Direct effects of prolactin and dopamine on the gonadotroph response to GnRH

Henderson, Helen L.; Townsend, Julie; Tortonese, Domingo J.

doi:10.1677/joe-07-0536

Cited by 46 publications

(33 citation statements)

References 50 publications

(36 reference statements)

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“…We observed a clear dose-response curve (data not shown), with maximal stimulation at 10 Ϫ8 M (Fig. 8), consistent with previous reports (49). We then examined the inhibitory effect of mRFRP at concentrations of 10 Ϫ7 to 10 8-CPT-cAMP (a cell-permeable cAMP analog) for 10 min.…”

Section: Inhibitory Effect Of Mrfrp On Lh Releasesupporting

confidence: 88%

Gonadotropin-Inhibitory Hormone Inhibits GnRH-Induced Gonadotropin Subunit Gene Transcriptions by Inhibiting AC/cAMP/PKA-Dependent ERK Pathway in LβT2 Cells

et al. 2012

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A neuropeptide that directly inhibits gonadotropin secretion from the pituitary was discovered in quail and named gonadotropin-inhibitory hormone (GnIH). The presence and functional roles of GnIH orthologs, RF-amide-related peptides (RFRP), that possess a common C-terminal LPXRF-amide (X ϭ L or Q) motif have also been demonstrated in mammals. GnIH orthologs inhibit gonadotropin synthesis and release by acting on pituitary gonadotropes and GnRH neurons in the hypothalamus via its receptor (GnIH receptor). It is becoming increasingly clear that GnIH is an important hypothalamic neuropeptide controlling reproduction, but the detailed signaling pathway mediating the inhibitory effect of GnIH on target cells is still unknown. In the present study, we investigated the pathway of GnIH cell signaling and its possible interaction with GnRH signaling using a mouse gonadotrope cell line, L␤T2. First, we demonstrated the expression of GnIH receptor mRNA in L␤T2 cells by RT-PCR. We then examined the inhibitory effects of mouse GnIH orthologs [mouse RFRP (mRFRP)] on GnRH-induced cell signaling events. We showed that mRFRP effectively inhibited GnRH-induced cAMP signaling by using a cAMP-sensitive reporter system and measuring cAMP levels, indicating that mRFRP function as an inhibitor of adenylate cyclase. We further showed that mRFRP inhibited GnRH-stimulated ERK phosphorylation, and this effect was mediated by the inhibition of the protein kinase A pathway. Finally, we demonstrated that mRFRP inhibited GnRHstimulated gonadotropin subunit gene transcriptions and also LH release. Taken together, the results indicate that mRFRP function as GnIH to inhibit GnRH-induced gonadotropin subunit gene transcriptions by inhibiting adenylate cyclase/cAMP/protein kinase A-dependent ERK activation in L␤T2 cells. (Endocrinology 153: 2332-2343, 2012)

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Section: Inhibitory Effect Of Mrfrp On Lh Releasesupporting

confidence: 88%

Gonadotropin-Inhibitory Hormone Inhibits GnRH-Induced Gonadotropin Subunit Gene Transcriptions by Inhibiting AC/cAMP/PKA-Dependent ERK Pathway in LβT2 Cells

et al. 2012

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“…Prolactin (PRL), the hormone product of lactotroph cells, acts on gonadotrophs cells to modulate the secretion of LH (Cheung 1983, Hodson et al 2010a. Lactotrophs are also estrogen sensitive, and gonadotrophs express PRL receptors (Henderson et al 2008). This evidence further signifies that, in addition to their function in the gonadotroph cells, the genes presented in this study may further modify the LH surge through their actions in lactotroph physiology.…”

Section: Discussionsupporting

confidence: 52%

Identification of estradiol/ERα-regulated genes in the mouse pituitary

Kim¹,

Gieske²,

Trudgen³

et al. 2011

Journal of Endocrinology

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Estrogen acts to prime the pituitary prior to the GnRHinduced LH surge by undiscovered mechanisms. This study aimed to identify the key components that mediate estrogen action in priming the pituitary. RNA extracted from the pituitaries of metestrous (low estrogen) and proestrus (high estrogen) stage mice, as well as from ovariectomized wildtype and estrogen receptor a (ERa) knockout mice treated with 17b-estradiol (E 2 ) or vehicle, was used for gene expression microarray. Microarray data were then aggregated, built into a functional electronic database, and used for further characterization of E 2 /ERa-regulated genes. These data were used to compile a list of genes representing diverse biological pathways that are regulated by E 2 via an ERa-mediated pathway in the pituitary. This approach substantiates ERa regulation of membrane potential regulators and intracellular vesicle transporters, among others, but not the basic components of secretory machinery. Subsequent characterization of six selected genes (Cacna1a, Cacna1g, Cited1, Abep1, Opn3, and Kcne2) confirmed not only ERa dependency for their pituitary expression but also the significance of their expression in regulating GnRH-induced LH secretion. In conclusion, findings from this study suggest that estrogen primes the pituitary via ERa by equipping pituitary cells with critical cellular components that potentiate LH release on subsequent GnRH stimulations.

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“…The most probable mechanism of noncycling caused by high levels of serum PRL is inhibition of gonadotropin releasing hormone (GnRH) secretion by a PRL-induced increase in dopamine secretion [6]. A previous paper reported that the LH mRNA response to GnRH was suppressed by PRL [18]. Moreover, PRL inhibits the expression of LH receptors (LH-R) in rats in a dose-dependent manner in granulosa cells treated with FSH [20].…”

Section: Discussionmentioning

confidence: 99%

Prolactin Secretion and Ovarian Function in Cycling and Non-Cycling African Female Elephants (Loxodonta africana)

Yamamoto

Watanabe

et al. 2010

J. Vet. Med. Sci.

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ABSTRACT. Reproduction of captive elephants in zoos has shown a low fecundity and requires improvement. One of the reasons for low fecundity is ovarian dysfunction in many female elephants. To investigate whether prolactin has a correlation with ovarian function in female elephants, the serum concentrations of prolactin, progesterone and estradiol-17 in four African female elephants (one cycling female and three non-cycling female elephants) were measured. Cyclic patterns of prolactin and estradiol-17 were observed in the cycling female elephant, which tended to be high during the follicular phase and low during the luteal phase. On the other hand, a cyclic pattern of prolactin was not observed in the non-cycling female elephants. One of the three non-cycling females (Mako) had developed breasts and showed significantly higher average levels of prolactin than the other female elephants. These results suggested that high concentrations of circulating estradiol-17 during the follicular phase stimulated prolactin secretion. They also suggested that hyperprolactinemia in Mako was one of the causes of the developed mammary glands and ovarian dysfunction.

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Direct effects of prolactin and dopamine on the gonadotroph response to GnRH

Cited by 46 publications

References 50 publications

Gonadotropin-Inhibitory Hormone Inhibits GnRH-Induced Gonadotropin Subunit Gene Transcriptions by Inhibiting AC/cAMP/PKA-Dependent ERK Pathway in LβT2 Cells

Gonadotropin-Inhibitory Hormone Inhibits GnRH-Induced Gonadotropin Subunit Gene Transcriptions by Inhibiting AC/cAMP/PKA-Dependent ERK Pathway in LβT2 Cells

Identification of estradiol/ERα-regulated genes in the mouse pituitary

Prolactin Secretion and Ovarian Function in Cycling and Non-Cycling African Female Elephants (Loxodonta africana)

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