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Morphological Evidence that Luteinizing Hormone-Releasing Hormone Neurons Participate in the Suppression by Estradiol of Pituitary Luteinizing Hormone Secretion in Ovariectomized Rats

 

作者: Joan C. King,   Edythe L.P. Anthony,   David A. Damassa,   Karen E. Elkind-Hirsch,  

 

期刊: Neuroendocrinology  (Karger Available online 1987)
卷期: Volume 45, issue 1  

页码: 1-13

 

ISSN:0028-3835

 

年代: 1987

 

DOI:10.1159/000124698

 

出版商: S. Karger AG

 

关键词: LHRH;LH;Estradiol;Negative feedback;Hypothalamus;Ovariectomy;Immunocytochemistry;Electron microscopy

 

数据来源: Karger

 

摘要:

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 fema

 

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