Morphological evidence that luteinizing hormone-releasing hormone neurons participate in the suppression by estradiol of pituitary luteinizing hormone secretion in ovariectomized rats.
Morphological evidence that luteinizing hormone-releasing hormone neurons participate in the suppression by estradiol of pituitary luteinizing hormone secretion in ovariectomized rats.
复制标题
形态学证据表明，黄体生成素释放激素神经元参与雌二醇对卵巢切除大鼠垂体黄体生成素分泌的抑制。
DOI：
10.1159/000124698
复制
发表时间：
1987
影响因子：
4.1
通讯作者：
Elkind-Hirsch,KE
中科院分区：
文献类型：
--
作者：
King,JC;Anthony,EL;Damassa,DA;Elkind-Hirsch,KE
Morphological characteristics of LHRH neurons identified by immunocytochemistry were studied using light and electron microscopy in female rats in which estradiol was replaced at the time of ovariectomy (‘pseudo-intact’ rats) or 3 weeks after ovariectomy (long-term ovariectomized, estradiol-treated). While estradiol levels were equivalent in these two groups, the rise in LH after ovariectomy was prevented by the immediate administration in the pseudo-intact rats, while the augmented plasma LH levels present three weeks following ovariectomy were only reduced by 50% as a result of delayed estradiol treatment. The LHRH content of the medial basal hypothalamus (MBH) including the median eminence (ME) was greater in pseudo-intact females than in untreated long-term ovariectomized control females or long-term ovariectomized, estradiol-treated females, both 1 and 14 days after estradiol exposure. Immunocytochemistry revealed fewer LHRH-immunopositive neuronal processes coursing throughout the MBH and terminating in the ME of long-term ovariectomized, estradiol-treated rats compared to those in pseudo-intact rats. However, within individual neurovascular terminals in the ME, image analysis revealed that the area of reaction product was greater in long-term ovariectomized, estradiol-treated animals. Equivalent amounts of LHRH were assayed in the MBH within each group of animals by several LHRH antisera regardless of their different binding requirements (R42, IJ29 and A-R743), suggesting that the predominant moiety present in neuronal terminals is the fully mature decapeptide. In contrast, in the preoptic area-anterior hypothalamus (POA-AH) these antisera assayed amounts of LHRH that varied as a function of binding characteristics, although the quantities did not vary with the estradiol treatment schedule. Immunocytochemical results paralleled these assay data; antisera requiring an interior sequence of amino acids (A-R743 and A-R419) detected approximately 3 times as many immunoreactive perikarya in the POA-AH as did an antiserum requiring the free amidated C terminal (IJ29). The estradiol treatment schedules had no effect on the total number of LHRH-immunopositive neurons detected by each antiserum or the distribution of LHRH-immunopositive neuronal perikarya. These data support the hypothesis that the predominant moieties present in neuronal cell bodies are precursor forms. The fine-structural characteristics of LHRH-immunopositive neuronal cell bodies are consistent with greater secretory and biosynthetic activity in LHRH neurons of long-term ovariectomized, estradiol-treated rats. We hypothesize that the activity of LHRH neurons in these females is enhanced in comparison to pseudo-intact females and, secondly, that this increased activity contributes to the augmented secretion of LH in long-term ovariectomized, estradiol-treated females.
