Background During development, the placenta can be said to be the most important organ, however, the most poorly researched. There is currently a broader understanding of how specific insults during development affect the fetal brain, and also the importance of placental signaling in neurodevelopmental programming. Epigenetic responses to maternal and fetal signals are an obvious candidate for transforming early life inputs into long‐term programmatic outcomes. As a mediator of maternal and environmental signals to the developing fetus, epigenetic processes within the placenta are particularly powerful such that alterations of placental gene expression, downstream function, and signalling during foetal development have the potential for dramatic changes in developmental programming. Summary In this article, we reviewed emerging evidence for a placental role in prenatal neurodevelopmental programming with a specific focus on nutrient and prenatal stress signals integration into chromatin changes; this new understanding, we hope will provide the means for lowering developmentally based disorder risk, and new therapeutic targets for treatment in adulthood. Key messages Based on this review, the placenta is a potent micro‐environmental player in neurodevelopment as it orchestrates a series of complex maternal–foetal interactions. Maternal insults to this microenvironment will impair these processes and disrupt foetal brain development resulting in the prenatal programming of neurodevelopmental disorders. These findings should inspire advance animal model and human research drive to appraise gene–environment impacts during pregnancy that will target the developmental cause of adult‐onset mental disorders.

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The interaction between MDMA and Nicotine affects multiple brain centres and neurotransmitter systems (serotonin, dopamine and glutamate) involved in motor coordination and cognition. In this study, we have elucidated the effect of prolonged (10 days) MDMA, Nicotine and a combined Nicotine-MDMA treatment on motor-cognitive neural functions. In addition, we have shown the correlation between the observed behavioural change and neural structural changes induced by these treatments in BALB/c mice. We observed that MDMA (2 mg/Kg body weight; subcutaneous) induced a decline in motor function, while Nicotine (2 mg/Kg body weight; subcutaneous) improved motor function in male periadolescent mice. In combined treatment, Nicotine reduced the motor function decline observed in MDMA treatment, thus no significant change in motor function for the combined treatment versus the control. Nicotine or MDMA treatment reduced memory function and altered hippocampal structure. Similarly, a combined Nicotine-MDMA treatment reduced memory function when compared with the control. Ultimately, the metabolic and structural changes in these neural systems were seen to vary for the various forms of treatment. It is noteworthy to mention that a combined treatment increased the rate of lipid peroxidation in brain tissue.

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