The possible existence of extrapituitary melanocyte stimulating hormone (MSH) in various regions of the rat brain has been studied in intact and hypophysectomized rats. Using a sensitive and specific radioimmunoassay (RIA), αMSH has been found in a number of brain regions in intact rats. The standard curves of synthetic αMSH and the dilution curves for pars intermedia nervosa (PIN), pars distalis (PD), hypothalamus and thalamus extracts were strictly parallel. The αMSH concentrations were measured in PIN (6,225 ± 962 ng/mg wet tissue); PD (12.5 ± 1.41 ng/mg); pineal (380 ± 29 ng/g wet tissue); hypothalamus (645 ± 161 ng/g) and thalamus (33.3 ± 5.26 ng/g). In rats hypophysectomized for 1 or 2 months, the highest concentrations of immunoreactive αMSH were found in pineal (353 ± 140 ng/g wet tissue), hypothalamus (85.8 ±14.1 ng/g) and thalamus (39.8 ± 13.9 ng/g). Hypophysectomy significantly reduced hypothalamic MSH content and concentration but did not alter MSH concentration in pineal and thalamus. From these results, we conclude that hypothalamic αMSH is, in part, of hypophyseal origin while pineal and thalamus «MSH does not originate from the pituitary. After Sephadex G-25 gel filtration, synthetic αMSH and PIN extracts showed a single peak of both bioactive and immunoreactive αMSH. In the same conditions, extracts from the 5 brain regions studied in hypophysectomized rats chromatographed as a single peak of immunoreactive MSH but as 2 peaks of apparent bioactive MSH, 1 concident with synthetic αMSH and the other far after the salt volume. We conclude that αMSH is found in a number of brain areas and its presence after hypophysectomy would indicate synthesis within the central nervous system.
In the human adrenal cortex, serotonin (5-HT) is contained in mast-like cells, and we have shown that 5-HT stimulates aldosterone secretion, suggesting that 5-HT may control glomerulosa cells through a paracrine mechanism. Concurrently, the presence of 5-hydroxyindolacetic acid in human adrenocortical extracts indicates that 5-HT may be metabolized after local release by mast cells. The aim of the present study was to investigate in vitro the production and metabolism of 5-HT by the human adrenal cortex. Perifused adrenal slices released spontaneously detectable amounts of 5-HT (0.74 +/- 0.38 fmol/mg wet tissue.min). The mast cell-depleting drug compound 48/80 induced a burst of 5-HT secretion followed by a gradual increase in aldosterone production. Administration of the specific 5-HT(4) receptor antagonist GR 113808 (10(-6) M) did not affect compound 48/80-induced 5-HT release but abolished the stimulatory effect of compound 48/80 on aldosterone secretion, indicating that 5-HT released locally is responsible for a paracrine control of steroidogenesis. Incubation of cells from the human adrenal cortex with 5-HT (10(-5) M) provoked the formation of the 5-HT metabolite 5-hydroxytryptophol. The type A monoamine oxidase (MAO) inhibitor clorgyline (10(-6) M) suppressed the metabolism of 5-HT into 5-hydroxytryptophol. Immunocytochemical staining of cultured cells revealed the presence of a subpopulation of MAO-A-positive cells. Double labeling with an antiserum against chromogranin A showed that MAO-A was actually contained in chromaffin cells. Similarly, immunohistochemical staining of adrenal slices showed that MAO-A was expressed in chromaffin cells located both in the medulla and in intracortical rays. In conclusion, the present study shows that, in the human adrenal cortex, 5-HT, released by mast-cells, may stimulate aldosterone secretion in a paracrine manner. Our data also indicate that 5-HT is metabolized by MAO-A located in intracortical chromaffin cells.
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