ArticleScientific reports2020
Repeated stress exposure in mid-adolescence attenuates behavioral, noradrenergic, and epigenetic effects of trauma-like stress in early adult male rats.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Time-Dependent Effects of Neonatal Methamphetamine Exposure on Catecholamines but Not Oxidative Stress in the Hippocampus and Striatum of Male Rats.Neurotoxicity research · 2026Article
- Exposure to early-life stress uncovers shared biological signatures underlying vulnerability in the habenula and insular cortex of male and female adult rats.Neurobiology of stress · 2025Article
- Analysis of the significance and gender differences in the factors influencing antisocial behaviors among adolescents.Scientific reports · 2025Article
- Person-centered analyses reveal that developmental adversity at moderate levels and neural threat/safety discrimination are associated with lower anxiety in early adulthood.Communications psychology · 2025Article
- Development of the rodent prefrontal cortex: circuit formation, plasticity, and impacts of early life stress.Frontiers in neural circuits · 2025Review
- Shifts in naturalistic behaviors induced by early social isolation stress are associated with adult binge-like eating in female rats.Frontiers in behavioral neuroscience · 2024Article
- Preclinical Models of Chronic Stress: Adaptation or Pathology?Biological psychiatry · 2023Review
- Adolescent Stress Confers Resilience to Traumatic Stress Later in Life: Role of the Prefrontal Cortex.Biological psychiatry global open science · 2023Article
- Low- and high-cocaine intake affects the spatial and temporal dynamics of class IIa HDAC expression-activity in the nucleus accumbens and hippocampus of male rats as measured by [18F]TFAHA PET/CT neuroimaging.Addiction neuroscience · 2022Article
- IL-1 Receptor-1 onBrain, behavior, & immunity - health · 2022Article
- Catatonia in autism and other neurodevelopmental disabilities: a state-of-the-art review.Npj mental health research · 2022Review
- A Role for Histone Deacetylases in the Biology and Treatment of Post-Traumatic Stress Disorder: What Do We Know and Where Do We Go from Here?Complex psychiatry · 2022Review
- Decoding Shared Versus Divergent Transcriptomic Signatures Across Cortico-Amygdala Circuitry in PTSD and Depressive Disorders.The American journal of psychiatry · 2022Article
- Peptide LCGA-17 Attenuates Behavioral and Neurochemical Deficits in Rodent Models of PTSD and Depression.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Chronic adolescent stress increases exploratory behavior but does not appear to change the acute stress response in adult male C57BL/6 mice.Neurobiology of stress · 2021Article
- Traumatic Stress, Chronic Ethanol Exposure, or the Combination, Alter Cannabinoid System Components in Reward and Limbic Regions of the Mouse Brain.Molecules (Basel, Switzerland) · 2021Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Stress in adolescence can regulate vulnerability to traumatic stress in adulthood through region-specific epigenetic activity and catecholamine levels. We hypothesized that stress in adolescence would increase adult trauma vulnerability by impairing extinction-retention, a deficit in PTSD, by (1) altering class IIa histone deacetylases (HDACs), which integrate effects of stress on gene expression, and (2) enhancing norepinephrine in brain regions regulating cognitive effects of trauma. We investigated the effects of adolescent-stress on adult vulnerability to severe stress using the single-prolonged stress (SPS) model in male rats. Rats were exposed to either (1) adolescent-stress (33-35 postnatal days) then SPS (58-60 postnatal days; n = 14), or (2) no adolescent-stress and SPS (58-60 postnatal days; n = 14), or (3) unstressed conditions (n = 8). We then measured extinction-retention, norepinephrine, HDAC4, and HDAC5. As expected, SPS exposure induced an extinction-retention deficit. Adolescent-stress prior to SPS eliminated this deficit, suggesting adolescent-stress conferred resiliency to adult severe stress. Adolescent-stress also conferred region-specific resilience to norepinephrine changes. HDAC4 and HDAC5 were down-regulated following SPS, and these changes were also modulated by adolescent-stress. Regulation of HDAC levels was consistent with the pattern of cognitive effects of SPS; only animals exposed to SPS without adolescent-stress exhibited reduced HDAC4 and HDAC5 in the prelimbic cortex, hippocampus, and striatum. Thus, HDAC regulation caused by severe stress in adulthood interacts with stress history such that seemingly conflicting reports describing effects of adolescent stress on adult PTSD vulnerability may stem in part from dynamic HDAC changes following trauma that are shaped by adolescent stress history.
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