ABSTRACT
The notion of epigenetics offers a putative interface between genetic and environmental factors that interact to provide the phenotypic expression. The impact of the environment on gene expression (epigenetics) and the convergence of genes and environment along common biological pathways induce greater effects than either those of genes or environment in isolation (van Winkel et al., 2010). Transgenerational epigenetic inheritance, i.e., the survival of epigenetic modišcations over generations, provides a process through which maternal nurturing behavior may in·uence the development and health of the offspring (Franklin and Mansuy, 2010a, 2010b; Franklin et al., 2010; Jablonka and Raz, 2009; Nadeau, 2009). In order to clarify the phenomena; modulating physiological phenotypes over generations, Ho and Burggren (2010) discuss:
1. How the concepts of epigenetics and maternal in·uence overlap with and are distinct from each other
2. Based on these notions, analyses that provide illustrations of existing animal physiological studies
3. A construct that provides integration of these concepts into the design underlying animal physiology studies
As described by Kappeler and Meaney (2010), the parental regulation of DNA methylation provides a plausible and prototypic candidate mechanism for parental effects on phenotypic variation. Mother-offspring interactions in rodents have demonstrated that parental signals in·uence the DNA methylation and set the cascade, leading to stable changes in gene expression in motion. In the mood disorders (bipolar and major depressive disorder), a broad range of studies have documented alterations of mitochondrial, oligodendrocytes, and myelin-related genes. These include
25.1 Introduction .......................................................................................................................... 513 25.2 Epigenetics of Depressive Disorders .................................................................................... 516 25.3 Epigenetics of Schizophrenia ............................................................................................... 519 25.4 Epigenetics in Intervention ................................................................................................... 523 25.5 Conclusions ........................................................................................................................... 524 Acknowledgments .......................................................................................................................... 526 References ...................................................................................................................................... 526
signaling and olidendroglial-related genes in depression and γ-aminobutyric acid (GABA)- glutamate related genes in depression and suicide (Sequeira and Turecki, 2006). The epigenetic modišcations of DNA methylation and chromatin remodeling are necessary, for example, for maintaining and regulating adult hippocampal neurogenesis but are associated, nevertheless, in the neuropsychiatric disorders. Epigenetic mechanisms contribute critical roles in encoding experience and environmental stimuli into stable, behaviorally meaningful alterations in gene expression (Hsieh and Eisch, 2010), but the adaptive aspect may take on a dysregulatory role. Early-life stressful events can provoke long-lasting memory traces on individuals’ genes, thereby programming a persisting risk for depression; for example, postnatal stress in mice marks the arginine vasopressin gene, resulting in hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis together with behavioral and endocrine mobilizations. Murgatroyd et al. (2010a) describe how epigenetic memory evolves by a dual-step process that the epigenetic reader and writer, MeCP2, coordinates. The initial derepression of arginine vasopressin is driven by neuronal activity, causing Ca2+/calmodulin kinase-dependent phosphorylation and dissociation of MeCP2; then subsequent hypomethylation at the AVP enhancer develops gradually to sustain derepression. The MeCP2 occupancy uncouples from the initial stimulus proceeding to the hard coding of early-life experience at the level of DNA methylation by a transition to a persistent irreversible epigenetic memory (Murgatroyd et al., 2009, 2010b).
