Journal of Cellular and Molecular Physiology(JCMP)
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Molecular Mechanisms for Reprogramming Hippocampal Development and Function by Early-Life StressSubmit Manuscript on this topic
The early postnatal period is a crucial stage for hippocampal development. During this critical period, the neonatal hippocampus is extremely sensitive to the detrimental consequences of adverse environmental factors such as separation from the mother. Extensive clinical and preclinical evidence has shown that traumatic events early in life have profound and persistent effects on hippocampal function and behavior.
The mechanisms of the long-term effects of early-life stress on hippocampal plasticity and hippocampus-dependent learning and memory are being unraveled. Nonetheless, a few key issues remain to be addressed. For example, how early-life stress acutely influences the developmental processes such as neurogenesis, apoptosis, dendritic outgrowth, and synaptogenesis? Do these potential structural changes have functional importance, for example, changing the electrophysiological properties of the neurons and neural circuits? Which molecules and signaling cascades are responsible for these cellular and physiological changes? Do glucocorticoids and receptors play the central role? Are the molecules responsible for the acute postnatal stress effects persistently dysregulated? Does early-life stress differentially influence hippocampal development in male and female offspring?
This research topic focuses on the acute and lasting effects of early-life stress on various developmental processes in the hippocampus, and aims to uncover the molecules that are responsible for early-life stress-programmed effects and underlie resilience or vulnerability to stress-related neuropsychiatric disorders later in life. We encourage researchers from relevant fields apply multidisciplinary approaches (developmental neurobiology, electrophysiology, and molecular and cellular neuroscience) and various postnatal stress paradigms (maternal separation, impoverished postnatal environment and pharmacological models) in different species (zebrafish, mouse, rat and non-human primates). We hope this initiative will be embraced by colleagues with high-quality original research or review articles that will further our understanding of early-life stress and brain development.