Abstract
Xenobiotics and environmental toxicants cause the perturbations during embryogenesis and fetal development resulting in congenital malformations. The most vulnerable is the neural tube development due to the critical window period after the conception of the closure, cellular proliferation and differentiation. Neurodevelopmental disorders are multifactorial conditions encompassing wide categories and broad classification. Structural defects reveal as overt anatomical defects while the functional defects become apparent in the postnatal period of brain growth. Autism spectrum disorder [ASD] is an example of functional neurodevelopmental defect. The emphasis in this review is on the fact that neural tube defects are both structural and functional caused by the same teratogens such as valproic acid [VPA]. Valproic acid [VPA] has been discussed as a model teratogen for the development of neural tube defects and autism spectrum disorder [ASD].
Highlights
Human pregnancy is complicated and even more complicated is finding the ways to study the structural and functional effects of teratogens
Out of all the phases of embryonic and fetal development the first trimester is at the most risk to the developmental complications resulting in birth defects
Understanding the mechanism of action and the pathologies created by VPA would be a gateway to know the pathology, prevention, and treatment landscapes for Autism Spectrum Disorder (ASD)-like conditions
Summary
Human pregnancy is complicated and even more complicated is finding the ways to study the structural and functional effects of teratogens. This review is focused on the structural and functional neurodevelopmental defects with emphasis on valproic acid [VPA] and autism spectrum disorder [ASD]. The functional defects in the neurological system which are not overt at birth but are the result of the prenatal insult at the same time of neural tube development may include autism spectrum disorders [ASD], developmental delays and learning disabilities [4]. VPA is one of the many environmental toxins having structural and functional neural tube defects, neurodevelopmental disorders and developmental delays. VPA exposure results in the accelerated dendritic patterns, neurite growth and neural proliferation through the HDAC inhibition mechanism of action These are the similar structural changes as of observed in ASD cortices and proposed underlying mechanism of brain hyper-excitability in ASD. This associates the VPA as a causative agent of ASD but on the other hand making the VPAexposed rodents, rats and mice, an ideal model to study ASD [24]
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