Progress and Challenges in the Search for the Mechanisms of Pulsatile Gonadotropin-Releasing Hormone Secretion

Constantin, Stéphanie

doi:10.3389/fendo.2017.00180

Cited by 26 publications

(14 citation statements)

References 146 publications

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“…These explant models: (1) contain a large number of primary GnRH neurons, olfactory sensory neurons and OECs; (2) allow one to perform single cell tracing and imaging; (3) are accessible to both molecular and pharmacological manipulations (Figure 3) (Wray et al, 1994; Klenke and Taylor-Burds, 2012). Although no brain is present, the GnRH cells mature in this model with respect to both processing of the peptide, extension of processes and cellular properties (Wray et al, 1994; Klenke and Taylor-Burds, 2012; Constantin, 2017), suggesting that the cells in explants are equivalent to their counterparts in vivo , aging appropriate. In explants generated from mice, olfactory axon outgrowth, OEC migration and GnRH cell migration occur between days 1 and 7 (Wray et al, 1996).…”

Section: Migration Of Gnrh Neurons From the Nose To The Brainmentioning

confidence: 86%

Nasal Placode Development, GnRH Neuronal Migration and Kallmann Syndrome

Cho

Shan

Whittington

et al. 2019

Front. Cell Dev. Biol.

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The development of Gonadotropin releasing hormone-1 (GnRH) neurons is important for a functional reproduction system in vertebrates. Disruption of GnRH results in hypogonadism and if accompanied by anosmia is termed Kallmann Syndrome (KS). From their origin in the nasal placode, GnRH neurons migrate along the olfactory-derived vomeronasal axons to the nasal forebrain junction and then turn caudally into the developing forebrain. Although research on the origin of GnRH neurons, their migration and genes associated with KS has identified multiple factors that influence development of this system, several aspects still remain unclear. This review discusses development of the olfactory system, factors that regulate GnRH neuron formation and development of the olfactory system, migration of the GnRH neurons from the nose into the brain, and mutations in humans with KS that result from disruption of normal GnRH/olfactory systems development.

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Section: Migration Of Gnrh Neurons From the Nose To The Brainmentioning

confidence: 86%

Nasal Placode Development, GnRH Neuronal Migration and Kallmann Syndrome

Cho

Shan

Whittington

et al. 2019

Front. Cell Dev. Biol.

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“…Independent of location, the majority of GnRH cells send their processes to the median eminence, where GnRH is secreted into the portal capillary system. When secretion of the GnRH peptide is pulsatile, gonadotropes of the anterior pituitary are activated and gonadal steroids released (Constantin, 2017;Shan and Wray, 2018). A dual origin for GnRH neuroendocrine cells has been proposed from studies in both zebrafish and mice (Whitlock et al, 2003;Forni et al, 2011).…”

Section: Discussion and Summarymentioning

confidence: 99%

Heterogeneous Origin of Gonadotropin Releasing Hormone-1 Neurons in Mouse Embryos Detected by Islet-1/2 Expression

Shan

Saadi

Wray

2020

Front. Cell Dev. Biol.

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In vertebrates, Gonadotropin releasing hormone-1 (GnRH) neuroendocrine cells originate in the olfactory placode and migrate into the forebrain where they regulate reproduction. However, the embryonic lineage of their progenitors remains controversial. Most GnRH neurons are derived from placodal ectodermal progenitor cells, but data from lineage tracing in zebrafish (Whitlock et al., 2003) and mouse (Forni and Wray, 2012) indicate that some GnRH progenitor cells have a neural crest (NC) origin. In contrast, a recent study in zebrafish (Aguillon et al., 2018), using Islet-1/2 expression, identified this LIM-homeodomain protein in all developing GnRH neuroendocrine cells, and the authors concluded a homogenous origin from progenitors within the preplacodal ectoderm. Evidence in different animal models and systems suggests that expression of Islet-1 plays a pivotal role in cell fate specification and differentiation. Thus, expression of Islet-1/2 in all GnRH cells in the nasal placode may not be lineage dependent but rather initiated locally in the placode as part of the program for GnRH cell specification and/or differentiation. This study addresses this issue and shows two populations of olfactory derived GnRH neurons in embryonic mouse: Islet-1/2(+) and Islet-1/2(−). Notably, triple-label immunofluorescence using the NC lineage tracer Wnt1, showed that GnRH neurons derived from Wnt1 progenitors are Islet-1/2(−). These results are consistent with two separate origins of GnRH neuroendocrine cells and suggest that either (1) NC-derived GnRH cells differentiate earlier than PE-derived GnRH cells or (2) different programs are used for cell specification in NC-vs. PE-derived GnRH cells.

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“…Kisspeptin, a C-terminally amidated neuropeptide and endogenous ligand of metabotropic Kiss1R (GPRS54) receptor plays an essential role in the hypophyseal regulation of the ovarian cycle (Constantin 2017, Navarro et al 2015. The core molecule kisspeptin-54 is proteolytically cleaved into several smaller peptides kisspeptin-13 and 14 ( Fig.1.).…”

Section: Kisspeptin In Anxiety Responses Depression and Anorexia Nermentioning

confidence: 99%

The potential role of the novel hypothalamic neuropeptides nesfatin-1, phoenixin, spexin and kisspeptin in the pathogenesis of anxiety and anorexia nervosa

Pałasz

Janas–Kozik

Borrow

et al. 2018

Neurochemistry International

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Due to the dynamic development of molecular neurobiology and bioinformatic methods several novel brain neuropeptides have been identified and characterized in recent years. Contemporary techniques of selective molecular detection e.g. in situ Real-Time PCR, microdiffusion and some bioinformatics strategies that base on searching for single structural features common to diverse neuropeptides such as hidden Markov model (HMM) have been successfully introduced. A convincing majority of neuropeptides have unique properties as well as a broad spectrum of physiological activity in numerous neuronal pathways including the hypothalamus and limbic system. The newly discovered but uncharacterized regulatory factors nesfatin-1, phoenixin, spexin and kisspeptin have the potential to be unique modulators of stress responses and eating behaviour. Accumulating basic studies revelaed an intriguing role of these neuropeptides in the brain pathways involved in the pathogenesis of anxiety behaviour. Nesfatin-1, phoenixin, spexin and kisspeptin may also distinctly affect the energy homeostasis and modulate food intake not only at the level of hypothalamic centres. Moreover, in patients suffered from anxiety and anorexia nervosa a significant, sex-related changes in the plasma neuropeptide levels occurred. It should be therefore taken into account that the targeted pharmacomodulation of central peptidergic signaling may be potentially helpful in the future treatment of certain neuropsychiatric and metabolic disorders. This article reviews recent evidence dealing with the hypothetical role of these new factors in the anxiety-related circuits and pathophysiology of anorexia nervosa.

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Progress and Challenges in the Search for the Mechanisms of Pulsatile Gonadotropin-Releasing Hormone Secretion

Cited by 26 publications

References 146 publications

Nasal Placode Development, GnRH Neuronal Migration and Kallmann Syndrome

Nasal Placode Development, GnRH Neuronal Migration and Kallmann Syndrome

Heterogeneous Origin of Gonadotropin Releasing Hormone-1 Neurons in Mouse Embryos Detected by Islet-1/2 Expression

The potential role of the novel hypothalamic neuropeptides nesfatin-1, phoenixin, spexin and kisspeptin in the pathogenesis of anxiety and anorexia nervosa

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