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      Growth Hormone-Releasing Hormone and Morphine Attenuate Growth Hormone Secretagogue-Induced Activation of the Arcuate Nucleus in the Male Rat

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          Growth hormone secretagogues (GHS) administered systemically selectively induce growth hormone (GH) release from the pituitary and the expression of Fos protein in arcuate nucleus neurons. Both the control of GH release and the expression of the GHS receptor in the arcuate nucleus are thought to be regulated, at least in part, by the negative feedback actions of GH. In this study, we utilized the immunocytochemical detection of Fos protein to examine the effects of morphine- and GH-releasing hormone (GHRH)-induced GH release on the activation of arcuate nucleus neurons following GHS administration. Given alone, two structurally different GHS induced significant amounts of Fos-LI in the arcuate nucleus of male rats, suggesting activation of cells in this region. Prior administration of morphine or GHRH significantly reduced the number of Fos-positive cells in the arcuate nucleus of rats injected with either GHS, although when given together, morphine and GHRH did not produce a greater reduction in Fos expression than when given alone. In no case was there a complete reduction in Fos expression, indicating that some arcuate nucleus neurons are not subject to the feedback effects of endogenous GH. These results provide evidence that, in the male rat, GH can feedback to the hypothalamus, altering the responsiveness of neurons involved in the central response to GHS.

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          Distribution of mRNA encoding the growth hormone secretagogue receptor in brain and peripheral tissues

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            Systemic administration of growth hormone-releasing peptide activates hypothalamic arcuate neurons.

            The synthetic hexapeptide growth hormone-releasing peptide selectively releases growth hormone in many species including man. Growth hormone-releasing peptide directly stimulates growth hormone release by an action at the level of the pituitary, at a different receptor site to that for the endogenous 44-amino acid peptide, growth hormone-releasing hormone, and when administered with growth hormone-releasing hormone has a synergistic effect. In addition to this pituitary action, we have suggested that the potent in vivo growth hormone-releasing activity of growth hormone-releasing peptide reflects a hypothalamic action and growth hormone-releasing peptide binding sites have been reported to be present in the hypothalamus. We have now found more direct evidence for a hypothalamic action of growth hormone-releasing peptide in two ways. First, we have found that a sub-population of hypothalamic neurons show strongly increased fos expression in response to systemic growth hormone-releasing peptide administration. Fos is the protein product of the immediate early gene, c-fos, which is induced in many neuronal systems following their activation. Second, extracellular recordings from putative growth hormone-releasing hormone neurons in the arcuate nucleus showed that growth hormone-releasing peptide also stimulates the firing of neurons in this area.

              Author and article information

              S. Karger AG
              August 1999
              16 August 1999
              : 70
              : 2
              : 101-106
              aDepartment of Biomedical Sciences, University Medical School, Edinburgh, UK and bHuffington Center on Aging, Baylor College of Medicine, Houston, Tex., USA
              54464 Neuroendocrinology 1999;70:101–106
              © 1999 S. Karger AG, Basel

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              Page count
              Figures: 2, References: 30, Pages: 6
              Growth Hormone-Releasing Hormone and Growth Hormone Secretagogues


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