Tissue levels of luteinizing hormone-releasing hormone in the preoptic area and hypothalamus, and serum concentrations of gonadotropins following anterior hypothalamic deafferentation and estrogen treatment of the female rat.
Tissue levels of luteinizing hormone-releasing hormone in the preoptic area and hypothalamus, and serum concentrations of gonadotropins following anterior hypothalamic deafferentation and estrogen treatment of the female rat.
复制标题
雌性大鼠下丘脑前部传入神经阻滞和雌激素治疗后,视前区和下丘脑的黄体生成素释放激素的组织水平以及促性腺激素的血清浓度。
DOI:
10.1210/endo-99-1-101
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发表时间:
1976
期刊:
影响因子:
4.8
通讯作者:
S. Kalra
中科院分区:
文献类型:
--
作者:
S. Kalra
Female rats were ovariectomized prior to anterior hypothalamic deafferentation (AHD) or sham AHD of the medial basal hypothalamus (MBH). LHRH in the MBH and the preoptic area (POA), and the blood concentrations of LHRH, FSH, and LH were measured following decapitation at the end of 30 days in experiment 1 and 28 days in experiment 2. Interruption of anterior neural links of the MBH resulted in a drastic reduction in the amounts of LHRH in the MBH and a significant increment in the POA. The circulating levels of FSH (experiments 1 and 2) and LH (experiment 2) were significantly depressed whereas serum LHRH was unaltered following deafferentation. In experiment 3, rats were ovariectomized 25 days following either AHD or sham AHD, and were given estradiol benzoate (EB, 10 mug/rat in oil, SC) or oil alone on day 7 postovariectomy and sacrificed 2 days later. Relative to sham AHD, a reduction in the MBH LHRH and a pronounced elevation in the POA LHRH was observed in AHD rats. Serum LH and FSH concentrations were also significantly decreased. EB treatment significantly lowered serum gonadotropins, whereas LHRH levels in the MBH of both AHD and sham AHD rats increased two-fold. Serum LHRH concentrations were also significantly reduced in AHD rats following EB injection. These studies indicate that 1) since a substantial portion of the LHRH activity normally detected in the MBH of female rats appears to be derived from that synthesized in the rostral regions, it is logical to infer that POA LHRH may be involved in the tonic as well as the cyclic discharge of LH, and 2) an increase in the LHRH content of the MBH after estrogen treatment may be due to a partial inhibition in release and/or an increased rate of synthesis of LHRH in the MBH.