Evidence map›Paper›PMID 41093944›Full record

ArticleScientific reports2025

Persistent open chromatin state in early-life stress-activated cells of the VTA.

Rebekah L Rashford, Michael DeBerardine, Shu Dan, Shannon N Bennett, Catherine Jensen Peña

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Altered Postnatal Chromatin Development in the Nucleus Accumbens Primes Enduring Stress Sensitivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  2. Epigenetic Signatures of Social Defeat Stress Varying Duration.International journal of molecular sciences · 2025
    Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Rebekah L RashfordPrinceton Neuroscience Institute, Princeton University, Princeton, NJ, 08544, USA.
Michael DeBerardinePrinceton Neuroscience Institute, Princeton University, Princeton, NJ, 08544, USA.
Shu DanPrinceton Neuroscience Institute, Princeton University, Princeton, NJ, 08544, USA.
Shannon N BennettPrinceton Neuroscience Institute, Princeton University, Princeton, NJ, 08544, USA.
Catherine Jensen PeñaPrinceton Neuroscience Institute, Princeton University, Princeton, NJ, 08544, USA. cpena@princeton.edu.

Funding

Epigenetic priming of response to future stressorsR01MH129643 · NIMH · PRINCETON UNIVERSITY · PI Catherine Jensen Pena · 2022 to 2026
$3.8M
Epigenetic and cellular markers of stress sensitization by early life stress in miceR00MH115096 · NIMH · PRINCETON UNIVERSITY · PI PENA, CATHERINE JENSEN · 2019 to 2021
$746k
Promoting Resilience to Early Life Stress through Epigenetic EditingF31MH131351 · NIMH · PRINCETON UNIVERSITY · PI RASHFORD, REBEKAH · 2022 to 2023
$58k
New York Stem Cell Foundation Robertson Neuroscience InvestigatorNIMH NIH HHS F31 MH131351NIMH NIH HHS F31MH131351NIMH NIH HHS R00 MH115096NIMH NIH HHS R00MH115096NIMH NIH HHS R01 MH129643
6 · The paper itself

Abstract

Early-life stress sensitizes individuals to subsequent stressors to increase lifetime risk for psychiatric disorders. Within the ventral tegmental area (VTA), a mesolimbic brain region implicated in stress response and mental health, early-life stress causes long-lasting changes in gene expression and chromatin modifications that in turn cause latent physiological and behavioral sensitivity to stress. These molecular consequences of early-life stress are indicative of epigenetic priming, a form of molecular memory in which developmental or environmental cues open chromatin at enhancers to facilitate transcriptional response to stimuli. However, the long term impact of early-life stress on chromatin architecture in the VTA was not yet known. Using a combination of activity-dependent cellular tagging and ATAC-sequencing, we find that early-life stress opens chromatin specifically in stress-activated cells of the VTA, that this remodeling persists into adulthood, and that opening chromatin at cis-regulatory elements including enhancers augments transcriptional response to adult stress. Together, this data supports enhancer priming within ELS-responsive cells in the VTA as a biological mechanism for lifelong stress sensitivity.

Indexed as

ChromatinStress, PsychologicalVentral Tegmental AreaAnimalsChromatin Assembly and DisassemblyEnhancer Elements, GeneticEpigenesis, GeneticMaleMiceChromatinActivity-dependent genetic labeling (TRAP)ATAC-seqEarly life stressEpigenetic primingEpigeneticsVentral tegmental area

Identifiers

PMID41093944
PMCPMC12528658

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.