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Harsh Parenting Predicts Novel HPA Receptor Gene Methylation and NR3C1 Methylation Predicts Cortisol Daily Slope in Middle Childhood

ABSTRACT: Harsh Parenting Predicts Novel HPA Receptor Gene Methylation and NR3C1 Methylation Predicts Cortisol Daily Slope in Middle Childhood

PROVIDER: PRJNA612861 | ENA |

REPOSITORIES: ENA

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Harsh Parenting Predicts Novel HPA Receptor Gene Methylation and NR3C1 Methylation Predicts Cortisol Daily Slope in Middle Childhood

Project description:Adverse experiences in childhood are associated with altered hypothalamic pituitary adrenal axis function and negative health outcomes throughout life. It is now commonly accepted that abuse and neglect can alter epigenetic regulation of HPA genes. Accumulated evidence suggests harsh parenting practices such as spanking are also strong predictors of negative health outcomes. We predicted harsh parenting at 2.5 years old would predict HPA gene DNA methylation similarly to abuse and neglect, and cortisol output at 8.5 years old. Saliva samples were collected three times a day across three days to estimate cortisol diurnal slopes. Methylation was quantified using the Illumina Infinium MethylationEPIC array BeadChip (850K) with DNA collected from buccal cells. We used principal components analysis to compute a summary statistic for CpG sites across candidate genes. The first and second components were used as outcome variables in mixed linear regression analyses with harsh parenting as a predictor variable. We found harsh parenting significantly predicted methylation of several HPA axis genes, including novel gene associations with AVPRB1, CRHR1, CRHR2, and MC2R (FDR corrected p < 0.05). Further, we found NR3C1 methylation predicted a steeper diurnal cortisol slope. Our results extend the current literature by demonstrating harsh parenting may influence DNA methylation similarly to more extreme early life experiences such as abuse and neglect. Further, we show NR3C1 methylation is associated with diurnal HPA function. Elucidating the molecular consequences of harsh parenting on health can inform best parenting practices and provide potential treatment targets for common complex disorders.

2021-04-01 | GSE147058 | GEO

Harsh Parenting Predicts Novel HPA Receptor Gene Methylation and NR3C1 Methylation Predicts Cortisol Daily Slope in Middle Childhood.

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Cell Type-Specific Hormonal Signaling Configures Hypothalamic Circuits for Parenting

Project description:Parenting behavior emerges from hormonally sensitive circuits, but how distinct circuit components are affected by, and contribute to, sex and state dependent changes in infant caregiving remains unclear. Using cell type-specific approaches, we characterized two circuit nodes that are differentially configured by hormones to modulate infant-evoked behavior. An excitatory neuronal population in the anteroventral periventricular nucleus is only active in lactating mothers, increases virgin female caregiving when artificially stimulated and confers oxytocin sensitivity in mothers through a prolactin--STAT5b pathway. These neurons function upstream of another preoptic area population involved in male and female parenting, thus boosting caregiving by mothers. By contrast, androgen signaling in the latter preoptic population reshapes their intrinsic properties to promote pup-directed aggression, revealing cell type-specific tuning of social behavior circuits.

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Ethological principles predict the neuropeptides co-opted to influence parenting

Project description:Ethologists predicted that parental care evolves by modifying suitable behavioural precursors in the asocial ancestor. Traits such as nest building, defensive and aggressive behaviours, and potentially shared resources evolve to offspring protection and defence, and feeding. From this ethological principle, we further predicted that the evolved mechanistic changes would reside in genetic pathways underlying these behavioural precursors. While gene expression is difficult to detect for some molecules like neuropeptides, we tested our hypothesis by measuring abundance of neuropeptides in different behavioural states using LC-MS in female burying beetles, Nicrophorus vespilloides. Parenting in this species is extensive and complex as caring adults regurgitate food to begging, dependent offspring. We identified neuropeptides by sampling peptide abundance in female brains collected from three different behavioural states: solitary virgins, actively parenting, or post-parenting solitary adults. We identified 133 peptides belonging to 18 neuropeptides. Of these 18, eight differed in abundance in one or more state. We found increased abundance during parenting in seven of the eight. None of the identified neuropeptides have previously been associated with parental care, but all have known roles in predicted behavioural precursors of mating, resource defence, feeding, or social tolerance. Two, tachykinin and sulfakinin, influence multiple pathways. Our study supports the prediction that appropriate behavioural precursors are likely targets of selection during the evolution of parenting. Evolutionary principles predicted neuropeptides influencing social behaviour, and our results provide several new candidate neuropeptides underpinning parenting.

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Project description:Sleep deprivation (SD) disrupts systemic homeostasis, yet its impact on lacrimal gland integrity through neuroendocrine–microbial pathways remains unclear. Using a male mice SD model, we show that chronic SD activates the hypothalamic-pituitary-adrenal (HPA) axis, elevates corticosterone, alters gut microbiota, and depletes short-chain fatty acids (SCFAs). These alterations coincide with lacrimal gland atrophy, reduced tear secretion, and increased CD4⁺/CD8⁺ T cell infiltration, accompanied by activation of IL-17-associated inflammatory pathways. Pharmacological inhibition of glucocorticoid synthesis with metyrapone preserves lacrimal gland structure and function while attenuating immune activation. Microbiome-directed interventions, including SCFA supplementation and fecal microbiota transplantation, rebalance gut communities, suppress proinflammatory T cell responses, and maintain lacrimal gland homeostasis. Transcriptomic and immunohistochemical analyses further reveal that all three interventions converge on downregulation of IL-17 signaling. Collectively, these findings establish an HPA-gut microbiome-lacrimal gland axis links neuroendocrine stress to microbial dysbiosis and ocular inflammation, and they suggest therapeutic strategies for SD-associated lacrimal gland dysfunction.

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Genome Methylation Predicts Age and Longevity of Bats

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