Role of Glia in the Regulation of Gonadotropin-Releasing Hormone Neuronal Activity and Secretion

Sharif, Ariane; Baroncini, Marc; Prévot, Vincent

doi:10.1159/000351867

Cited by 58 publications

(54 citation statements)

References 110 publications

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“…), including the ependymoglial cell tanycytes . Previous studies have shown the importance of the plastic interaction between tanycytes, endothelial cells and GnRH varicosities in the regulation of the HPG axis function. The present data suggest that such neurone/glia/vascular interactions are influenced by the metabolic status of animals affects the HPG axis.…”

Section: Discussionsupporting

confidence: 64%

Alteration in the relationship between tanycytes and gonadotrophin‐releasing hormone neurosecretory terminals following long‐term metabolic manipulation in the sheep

Neto

Clarke

Conductier

2017

J Neuroendocrinology

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The activity of the hypothalamic-pituitary gonadal axis is influenced by energy reserves, such that an increase or a decrease in adiposity may perturb the secretion and action of gonadotrophin-releasing hormone (GnRH). This is considered to be a result of the signalling of hormones such as leptin, which act upon neuronal systems controlling GnRH secretion. Other work shows plasticity in the relationship between tanycytes and GnRH neurosecretory terminals in the median eminence across the oestrous cycle and we hypothesised that a similar plasticity may occur with altered metabolic status. We studied Lean, Normal and Fat ovariectomised ewes, which displayed differences in gonadotrophin status, and investigated the relationship between tanycytes and GnRH neuroterminals. Under both Lean and Fat conditions, an altered anatomical arrangement between these two elements was observed in the vicinity of the blood vessels of the primary plexus of the hypophysial portal blood system. These data suggest that such plasticity is an important determinant of the rate of secretion of GnRH in animals of differing metabolic status and that this also contributes to the relative hypogonadotrophic condition prevailing with metabolic extremes.

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Section: Discussionsupporting

confidence: 64%

Alteration in the relationship between tanycytes and gonadotrophin‐releasing hormone neurosecretory terminals following long‐term metabolic manipulation in the sheep

Neto

Clarke

Conductier

2017

J Neuroendocrinology

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“…There is now a growing body of evidence indicating that cell-cell interactions involving nonneuronal cells such as vascular endothelial cells, astrocytes and specialized ependymoglial cells named tanycytes, which ensheathe the terminals of GnRH neurons, might be of critical importance in the regulation of GnRH secretion [123,124,125,126] (fig. 4a).…”

Section: Semaphorins and Neuroglial Plasticity In The Adult Hypothalamentioning

confidence: 99%

Shaping the Reproductive System: Role of Semaphorins in Gonadotropin-Releasing Hormone Development and Function

Giacobini¹

2015

Neuroendocrinology

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The semaphorin proteins, which contribute to the morphogenesis and homeostasis of a wide range of systems, are among the best-studied families of guidance cues. Much recent research has focused on the role of semaphorins in the development and adult activity of hormone systems and, reciprocally, how circulating reproductive hormones regulate their expression and function. Specifically, several reports have focused on the molecular mechanisms underlying the effects of semaphorins on the migration, survival and structural and functional plasticity of neurons that secrete gonadotropin-releasing hormone (GnRH), essential for the acquisition and maintenance of reproductive competence in mammals. Alterations in the development of this neuroendocrine system lead to anomalous or absent GnRH secretion, resulting in heterogeneous reproductive disorders such as congenital hypogonadotropic hypogonadism (CHH) or other conditions characterized by infertility or subfertility. This review summarizes current knowledge of the role of semaphorins and their receptors on the development, differentiation and plasticity of the GnRH system. In addition, the involvement of genetic deficits in semaphorin signaling in some forms of CHH in humans is discussed.

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“…R esearch over many years has indicated that a wide variety of classical neurotransmitters, neuropeptides, and other signaling molecules can modulate the activity of GnRH neurons to control gonadotropin secretion (1,2). Even though some transmitters, such as kisspeptin, are widely acknowledged as being of critical importance to GnRH neuron behavior, the functional hierarchy of most inputs remain unknown.…”

mentioning

confidence: 99%

RF9 Excitation of GnRH Neurons Is Dependent Upon Kiss1r in the Adult Male and Female Mouse

Liu

Herbison

2014

Endocrinology

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The neuropeptide FF receptor antagonist 1-adamantanecarbonyl-Arg-Phe-NH2 trifluoroacetate salt (RF9) has been found to be a remarkably potent activator of gonadotropin secretion in mammals. However, the mechanism of RF9 action on the reproductive axis is unknown. Using acute brain slice electrophysiology in genetically modified mouse models, we have investigated the possibility that RF9 may activate GnRH neurons. In transgenic GnRH-GFP male and female mice, RF9 was found to exert potent, dose-dependent, stimulatory effects on the firing rate of approximately 70% of GnRH neurons. These effects occurred directly on GnRH neurons and were independent of fast amino acid transmission. To assess RF9's action as an neuropeptide FF receptor antagonist at the GnRH neuron, its ability to antagonize the inhibitory effects of RFamide-related peptide-3 on GnRH neuron firing was examined. RF9 exhibited variable ability to prevent the inhibitory effects of RFamide-related peptide-3 on GnRH neurons. Whole-cell recordings from GnRH neurons showed that RF9 generated an inward current in GnRH neurons reminiscent of that evoked by kisspeptin. We therefore examined RF9 actions in kisspeptin receptor knockout mice. RF9 was found to have no effects at all on GnRH neurons in GnRH-GFP;Kiss1r-null mice, although these cells exhibited normal intrinsic electrical properties and remained responsive to GABA and glutamate. This study reveals that RF9 directly activates GnRH neurons in the mouse and that this is dependent upon Kiss1r expression.

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Role of Glia in the Regulation of Gonadotropin-Releasing Hormone Neuronal Activity and Secretion

Cited by 58 publications

References 110 publications

Alteration in the relationship between tanycytes and gonadotrophin‐releasing hormone neurosecretory terminals following long‐term metabolic manipulation in the sheep

Alteration in the relationship between tanycytes and gonadotrophin‐releasing hormone neurosecretory terminals following long‐term metabolic manipulation in the sheep

Shaping the Reproductive System: Role of Semaphorins in Gonadotropin-Releasing Hormone Development and Function

RF9 Excitation of GnRH Neurons Is Dependent Upon Kiss1r in the Adult Male and Female Mouse

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