ArticleEndocrinology2009
Kisspeptin-10 facilitates a plasma membrane-driven calcium oscillator in gonadotropin-releasing hormone-1 neurons.
Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- Kisspeptins in human reproduction-future therapeutic potential.Journal of assisted reproduction and genetics · 2012Pooled it
- Physiological roles of phosphoinositides and inositol phosphates: Implications for metabolic dysfunction-associated steatotic liver disease.Clinical science (London, England : 1979) · 2025Review
- Effect of CPP-related genes on GnRH secretion and Notch signaling pathway during puberty.Biomedical journal · 2023Review
- Acetylcholine regulation of GnRH neuronal activity: A circuit in the medial septum.Frontiers in endocrinology · 2023Article
- Estrogenic regulation of reproduction and energy homeostasis by a triumvirate of hypothalamic arcuate neurons.Journal of neuroendocrinology · 2022Review
- The electrophysiologic properties of gonadotropin-releasing hormone neurons.Journal of neuroendocrinology · 2022Review
- Hypothalamic Kisspeptin Neurons and the Control of Homeostasis.Endocrinology · 2022Review
- Physiological Characterization and Transcriptomic Properties of GnRH Neurons Derived From Human Stem Cells.Endocrinology · 2021Article
- Review
- Nitric oxide resets kisspeptin-excited GnRH neurons via PIP2 replenishment.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Puberty, A Sensitive Window of Hypothalamic Development and Plasticity.Endocrinology · 2021Review
- Mechanism of pulsatile GnRH release in primates: Unresolved questions.Molecular and cellular endocrinology · 2019Review
- Membrane-initiated estrogen signaling via Gq-coupled GPCR in the central nervous system.Steroids · 2019Review
- Effect of Kisspeptin on the Developmental Competence and Early Transcript Expression in Porcine Oocytes Parthenogenetically Activated with Different Methods.BioMed research international · 2018Article
- Spike and Neuropeptide-Dependent Mechanisms Control GnRH Neuron Nerve Terminal CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Progress and Challenges in the Search for the Mechanisms of Pulsatile Gonadotropin-Releasing Hormone Secretion.Frontiers in endocrinology · 2017Review
- Galanin Activates G Protein Gated Inwardly Rectifying Potassium Channels and Suppresses Kisspeptin-10 Activation of GnRH Neurons.Endocrinology · 2016Article
- Hypothalamic control of the male neonatal testosterone surge.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- Comprehensive Review on Kisspeptin and Its Role in Reproductive Disorders.Endocrinology and metabolism (Seoul, Korea) · 2015Review
- Membrane-initiated non-genomic signaling by estrogens in the hypothalamus: cross-talk with glucocorticoids with implications for behavior.Frontiers in endocrinology · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Kisspeptins, the natural ligands of the G-protein-coupled receptor (GPR)-54, are the most potent stimulators of GnRH-1 secretion and as such are critical to reproductive function. However, the mechanism by which kisspeptins enhance calcium-regulated neuropeptide secretion is not clear. In the present study, we used GnRH-1 neurons maintained in mice nasal explants to examine the expression and signaling of GPR54. Under basal conditions, GnRH-1 cells exhibited spontaneous baseline oscillations in intracellular calcium concentration ([Ca(2+)](i)), which were critically dependent on the operation of voltage-gated, tetrodotoxin (TTX)-sensitive sodium channels and were not coupled to calcium release from intracellular pools. Activation of native GPR54 by kisspeptin-10 initiated [Ca(2+)](i) oscillations in quiescent GnRH-1 cells, increased the frequency of calcium spiking in oscillating cells that led to summation of individual spikes into plateau-bursting type of calcium signals in a subset of active cells. These changes predominantly reflected the stimulatory effect of GPR54 activation on the plasma membrane oscillator activity via coupling of this receptor to phospholipase C signaling pathways. Both components of this pathway, inositol 1,3,4-trisphosphate and protein kinase C, contributed to the receptor-mediated modulation of baseline [Ca(2+)](i) oscillations. TTX and 2-aminoethyl diphenylborinate together abolished agonist-induced elevation in [Ca(2+)](i) in almost all cells, whereas flufenamic acid was less effective. Together these results indicate that a plasma membrane calcium oscillator is spontaneously operative in the majority of prenatal GnRH-1 neurons and is facilitated by kisspeptin-10 through phosphatidyl inositol diphosphate hydrolysis and depolarization of neurons by activating TTX-sensitive sodium channels and nonselective cationic channels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.