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大鼠卵巢代偿性肥大的5-羟色胺能机制研究

Study on serotoninergic mechanisms of compensatory ovarian hypertrophy in rats.

作者信息

Anisimov V N

出版信息

Endokrinologie. 1980 Mar;75(2):141-6.

PMID:7398587
Abstract

The increase of brain serotonin level following the treatment of hemicastrate adult female rats with L-tryptophane or Agr-1240 inhibits the compensatory ovarian hypertrophy (COH). The blockade of central serotoninergic receptors with typindole abolished the suppressive effect of estrogen on COH. The administration of L-DOPA abolished this effect of typindole. The dose-related inhibitory effect of melatonin on COH was shown. Serotoninergic systems are suggested to participate in the realisation of the negative feedback action of estrogen. The threshold of the hypothalamo-pituitary sensitivity to the suppressive estrogen effect is elevated in both pinealectomized and constant light-exposed rats.

摘要

用L-色氨酸或Agr-1240处理半去势成年雌性大鼠后,脑血清素水平的升高会抑制代偿性卵巢肥大(COH)。用替吲哚阻断中枢血清素能受体可消除雌激素对COH的抑制作用。给予左旋多巴可消除替吲哚的这种作用。褪黑素对COH的剂量相关抑制作用已得到证实。提示血清素能系统参与雌激素负反馈作用的实现。松果体切除和持续光照的大鼠下丘脑-垂体对雌激素抑制作用的敏感性阈值均升高。

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