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Estrogen-Sensitive Medial Preoptic Area Neurons Coordinate Hypothermia and Hypometabolism in Mice

ABSTRACT: Estrogen-Sensitive Medial Preoptic Area Neurons Coordinate Hypothermia and Hypometabolism in Mice

PROVIDER: PRJNA642124 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12097429.fastq.gz	Fastqsanger.gz
	SRR12097430.fastq.gz	Fastqsanger.gz
	SRR12097431.fastq.gz	Fastqsanger.gz
	SRR12097432.fastq.gz	Fastqsanger.gz
	SRR12097433.fastq.gz	Fastqsanger.gz

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Estrogen-Sensitive Medial Preoptic Area Neurons Coordinate Hypothermia and Hypometabolism in Mice

Project description:Homeotherms maintain a stable internal body temperature despite changing environments. During energy deficiency, some species can cease to defend their body temperature and enter a hypothermic and hypometabolic state known as torpor. Despite recent advances in our understanding of thermoregulation, the precise neurons that coordinate these profound thermoregulatory and metabolic changes remain largely unknown. Here, we demonstrate that estrogen-sensitive neurons in the medial preoptic area (MPA) are key drivers of hypothermia and hypometabolism in mice. We find that selectively activating estrogen-sensitive MPA neurons was sufficient to drive a coordinated depression of metabolic rate and body temperature similar to torpor, as measured by body temperature, physical activity, indirect calorimetry, heart rate, and brain activity. Inducing torpor with a prolonged fast revealed larger and more variable calcium transients from estrogen-sensitive MPA neurons during bouts of hypothermia. Finally, selective ablation of estrogen-sensitive MPA neurons demonstrated that these neurons are required for the full expression of fasting-induced torpor. Together, these findings suggest a role for estrogen-sensitive MPA neurons in directing the thermoregulatory and metabolic responses to energy deficiency.

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Transcription profiling of mouse bed nucleus of the stria terminalis and medial preoptic area

Project description:The effect of photoperiod on gene expression was assessed in punch samples of the bed nucleus of the stria terminalis and medial preoptic area. Long day mice were housed in 16L:8D and short day mice were housed in 8L:16D. Experiment Overall Design: For the medial preoptic area, independent samples were collected from long day (n=3) and short day (n=3) mice. For the bed nucleus of the stria terminalis independent samples were collected from long day (n=3) and short day (n=2) mice.

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Project description:Single nuclear RNA-sequencing from tissue dissected from the ventral medial preoptic area (VMPO) of the hypothalamus in saline and LPS injected mice

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Bulk single nuclear sequencing in the ventral medial preoptic area

Project description:Bulk single nuclear sequencing in the ventral medial preoptic area

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scRNAseq to understand hormonal control on pubertal transcription in the medial preoptic area

Project description:Pubertal maturation aids developments in emotion, cognition and reproduction. The conserved roles of elevated circulating gonadal sex steroids for the continued maturation of the nervous system via steroid hormone receptor mediated gene regulation is well documented. However, critical transcriptional dynamics mediated by steroids throughout puberty in molecularly defined circuitry remains elusive. We investigated pubertal transcriptional dynamics in the medial preoptic area (MPOA), a hypothalamic center for reproductive behaviors, in male and female mice at single cell resolution (scRNAseq).

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Effects of early life adversity on male reproductive behavior and the medial preoptic area

Project description:Early life adversity has been linked to altered reproductive development in humans, including changes in the timing of pubertal onset and sexual activity. One common form of early life adversity is having limited access to resources. This form of early life adversity can be modeled in rodents using the limited bedding and nesting model (LBN), in which rat dams and pups are placed in a low resource environment from postnatal day (PND) 2 through 9. Our laboratory has previously shown that male rats raised in LBN conditions have elevated levels of plasma estradiol compared to control males. Female rats, on the other hand, show no effect of LBN on plasma hormone levels, pubertal timing, or estrous cycle duration in adulthood. Here, we find that LBN males also show changes in adult reproductive behaviors. LBN males acquired the suite of reproductive behaviors more quickly than their control counterparts over the course of 3 weeks of testing, showing shorter latencies to mount, intromit, and ejaculate compared to controls prior to the final week of testing. We also characterized LBN-induced gene transcription changes across sex in the medial preoptic area (mPOA) which underlies reproductive behaviors. Interestingly, there was no effect of LBN on puberty onset (as measured by preputial separation) or masculinization of the sexually dimorphic nucleus of the preoptic area (SDN/POA; as measured by calbindin immunoreactivity) in males, suggesting LBN may not exert effects on hormone-dependent measures until after puberty.

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scRNAseq to understand hormonal control on pubertal transcription in the medial preoptic area

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Project description:The preoptic area (POA) of the hypothalamus is a key neural hub for thermoregulation, yet its role in modulating energy expenditure during caloric excess remains poorly defined. Here, we characterize prepronociceptin (PNOC)-expressing neurons in the medial POA (PNOCmPOA) that inhibit brown adipose tissue (BAT) thermogenesis and systemic energy expenditure. Chemogenetic activation of PNOCmPOA neurons reduced BAT activity, core temperature, energy expenditure, and glucose tolerance through inhibitory projections to the dorsomedial hypothalamus (DMH). In contrast, silencing or ablation of PNOCmPOA neurons increased BAT thermogenesis. Furthermore, PNOCmPOA activation promoted non-REM sleep, coupling thermoregulatory and arousal states. These findings define a hypothalamic circuit that limits postprandial arousal, thermogenesis, and energy dissipation, contributing to the pathophysiology of obesity. Targeting the PNOCmPOA→DMH pathway may provide a new therapeutic strategy to enhance BAT function in metabolic disease.

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