ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Gonadotropin-releasing hormone neurons express K(ATP) channels that are regulated by estrogen and responsive to glucose and metabolic inhibition.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 113 citations in OpenAlex.
- Article
- Cholinergic Control of GnRH Neuron Physiology and Luteinizing Hormone Secretion in Male Mice: Involvement of ACh/GABA Cotransmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Cycling matters: Sex hormone regulation of vascular potassium channels.Channels (Austin, Tex.) · 2023Review
- Epilepsy-associated increase in gonadotropin-releasing hormone neuron firing in diestrous female mice is independent of chronic seizure burden severity.Epilepsy research · 2022Article
- The electrophysiologic properties of gonadotropin-releasing hormone neurons.Journal of neuroendocrinology · 2022Review
- The modulation of potassium channels by estrogens facilitates neuroprotection.Frontiers in cell and developmental biology · 2022Review
- Hydrogen peroxide suppresses excitability of gonadotropin-releasing hormone neurons in adult mouse.Frontiers in endocrinology · 2022Article
- Neuromodulation or energy failure? Metabolic limitations silence network output in the hypoxic amphibian brainstem.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Role of potassium channels in female reproductive system.Obstetrics & gynecology science · 2020Article
- Insulin-induced hypoglycaemia suppresses pulsatile luteinising hormone secretion and arcuate Kiss1 cell activation in female mice.Journal of neuroendocrinology · 2019Article
- Changes in Both Neuron Intrinsic Properties and Neurotransmission Are Needed to Drive the Increase in GnRH Neuron Firing Rate during Estradiol-Positive Feedback.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Discovery and Characterization of VU0529331, a Synthetic Small-Molecule Activator of Homomeric G Protein-Gated, Inwardly Rectifying, Potassium (GIRK) Channels.ACS chemical neuroscience · 2019Article
- Proestrus Differentially Regulates Expression of Ion Channel and Calcium Homeostasis Genes in GnRH Neurons of Mice.Frontiers in molecular neuroscience · 2019Article
- Emerging insights into hypothalamic-pituitary-gonadal axis regulation and interaction with stress signalling.Journal of neuroendocrinology · 2018Review
- Neuroanatomical Framework of the Metabolic Control of Reproduction.Physiological reviews · 2018Review
- Emerging Concepts in Brain Glucose Metabolic Functions: From Glucose Sensing to How the Sweet Taste of Glucose Regulates Its Own Metabolism in Astrocytes and Neurons.Neuromolecular medicine · 2018Review
- Gonadotropin-Releasing Hormone (GnRH) Neuron Excitability Is Regulated by Estradiol Feedback and Kisspeptin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Increased cerebrospinal fluid levels of GABA, testosterone and estradiol in women with polycystic ovary syndrome.Human reproduction (Oxford, England) · 2017Observational
- Oleate induces KNeuroscience · 2017Article
- Dopaminergic inhibition of gonadotropin-releasing hormone neurons in the cichlid fish Astatotilapia burtoni.The Journal of experimental biology · 2016Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Gonadotropin-releasing hormone (GnRH) is released in a pulsatile manner that is dependent on circulating 17beta-estradiol (E2) and glucose concentrations. However, the intrinsic conductances responsible for the episodic firing pattern underlying pulsatile release and the effects of E2 and glucose on these conductances are primarily unknown. Whole-cell recordings from mouse enhanced green fluorescent protein-GnRH neurons revealed that the K(ATP) channel opener diazoxide induced an outward current that was antagonized by the sulfonylurea receptor 1 (SUR1) channel blocker tolbutamide. Single-cell reverse transcription (RT)-PCR revealed that the majority of GnRH neurons expressed Kir6.2 and SUR1 subunits, which correlated with the diazoxide/tolbutamide sensitivity. Also, a subpopulation of GnRH neurons expressed glucokinase mRNA, a marker for glucose sensitivity. Indeed, GnRH neurons decreased their firing in response to low glucose concentrations and metabolic inhibition. The maximum diazoxide-induced current was approximately twofold greater in E2-treated compared with oil-treated ovariectomized females. In current clamp, estrogen enhanced the diazoxide-induced hyperpolarization to a similar degree. However, based on quantitative RT-PCR, estrogen did not increase the expression of Kir6.2 or SUR1 transcripts in GnRH neurons. In the presence of ionotropic glutamate and GABA(A) receptor antagonists, tolbutamide depolarized and significantly increased the firing rate of GnRH neurons to a greater extent in E2-treated females. Finally, tolbutamide significantly increased GnRH secretion from the preoptic-mediobasal hypothalamus. Therefore, it appears that K(ATP) channels and glucokinase are expressed in GnRH neurons, which renders them directly responsive to glucose. In addition, K(ATP) channels are involved in modulating the excitability of GnRH neurons in an estrogen-sensitive manner that ultimately regulates peptide release.
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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.