ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Physiologic regulation of a tetrodotoxin-sensitive sodium influx that mediates a slow afterdepolarization potential in gonadotropin-releasing hormone neurons: possible implications for the central regulation of fertility.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 64 citations in OpenAlex.
- Dendritic interaction of timescales in afterdepolarization potentials and nonmonotonic spike-adding.Journal of computational neuroscience · 2026Article
- Altered Electrophysiology and Transcriptome of GnRH Neurons in Middle-Aged Female Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Estrogens rapidly shape synaptic and intrinsic properties to regulate the temporal precision of songbird auditory neurons.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- The electrophysiologic properties of gonadotropin-releasing hormone neurons.Journal of neuroendocrinology · 2022Review
- IInternational journal of molecular sciences · 2021Article
- Spike Activity in the Ventromedial Nucleus of Rat Hypothalamus during Aging.Bulletin of experimental biology and medicine · 2021Article
- Central aspects of systemic oestradiol negative- and positive-feedback on the reproductive neuroendocrine system.Journal of neuroendocrinology · 2020Review
- 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
- Proestrus Differentially Regulates Expression of Ion Channel and Calcium Homeostasis Genes in GnRH Neurons of Mice.Frontiers in molecular neuroscience · 2019Article
- 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
- GnRH Neuron Activity and Pituitary Response in Estradiol-Induced vs Proestrous Luteinizing Hormone Surges in Female Mice.Endocrinology · 2017Article
- A unified model for two modes of bursting in GnRH neurons.Journal of computational neuroscience · 2016Article
- Kisspeptin and Gonadotropin-Releasing Hormone Neuronal Excitability: Molecular Mechanisms Driven by 17β-Estradiol.Neuroendocrinology · 2015Review
- Optogenetic activation of GnRH neurons reveals minimal requirements for pulsatile luteinizing hormone secretion.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Orexin a suppresses gonadotropin-releasing hormone (GnRH) neuron activity in the mouse.Endocrinology · 2012Article
- 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
- Estradiol directly attenuates sodium currents and depolarizing afterpotentials in isolated gonadotropin-releasing hormone neurons.Brain research · 2012Article
- A simple integrative electrophysiological model of bursting GnRH neurons.Journal of computational neuroscience · 2012Article
- 17β-oestradiol regulation of gonadotrophin-releasing hormone neuronal excitability.Journal of neuroendocrinology · 2012Review
- Rapid nongenomic effects of oestradiol on gonadotrophin-releasing hormone neurones.Journal of neuroendocrinology · 2012Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The brain controls fertility through release of gonadotropin-releasing hormone (GnRH), but the mechanisms underlying action potential patterning and GnRH release are not understood. We investigated whether GnRH neurons exhibit afterdepolarizing potentials (ADPs) and whether these are modified by reproductive state. Whole-cell current-clamp recordings of GnRH neurons in brain slices from ovariectomized mice revealed a slow ADP (sADP) after action potentials generated by brief current injection. Generating two or four spikes enhanced sADP amplitude and duration. sADP amplitude was not affected by blocking selected neurotransmitter/neuromodulator receptors, delayed-rectifier potassium channels, calcium-dependent cation channels, or hyperpolarization-activated cation channels but was halved by the calcium channel blocker cadmium and abolished by tetrodotoxin. Cadmium also reduced peak latency. Intrinsic mechanisms underlying the sADP were investigated using voltage-clamp protocols simulating action potential waveforms. A single action potential produced an inward current, which increased after double and quadruple stimulation. Cadmium did not affect current amplitude but reduced peak latency. Pretreatment with blockers of calcium-activated potassium currents (I(KCa)) reproduced this shift and blocked subsequent cadmium-induced changes, suggesting cadmium changes latency indirectly by blocking I(KCa). Tetrodotoxin abolished the inward current, suggesting that it is carried by sodium. In contrast, I(KCa) blockers increased the inward current, indicating that I(KCa) may oppose generation of the sADP. Strong sADPs were suprathreshold, generating repetitive spontaneous firing. I(ADP), sADP, and excitability were enhanced by in vivo estradiol, which triggers a preovulatory surge of GnRH release. Physiological feedback modification of this inward current and resulting sADP may modulate action potential firing and subsequent GnRH release.
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Registered trials
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