Gonadotropes and Gonadotropin-Releasing Hormone Signaling

McArdle, Craig; Roberson, Mark S.

doi:10.1016/b978-0-12-397175-3.00010-7

Cited by 34 publications

(41 citation statements)

References 739 publications

(918 reference statements)

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“…As pointed out by Herbison (2015), GnRH neurons maintain a high content of their peptide, and it is therefore unlikely that regulation of GNRH1 expression plays a critical role in moment to moment control of either GnRH surges or pulses. GnRH action on the pituitary gonadotroph is mediated by G-protein coupled receptors that signal via Gq and or G 11 to activate phospholipase-C that leads to mobilization of Ca ++ by inositol phosphate3 (McArdle 2015). …”

Section: Gnrh Biosynthesis and Actionmentioning

confidence: 99%

60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-pituitary–gonadal axis

Plant

2015

Journal of Endocrinology

216

125

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This review provides an outline of how our understanding of the neuroendocrine control of the hypothalamo-pituitary–gonadal axis has evolved since the publication of Geoffrey Harris' renowned monograph in 1955. Particular attention is directed to the neurobiology underlying pulsatile GnRH release from the hypothalamus, the neuroendocrine control of ovarian cycles, puberty and seasonality of gonadal function, and to ideas that have emerged as a result of examining the relationship between growth and the reproductive axis. The review closes with i) a brief discussion of how knowledge gained as a result of pursing the early hypotheses of Harris has led to major clinical and therapeutic applications, and ii) a personal glimpse into the future of research in this fascinating area of biology.

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Section: Gnrh Biosynthesis and Actionmentioning

confidence: 99%

60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-pituitary–gonadal axis

Plant

2015

Journal of Endocrinology

216

125

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“…About 70% of the projections of these neurons terminate in the median eminence where GnRH can be released into the hypohyseal portal blood system and act as the central regulator of the HPG axis [32, 33]. The pattern of activity of these GnRH neurons is integral for the increase in release of the gonadotropins, luteinizing hormone (LH) and follicle stimulating hormone (FSH), from the pituitary gland [34]. Thus, activity of GnRH neurons is coupled to release, which is tightly regulated by GABAergic signaling (Han, 2004; Moenter, 2005).…”

Section: Gabaergic Regulation Of the Hpg Axismentioning

confidence: 99%

GABAergic regulation of the HPA and HPG axes and the impact of stress on reproductive function

Melón

Maguire

2016

The Journal of Steroid Biochemistry and Molecular Biology

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The hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) axes are regulated by GABAergic signaling at the level of corticotropin-releasing hormone (CRH) and gonadotropin-releasing hormone (GnRH) neurons, respectively. Under basal conditions, activity of CRH and GnRH neurons are controlled in part by both phasic and tonic GABAergic inhibition, mediated by synaptic and extrasynaptic GABAA receptors (GABAARs), respectively. For CRH neurons, this tonic GABAergic inhibition is mediated by extrasynaptic, δ subunit-containing GABAARs. Similarly, a THIP-sensitive tonic GABAergic current has been shown to regulate GnRH neurons, suggesting a role for δ subunit-containing GABAARs; however, this remains to be explicitly demonstrated. GABAARs incorporating the δ subunit confer neurosteroid sensitivity, suggesting a potential role for neurosteroid modulation in the regulation of the HPA and HPG axes. Thus, stress-derived neurosteroids may contribute to the impact of stress on reproductive function. Interestingly, excitatory actions of GABA have been demonstrated in both CRH neurons at the apex of control of the HPA axis and in GnRH neurons which mediate the HPG axis, adding to the complexity for the role of GABAergic signaling in the regulation of these systems. Here we review the effects that stress has on GnRH neurons and HPG axis function alongside evidence supporting GABAARs as a major interface between the stress and reproductive axes.

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“…However, this paradigm cannot be generally applied to GnRHR because type I mammalian GnRHR do not have COOH-terminal tails (16,17,30) and are therefore thought not to undergo agonist-induced phosphorylation or rapid homologous receptor desensitization (31-39). Nevertheless, there are multiple downstream negative feedback mechanisms shaping cellular responses to GnRH, and effects of GnRH on ERK, Ca 2+ and gonadotropin secretion do characteristically desensitize on constant stimulation (3,5,22,(40)(41)(42)(43). The situation with GnRH is more complicated however, because physiologically GnRH secretion is pulsatile and this pulsatility is essential for reproduction.…”

mentioning

confidence: 96%

“…Several Ca 2+ -regulated proteins are activated by GnRH and can also mediate transcriptional effects of GnRH. These include not only the conventional isoforms of PKC, but also the ubiquitous Ca 2+ sensor calmodulin (CaM), as well as calmodulin-dependent protein kinases (CaMK), the calmodulin dependent phosphatase calcineurin, and one of its major effectors, the Ca 2+ dependent transcription factor NFAT (nuclear factor of activated T-cells) (3,13,14). This brief overview omits *Manuscript Click here to view linked References many known components of the GnRH signaling network, which are reviewed in more detail elsewhere (1)(2)(3)(4)9,10,(15)(16)(17)(18)(19)(20)(21)(22)(23)(24).…”

mentioning

confidence: 99%

Gonadotropin-releasing hormone signaling: An information theoretic approach

Voliotis

Garner

Alobaid

et al. 2018

Molecular and Cellular Endocrinology

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Gonadotropin-releasing hormone (GnRH) is a peptide hormone that mediates central control of reproduction, acting via G-protein coupled receptors that are primarily G coupled and mediate GnRH effects on the synthesis and secretion of luteinizing hormone and follicle-stimulating hormone. A great deal is known about the GnRH receptor signaling network but GnRH is secreted in short pulses and much less is known about how gonadotropes decode this pulsatile signal. Similarly, single cell measures reveal considerable cell-cell heterogeneity in responses to GnRH but the impact of this variability on signaling is largely unknown. Ordinary differential equation-based mathematical models have been used to explore the decoding of pulse dynamics and information theory-derived statistical measures are increasingly used to address the influence of cell-cell variability on the amount of information transferred by signaling pathways. Here, we describe both approaches for GnRH signaling, with emphasis on novel insights gained from the information theoretic approach and on the fundamental question of why GnRH is secreted in pulses.

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Gonadotropes and Gonadotropin-Releasing Hormone Signaling

Cited by 34 publications

References 739 publications

60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-pituitary–gonadal axis

60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-pituitary–gonadal axis

GABAergic regulation of the HPA and HPG axes and the impact of stress on reproductive function

Gonadotropin-releasing hormone signaling: An information theoretic approach

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