Maternal programming of defensive responses through sustained effects on gene expression.

McGill Program for the Study of Behavior, Genes and Environment, McGill University, Canada.
Biological Psychology (Impact Factor: 3.47). 08/2006; 73(1):72-89. DOI: 10.1016/j.biopsycho.2006.01.009
Source: PubMed

ABSTRACT There are profound maternal effects on individual differences in defensive responses and reproductive strategies in species ranging literally from plants to insects to birds. Maternal effects commonly reflect the quality of the environment and are most likely mediated by the quality of the maternal provision (egg, propagule, etc.), which in turn determines growth rates and adult phenotype. In this paper we review data from the rat that suggest comparable forms of maternal effects on defensive responses stress, which are mediated by the effects of variations in maternal behavior on gene expression. Under conditions of environmental adversity maternal effects enhance the capacity for defensive responses in the offspring. In mammals, these effects appear to 'program' emotional, cognitive and endocrine systems towards increased sensitivity to adversity. In environments with an increased level of adversity, such effects can be considered adaptive, enhancing the probability of offspring survival to sexual maturity; the cost is that of an increased risk for multiple forms of pathology in later life.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective Early stress events severely impact brain and behaviour. From a neurobiological point of view early stress influences neuroanatomical structures and is associated with a dysregulation of the hypothalamic‐pituitary‐adrenal axis. The objective of this article is to review the epigenetic alterations implicated in brain adaptation to early stress events. MethodA review of empirical research of epigenetic alterations associated to early stress events was performed. ResultsNeuroanatomic and epigenetic alterations have been observed after early stress events. Epigenetics alterations include DNA methylation, histones modifications and microRNA (miRNA) expression. The most studied is largely the former, affecting genes involved in neuroendocrine, neurotransmission and neuroplasticity regulation after early stress exposition. It includes glucocorticoid receptor, FK506‐binding protein 5, arginine vasopressin, oestrogen receptor alpha, 5‐hydroxy‐tryptamine transporter and brain‐derived neurotrophic factor. Conclusion Epigenetic regulation is critical in the interplay between nature and nurture. Alterations in the DNA methylation as well as histones modifications and miRNA expression patterns could explain abnormal behaviours secondary to early stress events.
    Acta Neuropsychiatrica 10/2012; 24(5). · 0.61 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We review studies with human and nonhuman species that examine the hypothesis that epigenetic mechanisms, particularly those affecting the expression of genes implicated in stress responses, mediate the association between early childhood adversity and later risk of depression. The resulting studies provide evidence consistent with the idea that social adversity, particularly that involving parent-offspring interactions, alters the epigenetic state and expression of a wide range of genes, the products of which regulate hypothalamic-pituitary-adrenal function. We also address the challenges for future studies, including that of the translation of epigenetic studies towards improvements in treatments.
    Dialogues in clinical neuroscience 09/2014; 16(3):321-33.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Children of low socioeconomic status (SES) are at elevated risk for health problems across the lifespan. Observational studies suggest that nurturant parenting might offset some of these health risks, but their design precludes inferences about causal direction and clinical utility. Here we ask whether a psychosocial intervention, focused improving parenting, strengthening family relationships, and building youth competencies, can reduce inflammation in low-SES, African Americans from the rural South. The trial involved 272 mothers and their 11-y-old children from rural Georgia, half of whose annual household incomes were below the federal poverty line. Families were randomly assigned to a 7-wk psychosocial intervention or to a control condition. When youth reached age 19, peripheral blood was collected to quantify six cytokines that orchestrate inflammation, the dysregulation of which contributes to many of the health problems known to pattern by SES. Youth who participated in the intervention had significantly less inflammation on all six indicators relative to controls (all P values < 0.001; effect sizes in Cohen's d units ranged from -0.69 to -0.91). Mediation analyses suggested that improved parenting was partially responsible for the intervention's benefits. Inflammation was lowest among youth who received more nurturant-involved parenting, and less harsh-inconsistent parenting, as a consequence of the intervention. These findings have theoretical implications for research on resilience to adversity and the early origins of disease. If substantiated, they may also highlight a strategy for practitioners and policymakers to use in ameliorating social and racial health disparities.
    Proceedings of the National Academy of Sciences 07/2014; · 9.81 Impact Factor

Full-text (2 Sources)

Available from
May 28, 2014