Long-term treatment with estradiol induces reversible alterations in tuberoinfundibular dopaminergic neurons: a decreased responsiveness to prolactin.
Long-term treatment with estradiol induces reversible alterations in tuberoinfundibular dopaminergic neurons: a decreased responsiveness to prolactin.
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长期使用雌二醇治疗会引起结节漏斗部多巴胺能神经元的可逆性改变：对催乳素的反应性降低。
DOI：
10.1159/000123979
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发表时间：
1984
影响因子：
4.1
通讯作者：
Moore,KE
中科院分区：
文献类型：
--
作者：
Demarest,KT;Riegle,GD;Moore,KE
先前的研究表明，短期（3-5天）用雌二醇治疗会增加中隆起结节基底（TI）神经元末端多巴胺（DA）的周转率和合成率，这是由于这种激素能够增加催乳素的循环浓度。目前的研究是为了检查雌二醇对血清催乳素浓度和TIDA神经元活性的长期影响（通过服用脱羧酶抑制剂后正中隆起的DOPA积累率来估计）。切除卵巢2周的雌性大鼠皮下注射苯甲酸雌二醇硅胶胶囊，于6、12、18天后处死。血清催乳素浓度在第6、12和18天显著升高，DOPA积累速率在第6天升高，但在第12天没有升高，在第18天降低。DA在中隆起的浓度在第6天降低，在第12和18天进一步降低。尽管催乳素的循环浓度很高，但正中隆起的多巴积累率却很低，这表明长期雌二醇治疗降低了TIDA神经元对催乳素的反应能力。直接脑室内（icv）注射催乳素增加了假植入大鼠中央隆起的多巴积累速率，而雌二醇治疗18天的大鼠则没有。为了确定雌二醇的作用是否可逆，切除卵巢的大鼠被植入含有雌二醇的胶囊18天。然后取出胶囊，动物在18天后的不同时间被处死。取下胶囊后18 d内血清催乳素浓度升高恢复到对照组水平，中隆起处DA降低浓度升高，但18 d后仍低于对照组。另一方面，在取出胶囊18天后，正中隆起的DOPA积累率逐渐增加，达到大于对照组的值。这些结果表明，在去除雌二醇胶囊的大鼠中，TIDA神经元对催乳素的敏感性可能会反弹增加。在雌二醇后组的大鼠中，icv催乳素引起了多巴积累速率的更大增加，这一事实证实了这一点。这些结果表明，长期雌二醇治疗会降低TIDA神经元的活性，部分原因是它们对催乳素的反应减弱，而终止雌二醇治疗会导致TIDA神经元对催乳素的敏感性反弹增加。雌二醇诱导的TIDA神经元反应性降低似乎不是这种治疗引起的循环催乳素水平升高的结果，因为用氟哌啶醇慢性治疗11天或22天都会引起循环催乳素的类似升高，并伴有中隆起多巴积累率的相关增加。这些研究结果表明，雌二醇直接作用于催乳素反馈机制的某些组分，从而降低了TIDA神经元对催乳素的反应性。
Previous studies have demonstrated that short-term (3–5 days) treatment with estradiol increases the rate of turnover and synthesis of dopamine (DA) in terminals of tuberoinfundibular (TI) neurons in the median eminence by virtue of the ability of this hormone to increase circulating concentrations of prolactin. The present studies were undertaken to examine the long-term effects of estradiol on serum prolactin concentrations and TIDA neuronal activity (estimated by the rate of DOPA accumulation in the median eminence after the administration of a decarboxylase inhibitor). Female rats, ovariectomized for 2 weeks, were implanted subcutaneously with silastic capsules containing estradiol benzoate and sacrificed 6,12 and 18 days after capsule implantation. Serum prolactin concentrations were markedly increased at 6,12 and 18 days whereas the rate of DOPA accumulation was increased at 6 days but not at 12 days, and was decreased at 18 days. The concentration of DA in the median eminence was reduced at 6 days and further reduced at 12 and 18 days. The low rate of DOPA accumulation in the median eminence despite the high circulating concentrations of prolactin suggests that long-term estradiol treatment reduces the ability of TIDA neurons to respond to prolactin. This was confirmed by the finding that direct intracerebroventricular (icv) injections of prolactin increased the rate of DOPA accumulation in the median eminence of sham-implanted rats but not in 18 day estradiol-treated rats. To determine if the effects of estradiol were reversible, ovariectomized rats were implanted with estradiol-containing capsules for 18 days. The capsules were then removed and the animals sacrificed at various times up to 18 days later. The elevated serum concentrations of prolactin returned to control values within 18 days after removing the capsules, and the reduced DA concentrations in the median eminence increased but were still less than control after 18 days. On the other hand, the rate of DOPA accumulation in the median eminence increased progressively after removing the capsules reaching values greater than control by 18 days. These results suggest that there may be a rebound increase in the sensitivity of TIDA neurons to prolactin in rats that had the estradiol capsules removed. This was substantiated by the fact that icv prolactin caused a greater increase in the rate of DOPA accumulation in the postestradiol group of rats. These results suggest that long-term estradiol treatment reduces the activity of TI DA neurons, in part by attenuating their responsiveness to prolactin, and that termination of estradiol treatment results in a rebound increase in the sensitivity of TIDA neurons to prolactin. The decreased responsiveness of TIDA neurons induced by estradiol does not appear to be a consequence of elevated levels of circulating prolactin induced by this treatment, since chronic treatment with haloperidol for either 11 or 22 days induced similar elevations of circulating prolactin with an associated increase in the rate of DOPA accumulation in the median eminence. The results of these studies suggest that estradiol exerts a direct action on some component of the prolactin feedback mechanism so as to decrease the responsiveness of TIDA neurons to prolactin.
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