Project description:We found that oral administration of TCDD (1 µg/kg) to pregnant rats on gestational day 15 suppressed maternal production of prolactin, a pituitary hormone essential for nursing including milk production, during the lactational stage. To comprehensively investigate genes linked to the lower prolactin expression, we performed a DNA microarray analysis in the hypothalamus, which regulates the pituitary prolactin synthesis, of lactating dam rats.
Project description:We found that oral administration of TCDD (1 µg/kg) to pregnant rats on gestational day 15 suppressed maternal production of prolactin, a pituitary hormone essential for nursing including milk production, during the lactational stage. To comprehensively investigate genes linked to the lower prolactin expression, we performed a DNA microarray analysis in the pituitary of lactating dam rats.
Project description:Our previous studies have revealed that treatment of pregnant rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 1 M-NM-<g/kg) at gestational day (GD) 15 reduces the pituitary synthesis of luteinizing hormone (LH) during late fetal and early postnatal period, leading to imprinting of defects in sexual behaviors at adulthood. However, it remains obscure how the attenuation of pituitary LH links to sexual immaturity. To address this issue, we firstly performed a DNA microarray analysis to identify the gene(s) responsible for dioxin-induced sexual immaturity, using the pituitary and hypothalamus of male pups, at the age of postnatal day (PND)70, born from TCDD-treated dams. Among the reduced genes, we focused on gonadotropin-releasing hormone (GnRH) in the hypothalamus, because of its role in sexual behaviors suggested so far. The present study strongly suggests that maternal exposure to TCDD fixes the status of the lowered expression of GnRH in the offspring by reducing steroidogenesis at perinatal stage, and this is the mechanism for the imprinting of defects in sexual behaviors at adulthood. Total RNA was isolated from the pituitary and hypothalamus of PND70 male pups born from the dams treated with TCDD (1 M-NM-<g/kg) or vehicle at GD15, using an RNeasy Mini Kit (QIAGEN). To identify the gene(s) the altered expression of which is fixed and linked to defects in sexual behaviors, the profile of gene expression was analyzed using the Illumina RatRef-12 Expression BeadChip. This series includes two dataset; hypothalamic and pituitary samples (each case; N=3x2). The normalization applied each dataset.
Project description:Our previous studies have revealed that treatment of pregnant rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 1 μg/kg) at gestational day (GD) 15 reduces the pituitary synthesis of luteinizing hormone (LH) during late fetal and early postnatal period, leading to imprinting of defects in sexual behaviors at adulthood. However, it remains obscure how the attenuation of pituitary LH links to sexual immaturity. To address this issue, we firstly performed a DNA microarray analysis to identify the gene(s) responsible for dioxin-induced sexual immaturity, using the pituitary and hypothalamus of male pups, at the age of postnatal day (PND)70, born from TCDD-treated dams. Among the reduced genes, we focused on gonadotropin-releasing hormone (GnRH) in the hypothalamus, because of its role in sexual behaviors suggested so far. The present study strongly suggests that maternal exposure to TCDD fixes the status of the lowered expression of GnRH in the offspring by reducing steroidogenesis at perinatal stage, and this is the mechanism for the imprinting of defects in sexual behaviors at adulthood.
Project description:We have reported that mRNAs are present in bovine milk. But, it is unknown the roles of milk mRNAs. To clarify the roles of milk mRNAs, experimental animal such as rat study would be needed. However, it is unclear whether rat milk also contains mRNAs. Thus, we have employed microarray to show that rat milk also contains mRNAs. Milk samples were obtained at day 2, 9, and 16 postpartum from 3 rats. And serum samples were obtained from dam rats (n=3) at day 21 postpartum.