Paracrine cell to cell interactions determine the effects of pituitary adenylate cyclase activating polypeptide (PACAP) on in vitro prolactin release from rat pituitary cells

Benter, S; Leonhardt, Sabine; Wuttke, W.; Jarry, H.

doi:10.1055/s-0029-1211383

Cited by 14 publications

(11 citation statements)

References 8 publications

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“…In contrast, other studies have shown that PACAP can either slightly increase (Arbogast and Voogt, 1994) or inhibit ) PRL release from rat pituitary cells. To elucidate the origin of these apparent discrepancies, the effects of PACAP on PRL secretion have been compared in cultures of dispersed or aggregated cells and in pituitary fragments (Benter et al, 1995). In monolayer cultures, PRL release was inhibited by PACAP, whereas in cultures of aggregated cells and in pituitary fragments, PRL output was stimulated (Benter et al, 1995).…”

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confidence: 99%

“…To elucidate the origin of these apparent discrepancies, the effects of PACAP on PRL secretion have been compared in cultures of dispersed or aggregated cells and in pituitary fragments (Benter et al, 1995). In monolayer cultures, PRL release was inhibited by PACAP, whereas in cultures of aggregated cells and in pituitary fragments, PRL output was stimulated (Benter et al, 1995). These data suggest that cell-to-cell communication plays a crucial role in determining the type of action of PACAP on PRL secretion.…”

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confidence: 99%

“…Likewise, PACAP increases cAMP level and stimulates secretion of vascular endothelial growth factor, novel neurotrophin-1/B-cell-stimulating factor-3, and IL-6 in PITUITARY ADENYLATE CYCLASE-ACTIVATING POLYPEPTIDE the mouse folliculostellate-like cell line TtT/GF Gloddek et al, 1999;Lohrer et al, 2001;Vlotides et al, 2004). Because IL-6 is involved in the differentiation of pituitary cells (Renner et al, 1998) and because it stimulates the release of various adenohypophysial hormones (Renner et al, 1998), several indirect effects of PACAP on endocrine pituitary cells may be mediated through activation of folliculostellate cells (Benter et al, 1995). In support of this notion, PACAP, added on cocultures of TtT/GF folliculostellate cells with rat anterior pituitary cells, significantly reduces the effect of activin-A on FSH secretion through follistatin release (Katayama et al, 2000).…”

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Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

et al. 2009

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Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

et al. 2009

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“…Similarly, in ovine and bovine pituitary cells, PACAP had no effect on prolactin release [70,71]. Conversely, other studies demonstrated the stimulating effect of PACAP on prolactin release [72,73]. In prolactin-producing model GH3 cells that originate from rat pituitary somatolactotrophs, PACAP increases the synthesis and secretion of prolactin with a concomitant activation of ERK and cAMP/PKA pathways [74].…”

Section: Prolactin Synthesis and Secretion From Pituitary Lactotrophsmentioning

confidence: 99%

Interactions between Two Different G Protein-Coupled Receptors in Reproductive Hormone-Producing Cells: The Role of PACAP and Its Receptor PAC1R

Kanasaki

Oride

Hara

et al. 2016

IJMS

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Gonadotropin-releasing hormone (GnRH) and gonadotropins are indispensable hormones for maintaining female reproductive functions. In a similar manner to other endocrine hormones, GnRH and gonadotropins are controlled by their principle regulators. Although it has been previously established that GnRH regulates the synthesis and secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH)—both gonadotropins—from pituitary gonadotrophs, it has recently become clear that hypothalamic GnRH is under the control of hypothalamic kisspeptin. Prolactin, which is also known as luteotropic hormone and is released from pituitary lactotrophs, stimulates milk production in mammals. Prolactin is also regulated by hypothalamic factors, and it is thought that prolactin synthesis and release are principally under inhibitory control by dopamine through the dopamine D2 receptor. In addition, although it remains unknown whether it is a physiological regulator, thyrotropin-releasing hormone (TRH) is a strong secretagogue for prolactin. Thus, GnRH, LH and FSH, and prolactin are mainly regulated by hypothalamic kisspeptin, GnRH, and TRH, respectively. However, the synthesis and release of these hormones is also modulated by other neuropeptides in the hypothalamus. Pituitary adenylate cyclase-activating polypeptide (PACAP) is a hypothalamic peptide that was first isolated from sheep hypothalamic extracts based on its ability to stimulate cAMP production in anterior pituitary cells. PACAP acts on GnRH neurons and pituitary gonadotrophs and lactotrophs, resulting in the modulation of their hormone producing/secreting functions. Furthermore, the presence of the PACAP type 1 receptor (PAC1R) has been demonstrated in these cells. We have examined how PACAP and PAC1R affect GnRH- and pituitary hormone-secreting cells and interact with their principle regulators. In this review, we describe our understanding of the role of PACAP and PAC1R in the regulation of GnRH neurons, gonadotrophs, and lactotrophs, which are regulated mainly by kisspeptin, GnRH, and TRH, respectively.

