Oestrogen receptor-α and -β immunoreactivity in gonadotropin-releasing hormone neurones after ovariectomy and chronic exposure to oestradiol
Oestrogen receptor-α and -β immunoreactivity in gonadotropin-releasing hormone neurones after ovariectomy and chronic exposure to oestradiol
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DOI：
10.1111/j.1365-2826.2003.01115.x
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发表时间：
2003-12-01
影响因子：
3.2
通讯作者：
Tsai, HW
中科院分区：
文献类型：
--
作者：
Legan, SJ;Tsai, HW
雌二醇通过调节促性腺激素释放激素(GnRH)的释放，对黄体生成素(LH)的分泌起负反馈和正反馈作用。此外，无论是年轻的卵巢切除(OVX)大鼠，还是中年持续发情(PE)的大鼠，循环中雌二醇的慢性增加都会导致黄体生成素峰值逐渐减弱，直到雌二醇的正反馈作用消失。基于这些发现，以及关于雌激素对GnRH神经元的直接作用的模棱两可的证据，我们检验了这样的假设，即慢性雌激素通过减少含有雌激素受体(ER)α或β的GnRH神经元的比例来消除促黄体生成素激增。定期骑自行车的大鼠被摘除卵巢，其中一半立即接受雌二醇。3天、2周或4周后，分别于18.00 h灌流，免疫细胞化学染色观察GnRH与ERα或ERβ的共定位。76%的GnRH神经元表达ERβ，而几乎没有GnRH细胞表达ERα。去卵巢大鼠GnRH细胞表达ERα或β的比例不受雌二醇和去卵巢后时间的影响，无论其内侧到外侧或吻侧到尾部位置都是如此。结果表明，雌二醇的正反馈作用和去卵巢大鼠长期服用雌二醇后黄体生成素释放峰消失的机制，不是由含有雌激素受体的GnRH神经元比例的改变所介导的。
Oestradiol exerts negative- and positive-feedback actions on luteinizing hormone (LH) secretion by modulating gonadotropin-releasing hormone (GnRH) release. Furthermore, a chronic increase in circulating oestradiol in either young ovariectomized (OVX) rats, or in middle-aged persistent oestrous (PE) rats, causes a gradual attenuation of LH surges until the positive-feedback action of oestradiol disappears. Based on these findings, and on the equivocal evidence regarding a direct action of oestradiol on GnRH neurones, we tested the hypothesis that chronic oestradiol abolishes LH surges by decreasing the proportion of GnRH neurones containing oestrogen receptor (ER)alpha or beta. Regularly cycling rats were ovariectomized, and half immediately received oestradiol. Three days, or 2 or 4 weeks later, rats were perfused at 18.00 h, and GnRH was colocalized with ERalpha or ERbeta by immunocytochemistry. ERbeta was expressed in 76% of GnRH neurones, whereas virtually no GnRH cells were immunopositive for ERalpha. The proportion of GnRH cells expressing ERalpha or beta in OVX rats was not altered by oestradiol or time after OVX, and this was the case regardless of their medial to lateral, or rostral to caudal location. The results indicate that the mechanisms for the positive-feedback action of oestradiol, and the loss of LH surges in OVX rats after chronic oestradiol, are not mediated by changes in the proportion of oestrogen-receptor containing GnRH neurones.