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논문 기본 정보

자료유형
학술저널
저자정보
Kim, Ji-Eune (School of Life Sciences, The Catholic University of Koreae) Ko, Ji-Yun (School of Life Sciences, The Catholic University of Koreae) Kim, Young-il (School of Life Sciences, The Catholic University of Koreae) Yoon, Yong-Dal (Department of Biology, College of Natural Sciences, Hanyang Univesity) Cho, Byung-Nam (School of Life Sciences, The Catholic University of Koreae)
저널정보
한국통합생물학회 Korean journal of biological sciences Korean journal of biological sciences 제4권 제1호
발행연도
2000.1
수록면
71 - 76 (6page)

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The aim of this study was to investigate expression patterns of the prolactin (PRL) and c-fos genes by 17$\beta$-estradiol (17$\beta$-E) and stress in the mouse pituitary. In the pituitary, the levels of PRL mRNA were found high with some fluctuation at 30, 50, and 90 min whereas the levels of PRL mRNA were low at 120 min when ovariectomized female mice were injected with 17$\beta$-E or vehicle. PRL mRNA levels began to increase again at 4 h and remained high up to 24 h only in the 17$\beta$-E- treated mice. The overall changes in c-fos mRNA by 17$\beta$-E were very similar to those in PRL mRNA in the pituitary. Subsequent study revealed that these high initial levels of PRL and c-fos mRNAs were caused by stress during Injection, not by 17$\beta$-E, since vehicle injection alone into the ovariectomized mice could increase the levels of PRL and c-fos mRNAs. The stress-induced elevations of PRL and c-fos mRNAs were inhibited by bromocriptin, a dopamine agonist, suggesting that the dopaminergic system is involved in the action route of injection stress. In addition, the induced levels of c-fos mRNA by 17$\beta$-E and stress in the pituitary were very low compared with those in the uterus. The time course changes in c-fos mRNA level were different between the pituitary and uterus. Taken together, these data indicate that PRL and c-tos gene expression in the pituitary are regulated by 17$\beta$-E and stress in a parallel manner, supporting the notion that c-Fos plays a role in regulation of PRL gene expression.

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