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A psychological stressor conveyed by appetite-linked neurons

ABSTRACT: A psychological stressor conveyed by appetite-linked neurons

PROVIDER: PRJNA599010 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10828905_1.fastq.gz	Fastqsanger.gz
	SRR10828905_2.fastq.gz	Fastqsanger.gz
	SRR10828906_1.fastq.gz	Fastqsanger.gz
	SRR10828906_2.fastq.gz	Fastqsanger.gz
	SRR10828907_1.fastq.gz	Fastqsanger.gz

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A psychological stressor conveyed by appetite-linked neurons

Project description:We report RNA sequencing of individual neurons producing corticotropin-releasing hormone (CRH), which are the master regulators of blood levels of stress hormones. Analyses of individual transcriptomes reveal a large variety of neurotransmitter and neuromodulator receptors. Using the ligand information for different receptors expressed on CRHNs, we mapped the locations of upstream neurons expressing different ligands.

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A psychological stressor conveyed by appetite-linked neurons.

Project description:Mammals exhibit instinctive reactions to danger critical to survival, including surges in blood stress hormones. Hypothalamic corticotropin-releasing hormone neurons (CRHNs) control stress hormones but how diverse stressors converge on CRHNs is poorly understood. We used sRNA profiling to define CRHN receptors for neurotransmitters and neuromodulators and then viral tracing to localize subsets of upstream neurons expressing cognate receptor ligands. Unexpectedly, one subset comprised POMC (proopiomelanocortin)-expressing neurons in the arcuate nucleus, which are linked to appetite suppression. The POMC neurons were activated by one psychological stressor, physical restraint, but not another, a predator odor. Chemogenetic activation of POMC neurons induced a stress hormone response, mimicking a stressor. Moreover, their silencing markedly reduced the stress hormone response to physical restraint, but not predator odor. These findings indicate that POMC neurons involved in appetite suppression also play a major role in the stress hormone response to a specific type of psychological stressor.

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Project description:The paraventricular hypothalamus (PVH) is crucial for food intake control, yet the presynaptic mechanisms underlying PVH neurons remain unclear. Here, we show that RUVBL2 in the PVH is significantly reduced during energy deficit, and knockout (KO) of PVH RUVBL2 results in hyperphagic obesity in mice. RUVBL2-expressing neurons in the PVH (PVHRUVBL2) exert the anorexigenic effect by projecting to the arcuate hypothalamus, the dorsomedial hypothalamus, and the parabrachial complex. We further demonstrate that PVHRUVBL2 neurons form the synaptic connections with POMC and AgRP neurons in the ARC. PVH RUVBL2 KO impairs the excitatory synaptic transmission by reducing presynaptic boutons and synaptic vesicles near active zone. Finally, RUVBL2 overexpression in the PVH suppresses food intake and protects against diet induced obesity. Together, this study demonstrates an essential role for PVH RUVBL2 in food intake control, and suggests that modulation of synaptic plasticity could be an effective way to curb appetite and obesity.

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