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“…PACAP effects on PRL release are controversial and depend on the test system used (207–211). Whereas PACAP inhibits PRL release in monolayer cell cultures, it stimulates release in aggregate cell cultures and in vivo (207, 212). In studies where a stimulation of PRL release by PACAP was found in monolayer culture, the effect is probably on PRL gene expression and translation as it was only found after several hours of treatment (213).…”

Section: Gonadotrophs Signal To Lactotrophs Somatotrophs and Corticomentioning

confidence: 99%

Endogenous Cannabinoids: Structure and Metabolism

Bisogno

2008

J Neuroendocrinology

144

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D9 -Tetrahydrocannabinol (THC), the main psychoactive compound extracted from Cannabis sativa, is the most representative component of the mixture of therapeutic substances that are communally referred to as cannabinoids (1). It acts as an agonist at specific G-protein-coupled receptors, cannabinoid receptor subtypes CB 1 and CB 2 (2). The discovery of cannabinoid receptors has driven the investigation of the existence of their natural ligands and, soon after, endocannabinoids were identified. N-arachidonoyl-ethanolamine (AEA, anandamide) and 2-arachidonoyl glycerol (2-AG) are the two most studied endocannabinoids. They are biosynthesised 'on demand' by cleavage of their membrane lipid precursors N-arachidonoyl-phosphatidylethanolamine (N-ArPE) and sn-1-acyl-2-arachidonoylglycerols (DAGs) respectively, and then inactivated by intracellular hydrolysing enzymes. Cannabinoid receptors, endocannabinoids and enzymes that biosynthesise [N-acyl-phosphatidylethanolamine-selective phospholipase D (NAPE-PLD) and diacylglycerol lipase (DAGL)] and degrade [fatty acid amide hydrolase (FAAH) and the monoacylglycerol lipases (MAGL)] AEA and 2-AG, respectively, are key components in the endocannabinoid system (3). Despite a large number of excellent studies having contributed to the current understanding of the endocannabinoid regulation and function, further efforts are necessary to fully comprehend this signalling system. Here, a review on the current knowledge on structure and metabolism of the best studied endogenous cannabinoids is presented. In particular, this review concentrates on the mechanisms responsible for the biosynthesis and inactivation of the endocannabinoids, as well as on the several inhibitors of their metabolism identified to date. Endocannabinoids and related N-acyl-ethanolaminesEndocannabinoids are defined as endogenous compounds capable of binding to and functionally activating cannabinoid receptors. At least five endocannabinoids have been identified to date (Fig. 1). Anandamide, the amide between arachidonic acid and ethanolamine, was the first endogenous ligand to be reported at the end of 1992 (4) and additional polyunsaturated ethanolamines that bind to cannabinoid receptors, homolinolenylethanolamide and docosatetraenylethanolamide, have been isolated in the brain. Other endocannabinoids, all derived from arachidonic acid, were identified. The identification of 2-AG, the ester of arachidonic acid with glycerol, isolated from canine gut and brain has also been reported (5, 6). Subsequently, the first endocannabinoid characterised by ether bond, 2-arachidonyl glyceryl ether or noladin ether, was isolated from porcine brain (7) and N-arachidonoyldopamine (NADA), a selective CB 1 agonist and a potent agonist of vanilloid receptors, was discovered (8, 9). O-arachidonoylethanolamine, the ester derivative of ethanolamine with arachidonic acid, with the same molecular weight as anandamide but with opposite orientation of the polar ethanolamine moiety, was named virodhamine from the Sanskrit word virodha, ...

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Paracrine cell to cell interactions determine the effects of pituitary adenylate cyclase activating polypeptide (PACAP) on in vitro prolactin release from rat pituitary cells

Cited by 14 publications

References 8 publications

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

Interactions between Two Different G Protein-Coupled Receptors in Reproductive Hormone-Producing Cells: The Role of PACAP and Its Receptor PAC1R

Endogenous Cannabinoids: Structure and Metabolism

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