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      Hormonal Influences on the Estradiol-Induced and Age-Related Increases of Pituitary Dopamine in C57BL/6J Mice

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          Abstract

          Estradiol (E<sub>2</sub>) produces many-fold increases in the dopamine (DA) content of the anterior pituitary and also plays a role in the age-related increase in pituitary DA in female C57BL/6J mice. These studies address the following questions: (1) What are the time and dose characteristics of the E<sub>2</sub>-induced increase in pituitary DA and can other gonadal steroids – such as progesterone (P) and 5α-dihydrotestosterone – also influence pituitary DA? (2) Is the age-related increase in pituitary DA due entirely to an increase in the E<sub>2</sub>:P ratio seen in aging female mice, or can extra-ovarian factors also play a role? (3) Is the E2-induced (and therefore possibly the age-related) increase in pituitary DA secondary to an E<sub>2</sub>-induced increase in serum prolactin? In ovariectomized (OVX) mice, E2 implants increased pituitary DA in a time- and dose-dependent fashion. P implants administered to OVX mice simultaneously with E<sub>2</sub> antagonized the E<sub>2</sub>-induced increase in pituitary DA. Daily injections of 5α-dihydrotestosterone given in conjunction with E<sub>2</sub> implants had no effect on basal or E<sub>2</sub>-increased pituitary DA in OVX mice. Thus, E<sub>2</sub> is the only gonadal steroid examined which increases anterior pituitary DA. In intact aging mice, P attenuates the age-related increase in pituitary DA, supporting the hypothesis that the increased ratio of E<sub>2</sub>:P secreted by the ovaries of aging female mice is responsible for the age-related increase in pituitary DA. However, at advanced ages, intact male mice also showed modest increases in anterior pituitary DA. Therefore, extra-ovarian age changes, perhaps age changes intrinsic to the pituitary, also play a minor role in the age-related increase in pituitary DA. E<sub>2</sub> increases the secretion of prolactin, which can then feed back to increase secretion of DA from the tuberoinfundibular dopaminergic neurons, a source of pituitary DA. To determine if the E<sub>2</sub>-induced increase in pituitary DA was secondary to an E<sub>2</sub>-induced increase in serum prolactin, OVX mice were given pituitary grafts to increase serum prolactin independently of E<sub>2</sub> treatment. The E<sub>2</sub>-induced increase of pituitary DA is not mediated, but can be enhanced by prolactinemia.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1987
          1987
          02 April 2008
          : 46
          : 6
          : 481-487
          Affiliations
          aEthel Percy Andrus Gerontology Center and Department of Biological Sciences, University of Southern California, Los Angeles, Calif.; bWhittier Institute for Diabetes and Endocrinology, La Jolla, Calif., USA
          Article
          124869 Neuroendocrinology 1987;46:481–487
          10.1159/000124869
          3696379
          © 1987 S. Karger AG, Basel

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          Page count
          Pages: 7
          Categories
          Original Paper

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