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      In vitro Regulation of Pituitary ACTH Secretion in Inflammatory Disease Susceptible Lewis (LEW/N) and Inflammatory Disease Resistant Fischer (F344/N) Rats

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          Abstract

          We have previously shown that susceptibility to inflammatory disease in Lewis (LEW/N) rats is related to their limited hypothalamic-pituitary-adrenal (HPA) axis responses to a variety of inflammatory stimuli, while the relative resistance to inflammatory disease in Fischer (F344/N) rats is related to their potent HPA axis responses to these same stimuli. In vivo studies also showed that LEW/N pituitary ACTH responses to exogenous corticotropin-releasing hormone (CRH) were blunted compared to F344/N. To determine if there is a fundamental difference in pituitary corticotroph function between the two strains, independent of other factors influencing the HPA axis, we compared ACTH responses to a variety of stimuli in LEW/N and F344/N primary pituitary cell cultures. Here we show that in vitro basal ACTH secretion and peak ACTH response to CRH, forskolin and 8-bromo-cAMP are 50% lower in LEW/N than F344/N rats. However, these findings can be explained by other observations: diminished basal ACTH content, POMC mRNA, and a decreased number of corticotrophs, in pituitary cell cultures from LEW/N compared to F344/N rats. In addition, LEW/N corticotrophs were more sensitive to dexamethasone and to corticosterone suppression of CRH-stimulated ACTH secretion compared to F344/N. The data support the possibility of an HPA axis defect in LEW/N rats at the pituitary level which could be secondary to prolonged understimulation by hypothalamic CRH, or could also be partially related to enhanced glucocorticoid feedback inhibition.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1992
          1992
          07 April 2008
          : 56
          : 4
          : 474-482
          Affiliations
          aUnit on Neuroendocrine Immunology and Behavior, Clinical Neuroendocrinology Branch, bPediatric Endocrinology Branch, NICHD, cArthritis and Rheumatism Branch, NIAMS, NIMH and NIH, Bethesda, Md, USA
          Article
          126264 Neuroendocrinology 1992;56:474–482
          10.1159/000126264
          1335552
          © 1992 S. Karger AG, Basel

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          Page count
          Pages: 9
          Categories
          Original Paper

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