Cognitive ability and decline after early life stress exposure

AbstractAlcohol use disorders (AUDs) continue to be a significant public health problem. Early life stress and adversity have long-lasting effects on a wide range of behaviors, including responses to drugs of abuse. Epidemiological evidence indicates that exposure to early life stress contributes to alcohol use disorders and, while it is known that stress and alcohol both act on overlapping mesolimbic circuitry, the cellular mechanisms underlying the relationship between stress and alcohol intake are not well understood. Previous work has demonstrated that acute stress increases ethanol intake mediated by changes in GABA signaling within the ventral tegmental area (VTA). Here we investigated if adolescent stress exposure might elicit long-term, persistent increases in ethanol self-administration associated with altered VTA GABA signaling. To this end, we exposed adolescent postnatal day (PND) 28 male rats to 14 days of chronic variable stress (CVS) and then examined operant ethanol self-administration begun at least 30 days later. We found that adolescent stress exposure resulted in significantly increased ethanol self-administration in adulthood. In contrast, adult (PND 82) male rats exposed to the same CVS protocol did not display increased ethanol self-administration that was begun 30 days later. Furthermore, we found that adolescent stress exposure resulted in enhancement of ethanol-induced GABA signaling onto VTA dopamine neurons and impairments in VTA GABA chloride homeostasis. The results indicate that adolescence is a period vulnerable to stress, which produces long-term changes in VTA GABA signaling associated with increased ethanol self-administration behavior.

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Early life stress exposure associated with reduced polyunsaturated-containing lipids in low-income children

Pediatric Research ◽

10.1038/s41390-020-0989-0 ◽

2020 ◽

Author(s):

Jennifer L. LaBarre ◽

Alison L. Miller ◽

Katherine W. Bauer ◽

Charles F. Burant ◽

Julie C. Lumeng

Keyword(s):

Low Income ◽

Life Stress ◽

Early Life ◽

Early Life Stress ◽

Stress Exposure ◽

Low Income Children

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Sugar Consumption Produces Effects Similar to Early Life Stress Exposure on Hippocampal Markers of Neurogenesis and Stress Response

Frontiers in Molecular Neuroscience ◽

10.3389/fnmol.2015.00086 ◽

2016 ◽

Vol 8 ◽

Cited By ~ 3

Author(s):

Jayanthi Maniam ◽

Christopher P. Antoniadis ◽

Neil A. Youngson ◽

Jitendra K. Sinha ◽

Margaret J. Morris

Keyword(s):

Stress Response ◽

Life Stress ◽

Early Life ◽

Early Life Stress ◽

Stress Exposure ◽

Sugar Consumption

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FKBP5genotype and early life stress exposure predict neurobehavioral outcomes for preterm infants

Developmental Psychobiology ◽

10.1002/dev.21507 ◽

2017 ◽

Vol 59 (3) ◽

pp. 410-418 ◽

Cited By ~ 10

Author(s):

Amy L. D'Agata ◽

Stephen Walsh ◽

Dorothy Vittner ◽

Xiaomei Cong ◽

Jacqueline M. McGrath ◽

...

Keyword(s):

Preterm Infants ◽

Life Stress ◽

Early Life ◽

Early Life Stress ◽

Stress Exposure ◽

Neurobehavioral Outcomes

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Serotonin and early life stress interact to shape brain architecture and anxious avoidant behavior – a TPH2 imaging genetics approach

Psychological Medicine ◽

10.1017/s0033291720002809 ◽

2020 ◽

pp. 1-9 ◽

Cited By ~ 1

Author(s):

Congcong Liu ◽

Lei Xu ◽

Jialin Li ◽

Feng Zhou ◽

Xi Yang ◽

...

Keyword(s):

Life Stress ◽

Early Life ◽

Emotional Processing ◽

Tryptophan Hydroxylase ◽

Early Life Stress ◽

Imaging Genetics ◽

Stress Exposure ◽

Punishment Sensitivity ◽

Threat Avoidance ◽

The Impact

Abstract Background Early life stress has been associated with emotional dysregulations and altered architecture of limbic-prefrontal brain systems engaged in emotional processing. Serotonin regulates both, developmental and experience-dependent neuroplasticity in these circuits. Central serotonergic biosynthesis rates are regulated by Tryptophan hydroxylase 2 (TPH2) and transgenic animal models suggest that TPH2-gene associated differences in serotonergic signaling mediate the impact of aversive early life experiences on a phenotype characterized by anxious avoidance. Methods The present study employed an imaging genetics approach that capitalized on individual differences in a TPH2 polymorphism (703G/T; rs4570625) to determine whether differences in serotonergic signaling modulate the effects of early life stress on brain structure and function and punishment sensitivity in humans (n = 252). Results Higher maltreatment exposure before the age of 16 was associated with increased gray matter volumes in a circuitry spanning thalamic-limbic-prefrontal regions and decreased intrinsic communication in limbic-prefrontal circuits selectively in TT carriers. In an independent replication sample, associations between higher early life stress and increased frontal volumes in TT carriers were confirmed. On the phenotype level, the genotype moderated the association between higher early life stress exposure and higher punishment sensitivity. In TT carriers, the association between higher early life stress exposure and punishment sensitivity was critically mediated by increased thalamic-limbic-prefrontal volumes. Conclusions The present findings suggest that early life stress shapes the neural organization of the limbic-prefrontal circuits in interaction with individual variations in the TPH2 gene to promote a phenotype characterized by facilitated threat avoidance, thus promoting early adaptation to an adverse environment.

