ArticleEndocrinology2010
17 β-estradiol rapidly increases ATP-sensitive potassium channel activity in gonadotropin-releasing hormone neurons [corrected] via a protein kinase signaling pathway.
Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 45 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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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
45 citing papers in PubMed, 76 citations in OpenAlex.
- Role of Membrane Estrogen Receptor Alpha on the Positive Feedback of Estrogens on Kisspeptin and GnRH Neurons.eNeuro · 2024Article
- Cycling matters: Sex hormone regulation of vascular potassium channels.Channels (Austin, Tex.) · 2023Review
- The modulation of potassium channels by estrogens facilitates neuroprotection.Frontiers in cell and developmental biology · 2022Review
- Membrane-initiated estrogen signaling via Gq-coupled GPCR in the central nervous system.Steroids · 2019Review
- Extranuclear signaling by ovarian steroids in the regulation of sexual receptivity.Hormones and behavior · 2018Review
- Estradiol-Dependent Stimulation and Suppression of Gonadotropin-Releasing Hormone Neuron Firing Activity by Corticotropin-Releasing Hormone in Female Mice.Endocrinology · 2018Article
- The Arcuate Estrogen-Regulated Transcriptome: Estrogen Response Element-Dependent and -Independent Signaling of ERα in Female Mice.Endocrinology · 2017Article
- Estrogens, Neuroinflammation, and Neurodegeneration.Endocrine reviews · 2016Review
- Review
- BPA Directly Decreases GnRH Neuronal Activity via Noncanonical Pathway.Endocrinology · 2016Article
- Minireview: neural signaling of estradiol in the hypothalamus.Molecular endocrinology (Baltimore, Md.) · 2015Review
- Prolonged infusion of estradiol benzoate into the stalk median eminence stimulates release of GnRH and kisspeptin in ovariectomized female rhesus macaques.Endocrinology · 2015Article
- Kisspeptin and Gonadotropin-Releasing Hormone Neuronal Excitability: Molecular Mechanisms Driven by 17β-Estradiol.Neuroendocrinology · 2015Review
- Effects of STX, a novel estrogen membrane receptor agonist, on GnRH-induced luteinizing hormone secretion from cultured bovine anterior pituitary cells.The Journal of veterinary medical science · 2014Article
- Effects of estradiol on voltage-gated potassium channels in mouse dorsal root ganglion neurons.The Journal of membrane biology · 2014Article
- Cross-talk between reproduction and energy homeostasis: central impact of estrogens, leptin and kisspeptin signaling.Hormone molecular biology and clinical investigation · 2014Review
- Gq-mER signaling has opposite effects on hypothalamic orexigenic and anorexigenic neurons.Steroids · 2014Review
- GnRH neurons of young and aged female rhesus monkeys co-express GPER but are unaffected by long-term hormone replacement.Neuroendocrinology · 2014Article
- A selective membrane estrogen receptor agonist maintains autonomic functions in hypoestrogenic states.Brain research · 2013Review
- mRNA expression of ion channels in GnRH neurons: subtype-specific regulation by 17β-estradiol.Molecular and cellular endocrinology · 2013Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
17Beta-estradiol (E2) both inhibits and excites GnRH neurons via presynaptic as well as postsynaptic mechanisms. Although it has been demonstrated that E2 can alter the excitability of GnRH neurons via direct actions, the intracellular signaling cascades mediating these actions are not well understood. Previously we have shown that the activity of one of the critical ion channels needed for maintaining GnRH neurons in a hyperpolarized state, the ATP-sensitive potassium channel (K(ATP)) channel, is augmented by E2 in ovariectomized females. However, the mRNA expression of the K(ATP) channel subunits Kir6.2 and SUR1 are unchanged with in vivo E2 treatment. Therefore, to elucidate the cellular signaling mechanism(s) modulating the channel activity, we did whole-cell patch-clamp recording of enhanced green fluorescent protein-GnRH neurons from ovariectomized female mice to study the acute effects of E2. E2 dose-dependently (EC(50) = 0.6 nM) enhanced the diazoxide (channel opener)-activated K(ATP) channel currents by 1.2- to 2.0-fold, which was antagonized by ICI 182,780. E2-BSA was equally as effective as E2, whereas 17 alpha-estradiol [corrected] had no effect. The protein kinase A (PKA) activator forskolin mimicked the effects of E2, whereas the PKA inhibitor H89 and the protein kinase C (PKC) inhibitor bisindolylmaleimide I blocked the effects of E2. Similar to E2, STX, a membrane estrogen receptor (ER) agonist that does not bind to ERalpha or ERbeta, also potentiated the diazoxide-induced K(ATP) channel current by 1.5-fold. Therefore, E2 can potentiate K(ATP) channel activity in GnRH neurons through a membrane ER-activated PKC-PKA signaling pathway.
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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.