Developmental origin of abnormal dendritic growth in the mouse brain induced by in utero disruption of aryl hydrocarbon receptor signaling.

摘要: Increased prevalence of mental disorders cannot be solely attributed to genetic factors and is considered at least partly attributable chemical exposure. Among various environmental chemicals, in utero lactational dioxin exposure has been extensively studied known induce higher brain function abnormalities both humans laboratory animals. However, how the perinatal affects neuromorphological alterations remained largely unknown. Therefore, this study, we initially whether over-expression aryl hydrocarbon receptor (AhR), a receptor, would affect dendritic growth hippocampus developing brain. Transfecting constitutively active AhR plasmid into via electroporation on gestational day (GD) 14 induced abnormal branch growth. Further, observed that 14-day-old mice born dams administered with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dose: 0, 0.6, or 3.0 μg/kg) GD 12.5 exhibited disrupted amygdala. Finally, 16-month-old exposed TCDD as described above significantly reduced spine densities. These results indicated micromorphology may persist until adulthood later life.