A mechanism underlying the dioxin-produced sexual immaturity: an imprinting of the lowered expression of gonadotropin-releasing hormone

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This study suggests the novel mechanism that maternal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) fixes the status of a reduction in the hypothalamic expression of gonadotropin-releasing hormone (GnRH)in the offspring by reducing perinatal steroidogenesis, and this is the origin for imprinted defects in sexual behaviors at adulthood. The results obtained in this study were as follows:1) Areduction in GnRH mRNA by TCDD emerges from postnatal day 4 to adulthood.2) Intracerebroventricular infusion of GnRH into the TCDD-exposed pups after their growing up restored many defects in sexual behaviors. And3) Direct supplementation of gonadotropininto TCDD-exposed fetuses at GD17 rescueda TCDD-produced attenuation of hypothalamic GnRH mRNA in the male pups.