Growth Hormone-Releasing Factor Regulation by Somatostatin, Growth Hormone and Insulin-Like Growth Factor I in Fetal Rat Hypothalamic-Brain Stem Cell Cocultures

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Abstract
Information about growth hormone-releasing factor (GRF) regulation by somatostatin, GH and IGF-I is scarce and controversial. This could be due to the in vivo interactions among these signals and the lack of models for individualizing the action of one of them from the others upon GRF regulation. The aim of the present work was to study GRF regulation by these signals, using primary fetal rat hypothalamic-brain stem cell cocultures. Coculturing of these two cytotypes increases hypothalamic immunoreactive rat GRF (IR-rGRF) content in cells by 45% and in media by 36%. The effect of SS on GRF in cocultures was examined by using a multiple approach: (1) depleting endogenous SS by adding 1 mM cysteamine (CSH); (2) blocking endogenous SS by incubation with SS antiserum, and (3) incubating with synthetic SS 14 at different concentrations and exposure periods. 1 mM CSH depleted IR-SS content (pg/plate, mean ± SE) in cells (CSH-treated: 68 + 8 vs. control: 322 ± 10, p –10 –10–8M) could not modify IR-rGRF content in media and cells. The GH effect on IR-rGRF was studied in the absence of CSH and in CSH-induced SS-depleted cultures. GH (5 µM, 24 h) decreased (52%) the IR-rGRF content in media (GH-treated: 28.7 ± 4.6 vs. control: 60.2 ± 7; p M CSH again depleted IR-SS content and abolished the GH stimulatory effect. IGF-I (5.6 nM, 24 h) did not affect IR-rGRF content in media or in cells under either conditions (CSH and non-CSH-treated cultures). However, in these experiments IGF-I increased IR-SS content in the media (GH-treated: 322 ± 3 vs. control: 289 ± 9; p

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