Abstract
The neurodevelopmental hypothesis has been proposed in which impairments of neural cells and networks as a consequence of environmental events occurring in neurodevelopment are involved in the onset of psychiatric disorders during adolescence or early adulthood. Environmental events in neurodevelopment stage produce a variety of inflammatory mediators, whereas the relationship between prostaglandin E2 (PGE2) and psychiatric disorders is not clarified. We investigated the possibility of PGE2 as one of common molecules associated with vulnerability to neurodevelopmental disruptions induced by environmental events. PGE2 levels in brain were significantly increased after exposure to viral infection, hypoxia, and neglect as neonatal, compared to those after non‐exposure. Mice administered polyriboinosinic‐polycytidylic acid (Poly I : C) or PGE2 in neonatal exhibited pscychobehavioral and neuronal abnormalities in adult, being attenuated by a PGE2‐EP1 antagonist. Our findings suggest that PGE2 is one of potential common molecules associated with vulnerability to neurodevelopmental disruptions induced by environmental events, and PGE2 plays a crucial role in the development of behavioral and neuronal impairments, which are associated with activation of PGE2‐EP1. The approaches with such neurodevelopmental model will be invaluable for translational research on novel compounds, and also for providing insight into the pathogenesis and pathophysiology of psychiatric disorders.
