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dc.contributor.authorClifton, Donald K.en_US
dc.contributor.authorChowen-Breed, Julie A.en_US
dc.contributor.authorSteiner, Robert A.en_US
dc.contributor.authorZeitler, Philipen_US
dc.contributor.authorArgente, Jesusen_US
dc.date.accessioned2008-10-17T20:40:37Z
dc.date.available2008-10-17T20:40:37Z
dc.date.issued1990-09en_US
dc.identifier.citationEndocrinology. 1990 Sep;127(3):1362-8en_US
dc.identifier.urihttp://hdl.handle.net/1773/4316
dc.description.abstractSince intact adult male rats have higher GH pulse amplitude than do castrated animals and since GH-releasing hormone (GHRH) secretion is predominantly responsible for the production of these GH pulses, we hypothesized that testosterone stimulates GHRH synthesis in neurons of the hypothalamus. To test this hypothesis, we compared GHRH mRNA content in individual neurons of the arcuate (ARC) and ventromedial (VMH) nuclei among groups of intact (n = 3), castrated (n = 5), and castrated testosterone-replaced (n = 5) adult male rats. Cellular GHRH mRNA content was measured by using semiquantitative in situ hybridization with an 35S-labeled cRNA probe complementary to the coding sequence of rat GHRH mRNA. Castration resulted in an approximately 35% decline in GHRH mRNA signal relative to that in intact animals in both the ARC (P less than 0.005) and VMH (P less than 0.005). Replacement with testosterone at the time of castration completely prevented the decline in both areas. Testosterone can exert effects either through activation of the androgen receptor directly or through aromatization to estradiol; therefore, we also examined the effects on GHRH mRNA of replacement with 17 beta-estradiol (n = 5) or dihydrotestosterone (DHT), a nonaromatizable androgen (n = 4). Estradiol had no effect on the castration-induced decline in GHRH mRNA in either the ARC or VMH. In contrast, DHT partially prevented the postcastration decline in GHRH in the ARC (P less than 0.005), while having no statistically significant effect on GHRH mRNA in the VMH. These results clearly indicate that testosterone stimulates expression of GHRH mRNA in neurons of the hypothalamus. Furthermore, the failure of estradiol to substitute for testosterone and the ability of DHT to substantially support GHRH mRNA suggest that testosterone exerts its effects on GHRH gene expression predominantly through direct activation of the androgen receptor.en_US
dc.language.isoen_USen_US
dc.publisherEndocrine Societyen_US
dc.subjectGH-releasing hormoneen_US
dc.subjectmRNAen_US
dc.subjectraten_US
dc.subjecthypothalamusen_US
dc.subject.meshNucleic Acid Hybridizationen_US
dc.subject.meshNeurons, drug effects, metabolismen_US
dc.subject.meshRNA Probesen_US
dc.subject.meshRatsen_US
dc.subject.meshOrchiectomyen_US
dc.subject.meshEstradiol, pharmacologyen_US
dc.subject.meshTestosterone, pharmacologyen_US
dc.subject.meshRats, Inbred Strainsen_US
dc.subject.meshResearch Support, U.S. Gov't, P.H.S.en_US
dc.subject.meshAnimalsen_US
dc.subject.meshRNA, Messenger, biosynthesisen_US
dc.subject.meshHypothalamus, drug effects, metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshGene Expression, drug effectsen_US
dc.subject.meshSomatotropin-Releasing Hormone, geneticsen_US
dc.subject.meshArcuate Nucleus, metabolismen_US
dc.subject.meshDihydrotestosterone, pharmacologyen_US
dc.subject.meshVentromedial Hypothalamic Nucleus, metabolismen_US
dc.titleGrowth hormone-releasing hormone messenger ribonucleic acid in the hypothalamus of the adult male rat is increased by testosteroneen_US
dc.typeArticleen_US


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