Abstract
The environment in which a fetus develops is not only important for its growth and maturation but also for its long-term postnatal health and neurodevelopment. Several hormones including glucocorticosteroids, estrogens and progesterone, insulin growth factor and thyroid hormones, carefully regulate the growth of the fetus and its metabolism during pregnancy by controlling the supply of nutrients crossing the placenta. In addition to fetal synthesis, hormones regulating fetal growth are also expressed and regulated in the placenta, and they play a key role in the vulnerability of the developing brain and its maturation. This review summarizes the current understanding and evidence regarding the involvement of hormonal dysregulation associated with intra-uterine growth restriction and its consequences on brain development.
Highlights
This review summarizes the current understanding and evidence regarding the involvement of hormonal dysregulation associated with intra-uterine growth restriction and its consequences on brain development
Suboptimal fetal growth is likely to be a key factor of disruption in brain development and many neurodevelopmental disorders of motor and cognitive dysfunction have their origins in the antenatal period [2, 3]
Magnetic resonance imaging (MRI) has clearly revealed alterations of brain development in growth-restricted infants, involving both white and gray matter [8, 9] and including altered neural circuitry identified by diffusion MRI connectomics [10, 11] that correlate with functional cognitive, motor, and psychiatric deficits later in life [12, 13]
Summary
Glucocorticoids (GCs) are key mediators of stress responses involved during fetal development in the regulation of fetal growth and maturation of fetal tissues and organs [15, 16]. The 11β-HSD2 gene mutation produces IUGR which is associated with reduced placental activity of this enzyme highly expressed in the developing brain [28] These data, both in animals and in humans, strongly suggest that the effects of high circulating cortisol levels associated with IUGR could be potentiated by specific changes in gene expression involved in their biological response in many tissues including CNS. GCs regulate several developmental processes in the CNS, including hippocampal neurogenesis with variable effects on proliferation of progenitor cells, neurogenesis and astrogliogenesis in response to either low or high concentrations of cortisol [29]. Gómez-González et al showed that exposure to prenatal stress alters microglia maturation leading to an imbalance between immature and ramified microglia 1 day after birth in rat [46], and increased microglial activation in the hippocampus in juvenile animals [47, 48]
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