Direct Action of Serotonin on Prolactin, Growth Hormone, Corticotropin and Luteinizing Hormone Release in Cocultures of Anterior and Posterior Pituitary Lobes: Autocrine and/or Paracrine Action of Vasoactive Intestinal Peptide

Abstract

There is extensive evidence that serotonin (5-HT) is implicated in the neuroendocrine control regulating the secretion of several anterior pituitary hormones. It has also been reported that the posterior pituitary is necessary for prolactin (PRL) response to 5-HT as well as to suckling, in which 5-HT implication has been demonstrated. As we have previously shown that vasoactive intestinal peptide (VIP) mediates through an autocrine or paracrine action the PRL release induced by insulin-like growth factor I, thyrotropin-releasing hormone (TRH) and dopamine withdrawal, the aim of the present work was to determine whether 5-HT has a direct action on pituitary secretion and to study the possible role of pituitary VIP in this situation. Cells from the anterior pituitary lobe (AP) were cultured either alone or together with cells from the posterior pituitary lobe (PP). As melanotropes from PP express glucocorticoid receptors in vitro, both AP cultures and cocultures of AP/PP cells were incubated in the presence or absence of corticosterone (0.1 µg/ml), thus designing four experimental conditions. Then both AP and mixed cultures were incubated with 5-HT (100 nM) for 20, 45 and 180. The release of PRL, growth hormone (GH), corticotropin (ACTH) and luteinizing hormone (LH) was stimulated by 5-HT, but only in cocultures of AP/PP cells preincubated with corticosterone, whereas follicle-stimulating hormone and thyroid-stimulating hormone release was not modified. As AP cultures did not show any response to 5-HT, both in the presence or absence of corticosterone, and as melanotropes are the main cellular type present in the PP cultures, we studied the response of α-melanocyte-stimulating hormone (αMSH) to 5-HT in PP cells cultured with or without corticosterone. Serotonin did not modify αMSH release either in the absence or the presence of corticosterone. VIP release was also stimulated by 5-HT in the cocultures, and the time response profile was only similar to that of PRL. In order to study whether pituitary VIP is implicated in 5-HT action, cocultures preincubated with corticosterone were incubated in the presence of 5-HT, a VIP-receptor antagonist (VIP-At) or simultaneously with 5-HT plus VIP-At. PRL response to 5-HT was abolished by the simultaneous presence of VIP-At, whereas GH, ACTH and LH response remained unchanged. These data demostrate that: (1) 5-HT stimulates the secretion of PRL, GH, ACTH, LH and VIP acting directly at pituitary level on PP, probably by releasing an unidentified mediator from melanotropes; (2) glucocorticoids make the response of AP cells to 5-HT possible due to the presence of PP cells in the coculture; (3) PRL response to 5-HT is mediated through an autocrine and/or paracrine action of VIP.

Vasoactive Intestinal Peptide Can Modulate Immune and Endocrine Responses during Lipopolysaccharide-Induced Acute Inflammation

“…VIP stimulates the hypothalamus-pituitary axis, and through this mechanism increases secretion by the adrenal cortex. It acts through paracrine and autocrine mechanisms [23,24,36]. This peptide also stimulates the intramedullary CRH/ACTH system in the adrenal cortex and increases adrenal blood flow [23,37].…”

Effect of hydrocortisone on the pituitary response to growth hormone releasing hormone

“…The effects of cortisol on GH release from the pituitary may confound those studies using GH output to measure hypothalamic monoamine function. These effects may occur either directly or via an intermediary, such as 5-HT (Balsa et al 1998). A crucial factor in interpreting such studies is the extent to which subjects had hypercortisolaemia.…”

Identification of 5-hydroxytryptamine receptor gene polymorphisms modulating hyperprolactinaemia in antipsychotic drug-treated patients with schizophrenia

“…Initial studies failed to show a direct stimulatory effect of 5-HT on PRL release from pituitary tissue in vitro (Lamberts and MacLeod 1978;Garthwaite and Hagen 1979). However, later studies showed that stimulation of HTR2 affects PRL release by acting directly at the pituitary gland level (Meltzer et al 1983;Apfelbaum 1987;Balsa et al 1998). Stimulation of HTR2 not only promoted PRL release via the local autoparacrine action of VIP, but also directly by activating HTR2s on lactotrophs (Apfelbaum 1998 Souza (1986) described the presence of 5-HT2 binding sites in all three lobes of the rat pituitary gland.…”