Abstract
Early-life stress includes prenatal, postnatal, and adolescence stress. Early-life stress can affect the development of the hypothalamic-pituitary-adrenal (HPA) axis, and cause cellular and molecular changes in the developing hippocampus that can result in neurobehavioral changes later in life. Epidemiological data implicate stress as a cause of seizures in both children and adults. Emerging evidence indicates that both prenatal and postnatal stress can prime the developing brain for seizures and an increase in epileptogenesis. This article reviews the cellular and molecular changes encountered during prenatal and postnatal stress, and assesses the possible link between these changes and increases in seizure occurrence and epileptogenesis in the developing hippocampus. In addititon, the priming effect of prenatal and postnatal stress for seizures and epileptogenesis is discussed. Finally, the roles of epigenetic modifications in hippocampus and HPA axis programming, early-life stress, and epilepsy are discussed.
Highlights
The early-life environment is one of the most important factors affecting life-long health (Anand, 2000; van den Bergh et al, 2005; Lupien et al, 2009; Boksa, 2010; Strüber et al, 2014)
In humans, early-life stress can include prenatal stressors such as exposure to exogenous glucocorticoids, maternal infection (King et al, 2005; Sørensen et al, 2009; Jenkins, 2013), and birth complications, as well as postnatal stressors such as exposure to exogenous glucocorticoids, maternal postpartum depression, loss of a parent, exposure to family conflict and violence, neglect, or physical maltreatment (De Bellis, 2002; King et al, 2005; Frodl et al, 2010). Both prenatal and postnatal stress can increase the likelihood of seizures in early life (Joels, 2009; Koe et al, 2009) and epileptogenesis in later life
Infusion of CRH receptor 1 (CRHR1) antagonists immediately following this early-life stress prevented the learning and memory deficits, rescued long-term potentiation (LTP), and restored the integrity of the dendritic structure (Ivy et al, 2010). These findings provide direct evidence for a need for corticotrophin-releasing hormone (CRH)-CRHR1 signaling in the persistent effects of chronic early-life stress on hippocampal synapses
Summary
Early-life stress impacts the developing hippocampus and primes seizure occurrence: cellular, molecular, and epigenetic mechanisms. Early-life stress can affect the development of the hypothalamic-pituitary-adrenal (HPA) axis, and cause cellular and molecular changes in the developing hippocampus that can result in neurobehavioral changes later in life. Emerging evidence indicates that both prenatal and postnatal stress can prime the developing brain for seizures and an increase in epileptogenesis. This article reviews the cellular and molecular changes encountered during prenatal and postnatal stress, and assesses the possible link between these changes and increases in seizure occurrence and epileptogenesis in the developing hippocampus. The priming effect of prenatal and postnatal stress for seizures and epileptogenesis is discussed. The roles of epigenetic modifications in hippocampus and HPA axis programming, early-life stress, and epilepsy are discussed
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