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Gonadotropin Secretion following Intraventricular Norepinephrine Infusion into Neonatally Androgenized Female Rats

 

作者: Robert J. Handa,   Timothy P. Condon,   David I. Whitmoyer,   Roger A. Gorski,  

 

期刊: Neuroendocrinology  (Karger Available online 1986)
卷期: Volume 43, issue 3  

页码: 269-272

 

ISSN:0028-3835

 

年代: 1986

 

DOI:10.1159/000124539

 

出版商: S. Karger AG

 

关键词: Gonadotropin;Norepinephrine;Luteinizing hormone;Follicle-stimulating hormone;Androgenization

 

数据来源: Karger

 

摘要:

To determine whether norepinephrine (NE) will stimulate gonadotropin secretion in androgenized female rats, we administered NE (0.3 µM in 2 µl saline; pH 6.0–6.5) into the third ventricle of females which had been treated neonatally with two different doses of testosterone propionate (TP; 10 or 100 µg) on day 5 of life. This treatment rendered these animals anovulatory as evidenced by polyfollicular ovaries and a persistent vaginal estrus condition which occurred by 100 days of age. Those females which were determined to be anovulatory were ovariectomized 4 weeks prior to the stereotaxic implantation of an intracerebroventricular (ICV) cannula. Ten to twelve days following cannula placement, animals were primed with either estradiol benzoate (EB; 30 µg) or EB and progesterone (P; 5 mg). Two days following steroid priming, NE was infused into the third ventricle at 15.00 h and blood samples were taken via an intra-atrial catheter at 15-min intervals for 2 h before and 2 h after administration. In both TP-treated groups, NE caused rapid and significant (p < 0.01) elevations in plasma luteinizing hormone (LH) concentrations when animals were primed with EB as compared with control females given acid saline infusions (pH 6.0–6.5). Similar responses to NE were seen after additional priming with P at the same time as EB. Follicle-stimulating hormone (FSH) values did not increase following NE or saline infusion to any of the groups. These data suggest that the ability of the female to respond to NE with increases in plasma LH is present following androgenization, and the possibility exists that NE may be a component of the neural trigger for phasic LH secretion which is lost following neonatal exposure to a

 

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