ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Modeling of membrane excitability in gonadotropin-releasing hormone-secreting hypothalamic neurons regulated by Ca2+-mobilizing and adenylyl cyclase-coupled receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 64 citations in OpenAlex.
- Modelling KNDy neurons and gonadotropin-releasing hormone pulse generation.Current opinion in endocrine and metabolic research · 2022Review
- Mathematical models in GnRH research.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
- 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
- Calcium release-activated calcium channels and pain.Cell calcium · 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
- Article
- A unified model for two modes of bursting in GnRH neurons.Journal of computational neuroscience · 2016Article
- Optimal microdomain crosstalk between endoplasmic reticulum and mitochondria for Ca2+ oscillations.Scientific reports · 2015Article
- Simulated GABA synaptic input and L-type calcium channels form functional microdomains in hypothalamic gonadotropin-releasing hormone neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- A simple integrative electrophysiological model of bursting GnRH neurons.Journal of computational neuroscience · 2012Article
- Lessons from models of pancreatic beta cells for engineering glucose-sensing cells.Mathematical biosciences · 2010Review
- Two slow calcium-activated afterhyperpolarization currents control burst firing dynamics in gonadotropin-releasing hormone neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Pulsatile GnRH secretion: roles of G protein-coupled receptors, second messengers and ion channels.Molecular and cellular endocrinology · 2010Review
- An integrated model of electrical spiking, bursting, and calcium oscillations in GnRH neurons.Biophysical journal · 2009Article
- Kisspeptin-10 facilitates a plasma membrane-driven calcium oscillator in gonadotropin-releasing hormone-1 neurons.Endocrinology · 2009Article
- Dendrites determine the contribution of after depolarization potentials (ADPs) to generation of repetitive action potentials in hypothalamic gonadotropin releasing-hormone (GnRH) neurons.Journal of computational neuroscience · 2009Article
- A mathematical model for the actions of activin, inhibin, and follistatin on pituitary gonadotrophs.Bulletin of mathematical biology · 2008Article
- Synaptic integration in hypothalamic gonadotropin releasing hormone (GnRH) neurons.Neuroscience · 2008Article
- Dendritic action potential initiation in hypothalamic gonadotropin-releasing hormone neurons.Endocrinology · 2008Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Gonadotropin-releasing hormone (GnRH) secretion from native and immortalized hypothalamic neurons is regulated by endogenous Ca(2+)-mobilizing and adenylyl cyclase (AC)-coupled receptors. Activation of both receptor types leads to an increase in action potential firing frequency and a rise in the intracellular Ca(2+) concentration ([Ca(2+)](i)) and neuropeptide secretion. The stimulatory action of Ca(2+)-mobilizing agonists on voltage-gated Ca(2+) influx is determined by depletion of the intracellular Ca(2+) pool, whereas AC agonist-stimulated Ca(2+) influx occurs independently of stored Ca(2+) and is controlled by cAMP, possibly through cyclic nucleotide-gated channels. Here, experimental records from immortalized GnRH-secreting neurons are simulated with a mathematical model to determine the requirements for generating complex membrane potential (V(m)) and [Ca(2+)](i) responses to Ca(2+)-mobilizing and AC agonists. Included in the model are three pacemaker currents: a store-operated Ca(2+) current (I(SOC)), an SK-type Ca(2+)-activated K(+) current (I(SK)), and an inward current that is modulated by cAMP and [Ca(2+)](i) (I(d)). Spontaneous electrical activity and Ca(2+) signaling in the model are predominantly controlled by I(d), which is activated by cAMP and inhibited by high [Ca(2+)](i). Depletion of the intracellular Ca(2+) pool mimics the receptor-induced activation of I(SOC) and I(SK), leading to an increase in the firing frequency and Ca(2+) influx after a transient cessation of electrical activity. However, increasing the activity of I(d) simulates the experimental response to forskolin-induced activation of AC. Analysis of the behaviors of I(SOC), I(d), and I(SK) in the model reveals the complexity in the interplay of these currents that is necessary to fully account for the experimental results.
Indexed as
Identifiers
11125008PMC6773020W2103508991What OpenQuestion holds
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.