Burgett R A, Garris P A, Ben-Jonathan N
Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46223.
Brain Res. 1990 Oct 29;531(1-2):143-7. doi: 10.1016/0006-8993(90)90767-6.
Prolactin release is inhibited by dopamine and stimulated by estradiol. Dopamine is released from nerve terminals in the median eminence and posterior pituitary. Estradiol may act directly on the anterior pituitary or by modulating the two dopaminergic systems. Estradiol treatment induces the formation of prolactinomas in Fischer 334 rats. Therefore, this strain was chosen as the experimental model. The first objective was to determine whether estradiol differentially regulates the two dopaminergic systems. The second objective was to explore whether the anterior pituitary in estradiol-treated rats acquires the capability for de novo synthesis of dopamine. Rats were ovariectomized and implanted with estradiol capsules (OVEX + E2). Controls were untreated ovariectomized rats (OVEX). Three weeks thereafter, rats were killed. Anterior and posterior pituitaries and medial basal hypothalami (MBH) were removed and individually incubated for 60 min in Hank's balanced salt solution containing 10 microCi [3H-]tyrosine. The median eminence was then dissected from the MBH. Tissues were homogenized in perchloric acid and the supernatant fluids were extracted with alumina. Both endogenous and tritiated dopamine were simultaneously quantitated by HPLC. Prolactinoma formation in OVEX + E2 rats was confirmed by dramatic rise (50-fold) in plasma prolactin levels and marked enlargement (3-fold) of the anterior pituitary. Estradiol treatment caused a significant 60% reduction in both dopamine content and synthesis in the median eminence. In contrast, estradiol treatment affected neither dopamine content nor synthesis in the posterior pituitary. There was no evidence for de novo synthesis of dopamine in anterior pituitaries from either OVEX or OVEX + E2 rats. We conclude that the two dopaminergic systems which regulate prolactin secretion, exhibit a differential response to estradiol.
催乳素的释放受多巴胺抑制，受雌二醇刺激。多巴胺从中位隆起和垂体后叶的神经末梢释放。雌二醇可能直接作用于垂体前叶，或通过调节两个多巴胺能系统发挥作用。雌二醇处理可诱导Fischer 334大鼠形成催乳素瘤。因此，选择该品系作为实验模型。第一个目标是确定雌二醇是否对两个多巴胺能系统有不同的调节作用。第二个目标是探究经雌二醇处理的大鼠垂体前叶是否获得了从头合成多巴胺的能力。将大鼠卵巢切除并植入雌二醇胶囊（OVEX + E2）。对照组为未处理的卵巢切除大鼠（OVEX）。三周后，处死大鼠。取出垂体前叶和后叶以及内侧基底部下丘脑（MBH），分别在含有10微居里[3H-]酪氨酸的汉克平衡盐溶液中孵育60分钟。然后从MBH中分离出中位隆起。将组织在高氯酸中匀浆，上清液用氧化铝萃取。通过高效液相色谱法同时定量内源性和氚标记的多巴胺。OVEX + E2大鼠血浆催乳素水平显著升高（50倍）以及垂体前叶明显增大（3倍），证实了催乳素瘤的形成。雌二醇处理导致中位隆起中多巴胺含量和合成均显著降低60%。相比之下，雌二醇处理对垂体后叶中的多巴胺含量和合成均无影响。无论是OVEX大鼠还是OVEX + E2大鼠的垂体前叶，均没有证据表明存在多巴胺的从头合成。我们得出结论，调节催乳素分泌的两个多巴胺能系统对雌二醇表现出不同的反应。
