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An epigenomic shift in amygdala marks the transition to maternal behaviors in alloparenting virgin female mice

ABSTRACT: An epigenomic shift in amygdala marks the transition to maternal behaviors in alloparenting virgin female mice

PROVIDER: PRJNA765020 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15998300.fastq.gz	Fastqsanger.gz
	SRR15998218.fastq.gz	Fastqsanger.gz
	SRR15998219.fastq.gz	Fastqsanger.gz
	SRR15998220.fastq.gz	Fastqsanger.gz
	SRR15998221.fastq.gz	Fastqsanger.gz

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An epigenomic shift in amygdala marks the transition to maternal behaviors in alloparenting virgin female mice

Project description:In many species, adults care for young offspring that are not their own, a phenomenon called alloparenting. However, most nonparental adults must be sensitized by repeated or extended exposure to pups before robustly displaying of parental-like behaviors. To capture neurogenomic events underlying the transition to active parental caring behaviors, we analyzed brain gene expression and chromatin profiles of virgin female mice co-housed with mothers during pregnancy and after birth. After an initial display of antagonistic behaviors and a surge of defense-related gene expression, we observed a dramatic shift in the chromatin landscape specifically in amygdala of the pup-exposed virgin females, accompanied by a dampening of defense-related gene expression. This epigenetic shift coincided with hypothalamic expression of the oxytocin gene and the emergence of behaviors and gene expression patterns classically associated with maternal care. The results outline a neurogenomic program associated with dramatic behavioral changes and suggest molecular networks relevant to human postpartum mental health.

2022-01-26 | GSE184549 | GEO

An epigenomic shift in amygdala marks the transition to maternal behaviors in alloparenting virgin female mice.

Project description:Adults of many species will care for young offspring that are not their own, a phenomenon called alloparenting. However, in many cases, nonparental adults must be sensitized by repeated or extended exposures to newborns before they will robustly display parental-like behaviors. To capture neurogenomic events underlying the transition to active parental caring behaviors, we analyzed brain gene expression and chromatin profiles of virgin female mice co-housed with pregnant dams during pregnancy and after birth. After an initial display of antagonistic behaviors and a surge of defense-related gene expression, we observed a dramatic shift in the chromatin landscape specifically in amygdala of the pup-exposed virgin females compared to females co-housed with mother before birth, accompanied by a dampening of anxiety-related gene expression. This epigenetic shift coincided with hypothalamic expression of the oxytocin gene and the emergence of behaviors and gene expression patterns classically associated with maternal care. The results outline a neurogenomic program associated with dramatic behavioral changes and suggest molecular networks relevant to human postpartum mental health.

| S-EPMC8863255 | biostudies-literature

Loss of kdrl marks the shift from embryonic to adult HSPCs

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RNA-seq experiment on five mouse brain regions--hypothalamus, hippocampus, neocortex, cerebellum, and the amygdala --comparing expression in virgin females to primiparous females three weeks after pup weaning.

Project description:RNA-seq experiment on five mouse brain regions-- --comparing expression in virgin females to primiparous females three weeks after pup weaning. For each brain region there are 8 replicates, though three samples were not used in the final analysis based on inspection of PCA plots (1 sample from the Hippocampus, Cerebellum and Amygdala data sets; see details below).

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The basolateral amygdala-anterior cingulate pathway contributes to depression-like behaviors and comorbidity with chronic pain behaviors in male mice

Project description:While depression and chronic pain are frequently comorbid, underlying neuronal circuits, and their relevance for the understanding of psychopathology, remain poorly defined. Here we show in mice that hyperactivity of the neuronal pathway linking the basolateral amygdala to the anterior cingulate cortex is essential for chronic pain-induced depression. In naive male mice, we demonstrate that activation of this pathway is sufficient to trigger depressive-like behaviors, as well as transcriptomic alterations that recapitulate core molecular features of depression in the human brain. These alterations notably impact gene modules related to myelination and the oligodendrocyte lineage. Among these, we show that Sema4a, a hub gene significantly upregulated in both male mice and humans in the context of altered mood, is necessary for the emergence of depressive-like behaviors. Overall, these results place the BLA-ACC pathway at the core of pain and depression comorbidity, and unravel the role of impaired myelination and Sema4a in mood control.

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The basolateral amygdala-anterior cingulate pathway contributes to depression-like behaviors and comorbidity with chronic pain behaviors in male mice

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A double negative post-transcriptional regulatory circuit mediates the virgin behavioral state

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DNA methylation profiling of the amygdala, hippocampus, hypothalamus and adrenal gland of the pig using Reduced Representation Bisulfite Sequencing (RRBS)

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