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      Prolactin Stimulates Rat Hypothalamic Corticotropin-Releasing Hormone and Pituitary Adrenocorticotropin Secretion in vitro

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          Abstract

          In rats hyperprolactinemia increases corticotropin-releasing hormone (CRH) concentration and secretion in hypophysial portal blood and the serum concentration of adrenocorticotropic hormone (ACTH). To determine whether the stimulatory effect of prolactin (PRL) on CRH and ACTH in vivo is exerted directly on the hypothalamus, hypothalamic explants and primary anterior pituitary cell cultures from adult male and female rats were used. Hypothalami explanted from male and female rats were preincubated during 90 min and treated for 30 min with rat PRL (rPRL) at concentrations of 10<sup>–8</sup>, 10<sup>–7</sup>, and 10<sup>–6</sup> M (about 200, 2,000, and 20,000 ng/ml, respectively), corticosterone at concentrations of 10<sup>–7</sup>, 10<sup>–6</sup>, and 10<sup>–5</sup> M (about 35, 350 and 3,500 ng/ml, respectively), ACTH at concentrations ranging from 10<sup>–10</sup> to 10<sup>–7</sup> M (0.46, 4.6, 46, and 460 ng/ml, respectively), and graded concentrations of testosterone or estradiol. Concentrations of immunoreactive CRH (iCRH) were measured by radioimmunoassay. rPRL at 10<sup>–6</sup> M stimulated iCRH secretion by 360 and 400% of the basal iCRH output (about 14 pg/hypothalamus), respectively, from hypothalami explanted from male and female rats. ACTH and corticosterone did not suppress rPRL (10<sup>–6</sup> M) induced iCRH secretion. Corticosterone at the concentration of 10<sup>–6</sup> M potentiated rPRL (10<sup>–6</sup> M) induced iCRH secretion in hypothalami explanted from male, but not female rats. Gonadal steroids had no effect either on the basal or rPRL (10<sup>–6</sup> M) stimulated iCRH secretion, with the exception of estradiol which augmented the response to 10<sup>–6</sup> M rPRL by about fivefold, but only at the concentration of 10<sup>–8</sup> M (about 2.7 ng/ml). Pituitary cells were treated with rPRL, corticosterone, gonadal steroids, or CRH for 4 h. The concentrations of ACTH in the culture medium were measured by radioimmunoassay. rPRL at the concentration of 10<sup>–7</sup> M caused an ACTH release of 169 ± 8 and 185 ± 14% of basal values (about 2,000 pg/10<sup>5</sup> cells), respectively, in pituitary cells explanted from male and female rats, whereas at the concentration of 10<sup>–6</sup> M rPRL caused a release of 265 ± 15 (male) and 336 ± 62% (female). Corticosterone suppressed PRL (10<sup>–6</sup> M) induced ACTH release in a dose-dependent fashion, but the ACTH secretion did not reach basal levels. Inhibition of CRH-induced ACTH release by corticosterone was not reversed by the addition of 10-<sup>6</sup> M rPRL. Gonadal steroids had no effect. Rat growth hormone did not influence iCRH or ACTH secretion in these systems. We conclude that the activation of the hypothalamic-pituitary-adrenal axis observed during the course of hyperprolactinemia may be explained by a direct stimulatory effect of PRL on both hypothalamic CRH and pituitary ACTH secretions.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1991
          1991
          07 April 2008
          : 54
          : 3
          : 248-253
          Affiliations
          Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Md., USA
          Article
          125882 Neuroendocrinology 1991;54:248–253
          10.1159/000125882
          1658672
          © 1991 S. Karger AG, Basel

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          Pages: 6
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          Original Paper

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