ArticleMolecular neurobiology2019
Early-Life Adversity Induces Epigenetically Regulated Changes in Hippocampal Dopaminergic Molecular Pathways.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Epigenetic mechanisms affected by stress during adolescence and the increased risk for depression later in life: a systematic review.Molecular psychiatry · 2026Pooled it
- Aversive 22-kHz ultrasonic vocalization playback reveals differences in affective (dys)function following early life adversity in male and female juvenile rats.Behavioural brain research · 2026Article
- Different early-life adversity paradigms have disparate effects on maternal care, neuronal activation, and social behavior in developing mice.Neurobiology of stress · 2026Article
- Adverse effects of early-life stress: focus on the rodent neuroendocrine system.Neural regeneration research · 2024Review
- Translational models of stress and resilience: An applied neuroscience methodology review.Neuroscience applied · 2024Review
- Early life stress induces decreased expression of CB1R and FAAH and epigenetic changes in the medial prefrontal cortex of male rats.Frontiers in cellular neuroscience · 2024Article
- Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential.Signal transduction and targeted therapy · 2023Review
- By what molecular mechanisms do social determinants impact cardiometabolic risk?Clinical science (London, England : 1979) · 2023Review
- Epigenetic (re)programming of gene expression changes of CB1R and FAAH in the medial prefrontal cortex in response to early life and adolescence stress exposure.Frontiers in cellular neuroscience · 2023Article
- Epigenetic Mechanism of Early Life Stress-Induced Depression: Focus on the Neurotransmitter Systems.Frontiers in cell and developmental biology · 2022Review
- Early Life Stress-Induced Epigenetic Programming of Hippocampal NPY-Y2 Receptor Gene Expression Changes in Response to Adult Stress.Frontiers in cellular neuroscience · 2022Article
- Early social deprivation shapes neuronal programming of the social decision-making network in a cooperatively breeding fish.Molecular ecology · 2021Article
- Early Life Stress and Risks for Opioid Misuse: Review of Data Supporting Neurobiological Underpinnings.Journal of personalized medicine · 2021Review
- The Importance of Epigenetics in Diagnostics and Treatment of Major Depressive Disorder.Journal of personalized medicine · 2021Review
- Sex Differences in Affective Dysfunction and Alterations in Parvalbumin in Rodent Models of Early Life Adversity.Frontiers in behavioral neuroscience · 2021Review
- Maternal Separation Induces Long-Term Alterations in the Cardiac Oxytocin Receptor and CystathionineOxidative medicine and cellular longevity · 2020Article
- Hormesis in Health and Chronic Diseases.Trends in endocrinology and metabolism: TEM · 2019Review
- Unraveling the epigenetic landscape of depression: focus on early life stress .Dialogues in clinical neuroscience · 2019Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Early-life adversity (ELA) represents a major risk factor for the development of behavioral dysfunctions and mental disorders later in life. On the other hand, dependent on type, time point, and duration, ELA exposure can also induce adaptations, which result in better stress coping and resilience later in life. Guided by the hypothesis that chronic exposure to ELA results in dysfunctional brain and behavior, whereas short exposure to ELA may result in resilience, the behavioral and neurobiological consequences of long-term separation stress (LTSS) and short-term separation stress (STSS) were compared in a mouse model for ELA. In line with our hypothesis, we found that LTSS induced depressive-like behavior, whereas STSS reduced depressive-like behavioral symptoms. We then tested the hypothesis that the opposite behavioral outcomes of the two stress paradigms may be mediated by functional, epigenetically regulated changes of dopaminergic modulation in the hippocampal formation. We found that STSS exposure elevated dopamine receptor D1 (DRD1) gene expression and decreased gene expression of its downstream modulator DARPP-32 (32-kDa dopamine- and cAMP-regulated phosphoprotein), which was paralleled by decreased H3 acetylation at its gene promoter region. In contrast, LTSS elevated DARPP-32 gene expression, which was not paralleled by changes in histone acetylation and DRD1 gene expression. These findings indicate that short- and long-term neonatal exposure to ELA induces changes in dopaminergic molecular pathways, some of which are epigenetically regulated and which either alleviate or aggravate depressive-like symptoms later in life.
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Registered trials
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