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Early life stress, FK506 binding protein 5 gene (FKBP5) methylation, and inhibition-related prefrontal function: A prospective longitudinal study

Development and Psychopathology ◽

10.1017/s095457941700147x ◽

2017 ◽

Vol 29 (5) ◽

pp. 1895-1903 ◽

Cited By ~ 19

Author(s):

Madeline B. Harms ◽

Rasmus Birn ◽

Nadine Provencal ◽

Tobias Wiechmann ◽

Elisabeth B. Binder ◽

...

Keyword(s):

Inhibitory Control ◽

Life Stress ◽

Early Life ◽

Binding Protein ◽

Early Life Stress ◽

Stress Exposure ◽

Childhood Stress ◽

Fk506 Binding Protein ◽

Wide Range ◽

Prospective Longitudinal

AbstractIndividuals who have experienced high levels of childhood stress are at increased risk for a wide range of behavioral problems that persist into adulthood, yet the neurobiological and molecular mechanisms underlying these associations remain poorly understood. Many of the difficulties observed in stress-exposed children involve problems with learning and inhibitory control. This experiment was designed to test individuals' ability to learn to inhibit responding during a laboratory task. To do so, we measured stress exposure among a community sample of school-aged children, and then followed these children for a decade. Those from the highest and lowest quintiles of childhood stress exposure were invited to return to our laboratory as young adults. At that time, we reassessed their life stress exposure, acquired functional magnetic resonance imaging data during an inhibitory control task, and assayed these individuals' levels of methylation in the FK506 binding protein 5 (FKBP5) gene. We found that individuals who experienced high levels of stress in childhood showed less differentiation in the dorsolateral prefrontal cortex between error and correct trials during inhibition. This effect was associated only with childhood stress exposure and not by current levels of stress in adulthood. In addition, FKBP5 methylation mediated the association between early life stress and inhibition-related prefrontal activity. These findings are discussed in terms of using multiple levels of analyses to understand the ways in which adversity in early development may affect adult behavioral adaptation.

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Early life stress exposure worsens adult remote microglia activation, neuronal death, and functional recovery after focal brain injury

Brain Behavior and Immunity ◽

10.1016/j.bbi.2021.02.032 ◽

2021 ◽

Author(s):

Clarissa Catale ◽

Elisa Bisicchia ◽

Valeria Carola ◽

Maria Teresa Viscomi

Keyword(s):

Brain Injury ◽

Functional Recovery ◽

Neuronal Death ◽

Life Stress ◽

Early Life ◽

Early Life Stress ◽

Microglia Activation ◽

Stress Exposure ◽

Focal Brain Injury

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Early Life Stress and Child Temperament Style as Predictors of Childhood Anxiety and Depressive Symptoms: Findings from the Longitudinal Study of Australian Children

Depression Research and Treatment ◽

10.1155/2011/296026 ◽

2011 ◽

Vol 2011 ◽

pp. 1-9 ◽

Cited By ~ 16

Author(s):

Andrew J. Lewis ◽

Craig A. Olsson

Keyword(s):

Depressive Symptoms ◽

Longitudinal Study ◽

Life Stress ◽

Early Life ◽

Parental Education ◽

Early Life Stress ◽

Childhood Anxiety ◽

Infant Temperament ◽

Future Research ◽

Stress Exposure

Objective. The purpose of this study was to determine whether the relationship between stressful infant environments and later childhood anxiety and depressive symptoms varies as a function of individual differences in temperament style.Methods. Data was drawn from the Longitudinal Study of Australian Children (LSAC). This study examined 3425 infants assessed at three time points, at 1-year, at 2/3 years and at 4/5 years. Temperament was measured using a 12-item version of Toddler Temperament Scale (TTS) and was scored for reactive, avoidant, and impulsive dimensions. Logistic regression was used to model direct relationships and additive interactions between early life stress, temperament, and emotional symptoms at 4 years of age. Analyses were adjusted for socioeconomic status, parental education, and marital status.Results. Stressful family environments experienced in the infant's first year of life (high versus low) and high reactive, avoidant, and impulsive temperament styles directly and independently predicted anxiety and depressive problems in children at 4 years of age. There was no evidence of interaction between temperament and family stress exposure.Conclusions. Both infant temperament and stress exposures are independent and notable predictors of later anxiety and depressive problems in childhood. The risk relationship between stress exposure in infancy and childhood emotion problems did not vary as a function of infant temperament. Implications for preventive intervention and future research directions are discussed.

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