Topic
Developmental plasticity
About: Developmental plasticity is a research topic. Over the lifetime, 1721 publications have been published within this topic receiving 103438 citations.
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TL;DR: It is now apparent that there is substantial plasticity late in the Th17 program, which allows committed Th17 cells to transition from effectors that produce predominantly IL-17A andIL-17F, to effectors That produce predominantly IFNgamma, and raises new questions regarding the stability of epigenetic modifications that accompany induction of cytokine gene expression during T cell lineage development.
402 citations
TL;DR: It is suggested that experience-dependent competition in developing visual cortex is the outcome of two distinct, noncompetitive processes, a loss of deprived-eye responses followed by an apparently homeostatic increase in responses dependent on TNFalpha signaling.
396 citations
TL;DR: Findings from a range of nutritional studies examining maternal and/or postnatal nutritional excess suggest that maternal over‐nutrition is deleterious to the health of offspring and can result in a phenotype of the offspring that is characteristic of metabolic syndrome.
Abstract: Studies in both humans and experimental animals addressing the ‘Fetal Origins of Adult Disease’ hypothesis have established a relationship between an adverse intrauterine environment and offspring disease in adult life. This phenomenon, termed ‘fetal programming’ describes a process whereby a stimulus in utero establishes a permanent response in the fetus leading to enhanced susceptibility to later disease. However, the environment, during periods of developmental plasticity in postnatal life, can also ‘programme’ function. Thus, the terms ‘developmental programming’ and the ‘Developmental Origins of Adult Health and Disease’ are preferentially utilized. The ‘Thrifty Phenotype’ hypothesis explained the association between insufficient in utero nutrition and the later development of Type 2 diabetes. Most recently the ‘Predictive Adaptive Response’ hypothesis proposes that the degree of mismatch between the pre- and postnatal environments is an important determinant of subsequent disease. Epidemiological studies have indicated that fetal growth restriction correlates with later disease, implying that fetal nutritional deprivation is a strong programming stimulus. This prompted the development of experimental animal models using controlled maternal calorie, protein or macronutrient deficiency during key periods of gestation. However, in many societies, maternal and postnatal nutrition are either sufficient or excessive. Here, we examine findings from a range of nutritional studies examining maternal and/or postnatal nutritional excess. There is supportive evidence from a limited number of studies to test the ‘Predictive Adaptive Response’ hypothesis. These suggest that maternal over-nutrition is deleterious to the health of offspring and can result in a phenotype of the offspring that is characteristic of metabolic syndrome.
395 citations
TL;DR: To conduct research in this area, developmental plasticity must be disentangled from disruption and the adverse long-term effects of coping, and ways in which such distinctions may be made in practice are explored.
Abstract: Early experience has a particularly great effect on most organisms. Normal development may be disrupted by early environmental influences; individuals that survive have to cope with the damaging consequences. Additionally, the responses required to cope with environmental challenges in early life may have long-term effects on the adult organism. A further set of processes, those of developmental plasticity, may induce a phenotype that is adapted to the adult environment predicted by the conditions of early life. A mismatch between prediction and subsequent reality can cause severe health problems in those human societies where economic circumstances and nutrition are rapidly improving. Understanding the underlying mechanisms of plasticity is, therefore, clinically important. However, to conduct research in this area, developmental plasticity must be disentangled from disruption and the adverse long-term effects of coping. The paper reviews these concepts and explores ways in which such distinctions may be made in practice.
394 citations
University of Auckland1, University of Southampton2, University of Cambridge3, University College London4, Aga Khan University5, Russian Academy6, French Institute of Health and Medical Research7, Centre for Cellular and Molecular Biology8, University of Bristol9, Harvard University10, University of the West Indies11, Swarthmore College12, Tel Aviv University13, University of New Mexico14, University of London15, University of Sydney16, University of Chile17, Smithsonian Tropical Research Institute18
TL;DR: Developmental plasticity has been viewed traditionally in the context of major disruptions such as caused by teratogens, prematurity and growth retardation, but there is increasing appreciation of the role of developmental plasticity.
389 citations