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Inhibition of luteinizing hormone secretion during quiescent interval of testicular androgen production in immature mice
Authors:Y Ogasawara  T Yamane  Y Kitamura  K Uchida  K Wakabayashi  K Matsumoto
Affiliation:1. Department of Patholgy, Osaka University Medical School, Osaka 530, Japan;1. Institute for Cancer Research, Osaka University Medical School, Osaka 530, Japan;2. Shionogi Research Laboratory, Shionogi Co. Ltd., Osaka 553, Japan;3. Institute of Endocrinology, Gunma University, Maebashi 371, Japan;1. Oxford Brookes Centre for Nutrition and Health, Faculty of Health and Life Sciences, Oxford Brookes University, Oxford, UK;2. School of Biological, Health, and Sports Sciences, Technological University Dublin, Dublin, Ireland;1. Department of Systems Pharmacology, The University of Tokyo, Tokyo 113-0033, Japan;2. Laboratory for Synthetic Biology, RIKEN BDR, Suita, Osaka 565-0871, Japan;3. Department of Bioelectronics, FKE, Vienna University of Technology-TU Wien, Vienna, Austria;4. Section of Bioelectronics, Center for Brain Research, Medical University of Vienna, Vienna, Austria;5. Cold Spring Harbor Laboratories, Cold Spring Harbor, NY 11724, USA;6. Department of Biomedical Engineering, Boston University, Boston, MA, USA;7. Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA;1. Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA;2. Department of Genetic and Cellular Toxicology, ADME & Discovery Toxicology, Preclinical Development, Merck Research Laboratories, Merck & Co., Inc., West Point, PA 19486, USA;3. State Key Laboratory of Membrane Biology, Beijing Frontier Research Center for Biological Structure, Tsinghua-Peking Joint Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing 100084, China;4. Department of Biological Sciences, St. John’s University, Queens, NY 11439, USA;1. State Key Laboratory of Molecular Biology, Shanghai Key Laboratory of Molecular Andrology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, China;2. School of Life Science and Technology, ShanghaiTech University, Shanghai, China;3. School of Life Science, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou, China
Abstract:We reported [1] that the proliferation of seminal vesicle cells in mice takes place largely in the neonatal (days 0-15) and pubertal (days 25-35) periods and that between neonatal and pubertal proliferations, a quiescent interval of cell proliferation due to markedly diminished secretion of androgens occurs. The present study was carried out to investigate the mechanism for this quiescent interval of Leydig cell activity. Serum LH concentrations were moderate (0.29 ng NIH-LH-S1/ml) at 8 days of age, low (0.13 ng/ml) at 18 days, and high (0.78-0.60 ng/ml) at 30, 40 and 60 days. The LH level on day 18 was almost the same as that found in hypophysectomized adult mice (0.12 ng/ml). These changes with age in serum LH concentrations paralleled those for serum total androgen (testosterone plus 5 alpha-androgens) concentrations. The injection of HCG (1 IU/day) or LH releasing hormone (0.1 or 0.4 microgram/6h) for 1 or 2 days resulted in significant and marked increases on day 18 in testicular and serum androgen levels and/or the proliferation of seminal vesicle cells measured with 5-[125I]iodo-2'-deoxyuridine uptake by the whole seminal vesicles. These findings lead to the hypothesis that the quiescent interval of testicular androgen production due to inhibition of pituitary LH secretion occurs around day 20 in mice.
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