Journal of Fertilization: In Vitro - IVF-Worldwide, Reproductive Medicine, Genetics & Stem Cell Biol
Open Access

A Brief Note on Prenatal Programming of Foetal Nervous System

Mason Frithjof^{* *}Correspondence: Mason Frithjof, Department of Women and Children's Health, University of California, Orange, California, USA, Email:

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Description

The human placenta expresses the genes for propiomelanocortin and therefore the major stress hormone, Corticotropin-Releasing Hormone (CRH), altering the “fight or flight” stress system in the mother and fetus. As gestation progresses, the level of those stress hormones, as well as maternal adrenal cortical steroids, increases dramatically. These endocrine changes are necessary for fetal maturation, however, if the level is altered (e.g., in response to stress), they influence (program) the fetal nervous system with long-term consequences. The evidence indicates that fetal exposure to elevated levels of stress hormones (i) delays fetal nervous system maturation, (ii) restricts the neuromuscular development and alters the strain stress of the newborn, (iii) impairs mental development and will increase fearful behavior within the baby, and (iv) might lead to diminished gray matter volume in children. The studies reviewed indicate that fetal exposure to stress peptides and hormones exerts profound programming influences on the system and will increase the chance for emotional and cognitive impairment.

The Developmental Origins of Disease or Fetal Programming model predicts that early exposures to threats or adverse conditions have lifelong consequences that lead to poor health outcomes. The overwhelming majority of the studies in support of the programming model in humans are retrospective and most relied on surrogate measures of early expertise like low birth weight or preterm birth. The retrospective studies and the growing range of prospective studies have reportable that fetuses exposed to maternal stress at varied times throughout gestation are at greater risk for cardiovascular and metabolic disorders that shorten lifespan. The fetal exposure to peptides and hormones from the maternal HPA and placental stress system exerts profound programming influences on the brain. Programming could be a method by which a stimulus or exposure throughout a critical developmental period includes a long-lived or permanent influence on the brain, behavior, and risk for disease. Throughout these periods of rapid cell division, fetal organs are vulnerable to perturbation like stress.

The effects of stress/HPA and placental axis hormones are modulated by the activities of binding proteins and enzymes. As an example, concurrent with the increase in pCRH, maternal CRH-binding macromolecule (protein) rises and then falls near the end of gestation. Maternal plasma Cortisol-Binding Globulin (CBG) levels change across gestation. CBG is stimulated by estrogen, and these levels increase with advancing gestation till the end of gestation once there's a big decline in CBG. The level of placental 11β-HSD2 (which oxidizes adrenal cortical steroid into its inactive kind, cortisone) rises as gestation progresses before falling ensuring maturation of the fetal lungs, CNS, and different organ systems fully term births.

The maternal-fetal endocrine changes are adaptive and necessary for fetal maturation however if the level is elevated, for example in response to stress, it will have an effect on the mechanical phenomenon of fetal development. Rapidly evaporating pools of desert water lead to elevation of CRH within the median eminence of the larva survival is compromised. If the CRH response is blocked throughout environmental desiccation, then the speed of development is inactive and therefore the tadpole’s survival is compromised. This remarkable surveillance and response system has evolved and is preserved several species, as well as the human fetus, will find threats to survival and adjust its developmental trajectory.

The placenta collects information from its maternal host to prepare the fetus for postnatal survival. If the fetal/placental unit detects stress signals from the maternal surroundings (e.g., cortisol), the “placental clock" could also be advanced by activation of the promoter region of the CRH cistron gene that initiates the placental synthesis of the “master” stress endocrine hormone, pCRH. The rapid increase in circulating pCRH initiates the cascade of events leading to myometrial activation that will increase the chance of preterm birth. In parallel, the fetus adjusts its developmental trajectory and/or modifies its nervous system to confirm survival in hostile surroundings. Survival under these circumstances, however, is related to compromised motor, cognitive, and emotional operations and reduced region-specific brain gray matter volume. It is necessary to acknowledge that there are vast variations in reproductive physiology and also within the trajectory of fetal brain development, even in closely related species, like humans and nonhuman primates. These variations limit the validity of generalizing to humans from animal models. As an example, placental CRHmRNA is found among some primates, and, even among nonhuman primates, the timing of synthesis and release of pCRH is totally different than for humans (and apes).

Conclusion

Glucocorticoid receptors are present throughout the central system and glucocorticoids simply pass through the blood-brain barrier and influence multiple brain regions, as well as the hippocampus, amygdale, and anterior cortex. At high concentrations, adrenal cortical steroids might inhibit the growth and differentiation of the developing nervous system, and indicates that glucocorticoids are neurotoxins to hippocampal CA3 pyramidal cells. In embryonic hippocampal neurons, glucocorticoid induces neural death. Delayed myelination has been reportable within the corpus callosum in association with prenatal exogenous glucocorticoid exposure, which is consistent with findings that prenatal stress exposure affects the dimensions of the corpus callosum. Maternal exposure and response to adversity exert profound influences on the fetal nervous system. These effects “program” the nervous system with consequences that persist throughout the lifespan. The precise mechanisms of communication between mother and fetus aren't best-known; however, the roles of pCRH and maternal adrenal cortical steroids are getting apparent and can be the main focus of future analysis.