ArticleEndocrinology2008
Gonadotropin-releasing hormone-1 neuronal activity is independent of hyperpolarization-activated cyclic nucleotide-modulated channels but is sensitive to protein kinase a-dependent phosphorylation.
Article in Endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Vasoactive intestinal peptide excites GnRH neurons via KCa3.1, a potential player in the slow afterhyperpolarization current.Frontiers in cellular neuroscience · 2024Article
- The electrophysiologic properties of gonadotropin-releasing hormone neurons.Journal of neuroendocrinology · 2022Review
- Nitric oxide resets kisspeptin-excited GnRH neurons via PIP2 replenishment.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Modulation of Gonadotropin-Releasing Hormone Neuron Activity and Secretion in Mice by Non-peptide Neurotransmitters, Gasotransmitters, and Gliotransmitters.Frontiers in endocrinology · 2019Review
- Galanin Activates G Protein Gated Inwardly Rectifying Potassium Channels and Suppresses Kisspeptin-10 Activation of GnRH Neurons.Endocrinology · 2016Article
- Chloride Accumulators NKCC1 and AE2 in Mouse GnRH Neurons: Implications for GABAA Mediated Excitation.PloS one · 2015Article
- Episodic hormone secretion: a comparison of the basis of pulsatile secretion of insulin and GnRH.Endocrine · 2014Review
- Metabolic influences on reproduction: adiponectin attenuates GnRH neuronal activity in female mice.Endocrinology · 2014Article
- Novel role of KT5720 on regulating hyperpolarization-activated cyclic nucleotide-gated channel activity and dorsal root ganglion neuron excitability.DNA and cell biology · 2013Article
- mRNA expression of ion channels in GnRH neurons: subtype-specific regulation by 17β-estradiol.Molecular and cellular endocrinology · 2013Article
- Improved spatial direct method with gradient-based diffusion to retain full diffusive fluctuations.The Journal of chemical physics · 2012Article
- Culturing embryonic nasal explants for developmental and physiological study.Current protocols in neuroscience · 2012Article
- Physiology of the gonadotrophin-releasing hormone (GnRH) neurone: studies from embryonic GnRH neurones.Journal of neuroendocrinology · 2011Review
- The calcium oscillator of GnRH-1 neurons is developmentally regulated.Endocrinology · 2010Article
- Neuropeptide Y directly inhibits neuronal activity in a subpopulation of gonadotropin-releasing hormone-1 neurons via Y1 receptors.Endocrinology · 2010Article
- Involvement of G protein-coupled receptor 30 (GPR30) in rapid action of estrogen in primate LHRH neurons.Molecular endocrinology (Baltimore, Md.) · 2009Article
- Kisspeptin-10 facilitates a plasma membrane-driven calcium oscillator in gonadotropin-releasing hormone-1 neurons.Endocrinology · 2009Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Pulsatile release of GnRH-1 stimulates the anterior pituitary and induces secretion of gonadotropin hormones. GnRH-1 release is modulated by many neurotransmitters that act via G protein-coupled membrane receptors. cAMP is the most ubiquitous effector for these receptors. GnRH-1 neurons express hyperpolarization-activated cyclic nucleotide-modulated (HCN) channel protein in vivo. HCN channels are involved in neuronal pacemaking and can integrate cAMP signals. cAMP-dependent protein kinase (PKA) is also activated by cAMP signals, and PKA-dependent phosphorylation modulates voltage-activated channels. In this report, these two pathways were examined in GnRH-1 neurons as integrators of forskolin (FSK)-induced stimulation. The HCN3 isoform was detected in GnRH-1 neurons obtained from mouse nasal explants. ZD7288, a HCN channel blocker, significantly reduced the efficiency of FSK to stimulate GnRH-1 neurons, whereas blockade of PKA with Rp-adenosine-3',5'-cyclic monophosphorothioate triethylammonium did not attenuate the FSK-induced stimulation. To ensure that disruption of HCN channels on GnRH-1 neurons was responsible for reduction of FSK stimulation, experiments were performed removing gamma-aminobutyric acid (GABA), the major excitatory input to GnRH-1 neurons in nasal explants. Under these conditions, Rp-adenosine-3',5'-cyclic monophosphorothioate triethylammonium, but not ZD7288, altered the FSK-induced response of GnRH-1 neurons. These studies indicate that PKA-dependent phosphorylation is involved in the FSK-induced stimulation of GnRH-1 neurons rather than HCN channels, and HCN channels integrate the FSK-induced stimulation on GABAergic neurons. In addition, blockade of HCN channels did not modify basal GnRH-1 neuronal activity when GABAergic input was intact or removed, negating a role for these channels in basal GABAergic or GnRH-1 neuronal activity.
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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.