project description:ES cell-derived neurons of forebrain identity were isolated by magnetic sorting, cultured for 7 days and transduced with either Nurr1 or eGFP lentivirus. After an additional 12 h in culture, mRNA was isolated and subjected to microarray analysis.

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Project description:Nurr1 regulates claustral cell identity and hallucinogenic-like states

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NURR1 activation in skeletal muscle controls systemic energy homeostasis (ChIP-seq)

Project description:Skeletal muscle plays a central role in the control of metabolism and exercise tolerance. Analysis of muscle enhancers activated after exercise in mice revealed the orphan nuclear receptor NURR1/NR4A2 as a prominent component of exercise-responsive enhancers. We show that exercise enhances the expression of NURR1 and transgenic overexpression of NURR1 in skeletal muscle confers an endurance phenotype in mice. NURR1 expression in skeletal muscle is also sufficient to prevent hyperglycemia and hepatic steatosis by enhancing muscle glucose uptake and storage as glycogen. Furthermore, treatment of obese mice with putative NURR1 agonists increases energy expenditure, improves glucose tolerance, and confers a lean phenotype, mimicking the effects of exercise. These findings identify a key role for NURR1 in governance of skeletal muscle glucose metabolism and reveal a transcriptional link between exercise and metabolism. Our findings also identify NURR1 agonists as possible exercise mimetics with the potential to ameliorate obesity and other metabolic abnormalities.

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NURR1 activation in skeletal muscle controls systemic energy homeostasis (RNA-seq)

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Identification of genes modulated by Nurr1 overexpression

Project description:Identification of genes modulated by Nurr1 overexpression in HB-1 HB-1 cells overexpressing Nurr1

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