Growth hormone-releasing hormone messenger ribonucleic acid in the hypothalamus of the adult male rat is increased by testosterone

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Growth hormone-releasing hormone messenger ribonucleic acid in the hypothalamus of the adult male rat is increased by testosterone

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dc.contributor.author Clifton, Donald K. en_US
dc.contributor.author Chowen-Breed, Julie A. en_US
dc.contributor.author Steiner, Robert A. en_US
dc.contributor.author Zeitler, Philip en_US
dc.contributor.author Argente, Jesus en_US
dc.date.accessioned 2008-10-17T20:40:37Z
dc.date.available 2008-10-17T20:40:37Z
dc.date.issued 1990-09 en_US
dc.identifier.citation Endocrinology. 1990 Sep;127(3):1362-8 en_US
dc.identifier.uri http://hdl.handle.net/1773/4316
dc.description.abstract Since 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.iso en_US en_US
dc.publisher Endocrine Society en_US
dc.subject GH-releasing hormone en_US
dc.subject mRNA en_US
dc.subject rat en_US
dc.subject hypothalamus en_US
dc.subject.mesh Nucleic Acid Hybridization en_US
dc.subject.mesh Neurons, drug effects, metabolism en_US
dc.subject.mesh RNA Probes en_US
dc.subject.mesh Rats en_US
dc.subject.mesh Orchiectomy en_US
dc.subject.mesh Estradiol, pharmacology en_US
dc.subject.mesh Testosterone, pharmacology en_US
dc.subject.mesh Rats, Inbred Strains en_US
dc.subject.mesh Research Support, U.S. Gov't, P.H.S. en_US
dc.subject.mesh Animals en_US
dc.subject.mesh RNA, Messenger, biosynthesis en_US
dc.subject.mesh Hypothalamus, drug effects, metabolism en_US
dc.subject.mesh Male en_US
dc.subject.mesh Gene Expression, drug effects en_US
dc.subject.mesh Somatotropin-Releasing Hormone, genetics en_US
dc.subject.mesh Arcuate Nucleus, metabolism en_US
dc.subject.mesh Dihydrotestosterone, pharmacology en_US
dc.subject.mesh Ventromedial Hypothalamic Nucleus, metabolism en_US
dc.title Growth hormone-releasing hormone messenger ribonucleic acid in the hypothalamus of the adult male rat is increased by testosterone en_US
dc.type Article en_US


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