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Molecular profiling of lateral septum neurotensin neurons using viralTRAP

ABSTRACT: Molecular profiling of lateral septum neurotensin neurons using viralTRAP

PROVIDER: PRJNA647385 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12269905.fastq.gz	Fastqsanger.gz
	SRR12269906.fastq.gz	Fastqsanger.gz
	SRR12269907.fastq.gz	Fastqsanger.gz
	SRR12269908.fastq.gz	Fastqsanger.gz
	SRR12269909.fastq.gz	Fastqsanger.gz

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Molecular profiling of lateral septum neurotensin neurons using viralTRAP

Project description:The lateral septum contains a number of molecularly defined cell populations. We used the viral-TRAP protocol (Nectow et al.,2017) to profile lateral septum neurotensin neurons.

2020-08-30 | GSE154758 | GEO

Opioid-driven disruption of the septum reveals a role for neurotensin-expressing neurons in withdrawal

Project description:Because opioid withdrawal is an intensely aversive experience, persons with opioid use disorder (OUD) often relapse to avoid it. The lateral septum (LS) is a forebrain structure that is important in aversion processing, and previous studies have linked the LS to substance use disorders. It is unclear, however, which precise LS cell types might contribute to the maladaptive state of withdrawal. To address this, we used single-nucleus RNA-sequencing to interrogate cell type specific gene expression changes induced by chronic morphine and withdrawal. We discovered that morphine globally disrupts the transcriptional profile of LS cell types, but neurotensin-expressing neurons (Nts; LS-Nts neurons) are selectively activated by naloxone. Using two-photon calcium imaging and ex vivo electrophysiology, we next demonstrated that LS-Nts neurons receive enhanced glutamatergic drive in morphine-dependent mice and remain hyperactivated during opioid withdrawal. Finally, we showed that activating and silencing LS-Nts neurons during opioid withdrawal regulates pain coping behaviors and sociability. Together, these results suggest that LS-Nts neurons are a key neural substrate involved in opioid withdrawal and establish the LS as a crucial regulator of adaptive behaviors, specifically pertaining to OUD.

2025-05-15 | GSE236007 | GEO

Actvity-dependent profiling of lateral septum neurons following restraint stress

Project description:Actvity-dependent profiling of lateral septum neurons following restraint stress

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Actvity-dependent profiling of lateral septum neurons following restraint stress

Project description:We used the phospho-TRAP protocol (Knight et al., 2011) to profile lateral septum populations that are activated following 1 hour of restraint stress.

2020-08-30 | GSE154749 | GEO

Opioid-driven disruption of the septum reveals a role for neurotensin-expressing neurons in withdrawal

Project description:Opioid-driven disruption of the septum reveals a role for neurotensin-expressing neurons in withdrawal

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Impact of Chronic Olanzapine Administration on Gene Expression in the Mouse Lateral Septum

Project description:To explore the effects of long-term olanzapine treatment on gene expression in the lateral septum of female mice, we conducted a study using female C57BL/6 mice fed with olanzapine-supplemented chow for 12 weeks. The treated mice exhibited significant weight gain and lipid alterations compared to the control group. Subsequently, RNA-seq was performed on the lateral septum brain regions of both the treated and control mice, followed by gene expression profiling to analyze the data.

2024-07-03 | GSE268867 | GEO

A circuit from lateral septum neurotensin neurons to tuberal nucleus controls hedonic feeding.

Project description:Feeding behavior is regulated by both the homeostatic needs of the body and hedonic values of the food. Easy access to palatable energy-dense foods and the consequent obesity epidemic stress the urgent need for a better understanding of neural circuits that regulate hedonic feeding. Here, we report that neurotensin-positive neurons in the lateral septum (LSNts) play a crucial role in regulating hedonic feeding. Silencing LSNts specifically promotes feeding of palatable food, whereas activation of LSNts suppresses overall feeding. LSNts neurons project to the tuberal nucleus (TU) via GABA signaling to regulate hedonic feeding, while the neurotensin signal from LSNts→the supramammillary nucleus (SUM) is sufficient to suppress overall feeding. In vivo calcium imaging and optogenetic manipulation reveal two populations of LSNts neurons that are activated and inhibited during feeding, which contribute to food seeking and consumption, respectively. Chronic activation of LSNts or LSNts→TU is sufficient to reduce high-fat diet-induced obesity. Our findings suggest that LSNts→TU is a key pathway in regulating hedonic feeding.

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Molecular codes defining lateral hypothalamic sleep regulating neurons

Project description:Molecular codes defining lateral hypothalamic sleep regulating neurons

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Changes in neurotensin signalling drive hedonic devaluation in obesity

Project description:Calorie-rich foods, particularly those high in fat and sugar, evoke pleasure in both humans and animals. However, prolonged consumption of such foods may reduce their hedonic value, potentially contributing to obesity. Here, we investigated this phenomenon in mice on a chronic high-fat diet (HFD). While these mice preferred high-fat food over regular chow in their home cages, they showed reduced interest in calorie-rich foods in a no-effort setting. This paradoxical decrease in hedonic feeding has been reported previously, but its neurobiological basis remains unclear. We found that in regular diet mice, neurons in the lateral nucleus accumbens projecting to the ventral tegmental area (NAcLat→VTA) encoded hedonic feeding behaviors. In HFD mice, this behavior was reduced and uncoupled from neural activity. Optogenetic stimulation of the NAcLat→VTA pathway increased hedonic feeding in regular diet mice but not in HFD mice, though this behavior was restored when HFD mice returned to a regular diet. HFD mice exhibited reduced neurotensin expression and release in the NAcLat→VTA pathway. Furthermore, neurotensin knockout in the NAcLat and neurotensin receptor blockade in the VTA each abolished optogenetic-induced hedonic feeding behavior. Enhancing neurotensin signaling via overexpression normalized aspects of diet-induced obesity, including weight gain and hedonic feeding. Altogether, our findings identify a neural circuit mechanism linking the devaluation of hedonic foods with obesity.

2025-03-27 | GSE287548 | GEO

Chronic subanesthetic ketamine induces schizophrenic-like social deficits and alters translatome in the lateral septum

Project description:Schizophrenia is often marked by poor social functioning that can have a severe impact on quality of life and independence, but the underlying neural circuity is not well understood. Here we used a translational model of subanesthetic ketamine mice to delineate neural pathways in the brain linked to social deficits in schizophrenia. Mice treated with chronic ketamine exhibit profound social and sensorimotor deficits as previously reported. Using three-dimensional c-Fos immunolabeling and volume imaging (iDISCO), we show that ketamine treatment resulted in hypoactivation of the lateral septum (LS) in response to social stimuli. Chemogenetic activation of the LS rescued social deficits after ketamine treatment, while chemogenetic inhibition of previously active populations in the LS (i.e. social engram neurons) recapitulated social deficits in ketamine-naïve mice. We then examined the translatome of LS engram neurons and found upregulation of genes encoding potassium inwardly-rectifying channels and solute transporters as well as dysregulation of genes implicated in apoptotic processes, all of which could contribute to the hypoactivation of LS social engram neurons after chronic ketamine exposure. A number of ketamine-induced differentially expressed genes (DEGs), including those involved in mitochondrial function and neuroinflammatory pathways, were shared with human schizophrenia and mouse models of neurodevelopmental disorders.

2024-08-18 | GSE241234 | GEO

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