Serotoninergic regulation of corticosterone secretion in domestic fowl

Abstract

The effects of serotoninergic drugs on adrenocortical function in domestic fowl were examined. Administration of the serotonin receptor agonist 2-(1-piperazinyl)quinoline maleate (quipazine), an inhibitor of serotonin metabolism, N-methyl-N-2-propynylbenzylamine HCl (pargyline), as well as serotonin itself, all increased plasma concentrations of corticosterone. The maximum responses to serotonin and quipazine occurred 1 h after treatment. The quipazine-stimulated response was partly prevented by the serotonin antagonist cyproheptadine. Cockerels pretreated with dexamethasone, a synthetic steroid known to inhibit pituitary ACTH release, showed attenuated responses to subsequent quipazine, pargyline or serotonin injection. Serotonin, quipazine and cyproheptadine did not affect corticosterone release directly from the adrenal gland incubated in vitro, nor did they affect adrenal responsiveness to ACTH stimulation. The neurotoxin 5,6-dihydroxytryptamine injected into day-old chicks decreased plasma concentrations of corticosterone for up to 7 days after treatment, with corresponding decreases in the hypothalamic concentration of serotonin, but not dopamine or noradrenaline concentrations. These results show that adrenal corticosterone secretion is regulated by a central serotoninergic system, probably acting on the hypothalamo-pituitary-adrenal axis.

Inflammatory mediator-induced hypothalamic-pituitary-adrenal axis activation is defective in streptococcal cell wall arthritis-susceptible Lewis rats.

“…The greater LEW/N corticosterone response to quipazine compared to IL-la may result from the multiple pathways through which 5-HT and 5-HT agonists may stimulate the HPA axis since 5-HT is both a major CRH and a potent ACTH secretagogue (16)(17)(18)(19)(20)(21)(22)(23). The physiologic relevance of such a potential route of 5-HT stimulation of the HPA axis is, however, not clear, since it would be dependent on adequate systemic concentrations of 5-HT released from platelets during inflammation reaching central sites.…”

Platelet serotonin-binding and dexamethasone suppression test in melancholia and dysthymia

“…Although some reports have suggested that serotonergic mechanisms may be involved in the regulation of adrenal corticosterone secretion, the relationship between the serotonergic system and the hypothalamo-pituitary-adrenocortical axis (IIPAA) is still unclear. Some studies seem to support the fact that serotonergic agonists increase HPAA activity (Fuller, 1981;Cheung et al, 1986), while other studies have found an association between low cerebrospinal fluid 5-hydroxyindoleacetic acid and high HPAA activity (Stokes et al, 1987). Conversely, it has also been suggested that the pituitary-adrenal endocrine system may act on serotonergic neurons within specific hypothalamic sites (Jhanwar-Uniyal et al, 1987).…”