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Early-life prefrontal cortex inhibition and early-life stress lead to long-lasting behavioral, transcriptional, and physiological impairments

ABSTRACT: Early-life prefrontal cortex inhibition and early-life stress lead to long-lasting behavioral, transcriptional, and physiological impairments

PROVIDER: PRJNA1069767 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27747642_1.fastq.gz	Fastqsanger.gz
	SRR27747642_2.fastq.gz	Fastqsanger.gz
	SRR27747643_1.fastq.gz	Fastqsanger.gz
	SRR27747643_2.fastq.gz	Fastqsanger.gz

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Early-life prefrontal cortex inhibition and early-life stress lead to long-lasting behavioral, transcriptional, and physiological impairments

Project description:Early-life stress has been linked to multiple neurodevelopmental and neuropsychiatric deficits. Our previous studies have linked maternal presence/absence from the nest in developing rat pups to changes in prefrontal cortex activity. Furthermore, we have shown that these changes are modulated by serotonergic signaling. Here we test whether changes in prefrontal cortex activity during early-life affect the developing cortex leading to behavioral alterations in the adult. We show that inhibiting the prefrontal cortex of mouse pups leads to cognitive deficits in the adult comparable to those seen following maternal separation. Moreover, we show that activating the prefrontal cortex during maternal separation can prevent these behavioral deficits. To test how maternal separation affects the transcriptional profile of the prefrontal cortex we performed single-nucleus RNA sequencing. Maternal separation lead to differential gene expression almost exclusively in inhibitory neurons. Among others, we found changes in GABAergic and serotonergic pathways in these interneurons. Interestingly, both maternal separation and early-life prefrontal cortex inhibition led to changes in physiological responses in prefrontal activity to GABAergic and serotonergic antagonists that were similar to the responses of more immature brains. Prefrontal activation during maternal separation prevented these changes. These data point to a crucial role of prefrontal cortex activity during early-life in behavioral expression in adulthood

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Early-life gene expression in neurons modulates lasting epigenetic states.

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Early-life gene expression in neurons modulates lasting epigenetic states [ChIP-Seq]

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The Biological Residue of Low Early-Life Social Class

Project description:Research shows that children who are reared in households with low socioeconomic status are more vulnerable to heart disease, respiratory infection, and some cancers when they reach adulthood. This study conducted transcriptional profiling of PBMC in healthy adults who were low vs. high in early-life SES to explore the long-lasting genomic effects of early experience. Keywords: life stress, gene expression, inflammation, socioeconomic status Samples from 30 adults with low early-life SES and 30 adults with high early-life SES

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Early-life gene expression in neurons modulates lasting epigenetic states. [RNA-seq 2]

Project description:Early-life gene expression in neurons modulates lasting epigenetic states. [RNA-seq 2]

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The Biological Residue of Low Early-Life Social Class

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Early life stress affects the salmon microbiome

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Early-life gene expression in neurons modulates lasting epigenetic states [ChIP-Seq]

Project description:In mammals during the early postnatal period the environment plays a critical role in promoting the final steps in neuronal development. While epigenetic factors are thought to contribute to this process, the underlying molecular mechanisms remain poorly understood. Here we show that in the brain during early life the DNA methyltransferase DNMT3A transiently binds across transcribed regions of lowly expressed genes, and its binding specifies the pattern of DNA methylation at CA sequences (mCA) within these genes. We find that DNMT3A occupancy and mCA deposition within the transcribed regions of genes is negatively regulated by gene transcription and may be modified by early-life experience. Once deposited, mCA is bound by the methyl-DNA-binding protein MECP2 and functions in a rheostat-like manner to fine-tune the cell type-specific transcription of genes that are critical for brain function.

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