ArticleThe Journal of physiology2006
The SK channel blocker apamin inhibits slow afterhyperpolarization currents in rat gonadotropin-releasing hormone neurones.
Article in The Journal of physiology, 2006. 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, 47 citations in OpenAlex.
- Age-Dependent Regulation of Acetylcholine Release at the Neuromuscular Junction Mediated by GABA.Cells · 2025Article
- Vasoactive intestinal peptide excites GnRH neurons via KCa3.1, a potential player in the slow afterhyperpolarization current.Frontiers in cellular neuroscience · 2024Article
- A Pathogenic Missense Mutation in Kainate Receptors Elevates Dendritic Excitability and Synaptic Integration through Dysregulation of SK Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Synaptic disruption and CREB-regulated transcription are restored by KEMBO molecular medicine · 2021Article
- Proestrus Differentially Regulates Expression of Ion Channel and Calcium Homeostasis Genes in GnRH Neurons of Mice.Frontiers in molecular neuroscience · 2019Article
- Long-Term Depression of Intrinsic Excitability Accompanied by Synaptic Depression in Cerebellar Purkinje Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Kisspeptin and Gonadotropin-Releasing Hormone Neuronal Excitability: Molecular Mechanisms Driven by 17β-Estradiol.Neuroendocrinology · 2015Review
- Cross-talk between reproduction and energy homeostasis: central impact of estrogens, leptin and kisspeptin signaling.Hormone molecular biology and clinical investigation · 2014Review
- Kisspeptin inhibits a slow afterhyperpolarization current via protein kinase C and reduces spike frequency adaptation in GnRH neurons.American journal of physiology. Endocrinology and metabolism · 2013Article
- mRNA expression of ion channels in GnRH neurons: subtype-specific regulation by 17β-estradiol.Molecular and cellular endocrinology · 2013Article
- Kisspeptin excitation of GnRH neurons.Advances in experimental medicine and biology · 2013Review
- Orexin a suppresses gonadotropin-releasing hormone (GnRH) neuron activity in the mouse.Endocrinology · 2012Article
- 17β-oestradiol regulation of gonadotrophin-releasing hormone neuronal excitability.Journal of neuroendocrinology · 2012Review
- Regulation of endogenous conductances in GnRH neurons by estrogens.Brain research · 2010Review
- Identified GnRH neuron electrophysiology: a decade of study.Brain research · 2010Review
- Flufenamic acid modulates multiple currents in gonadotropin-releasing hormone neurons.Brain research · 2010Article
- 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
- Voltage-gated Ca2+ channel mRNAs and T-type Ca2+ currents in rat gonadotropin-releasing hormone neurons.The journal of physiological sciences : JPS · 2010Article
- Kisspeptin excites gonadotropin-releasing hormone neurons through a phospholipase C/calcium-dependent pathway regulating multiple ion channels.Endocrinology · 2008Article
- Small-conductance calcium-activated potassium channels control excitability and firing dynamics in gonadotropin-releasing hormone (GnRH) neurons.Endocrinology · 2008Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gonadotropin-releasing hormone (GnRH) neurones play an essential role in the hypothalamo-pituitary-gonadal axis. As for other neurones, the discharge pattern of action potentials is important for GnRH neurones to properly function. In the case of a luteinizing hormone (LH) surge, for example, GnRH neurones are likely to continuously fire for more than an hour. For this type of firing, GnRH neurones must have a certain intrinsic property. To address this issue, we investigated the voltage-gated Ca(2+) currents and Ca(2+)-activated voltage-independent K(+) currents underlying afterhyperpolarization, because they affect cell excitability. Dispersed GnRH neurones from adult GnRH-EGFP (enhanced green fluorescent protein) transgenic rats were cultured overnight and then used for an electrophysiological experiment involving the perforated patch-clamp configuration. The GnRH neurones showed five subtypes of voltage-gated Ca(2+) currents, i.e. the T-, L-, N-, P/Q- and R-types. The GnRH neurones also showed a slow afterhyperpolarization current (I(sAHP)), but not a medium one. It is reported that the SK channel blocker apamin (10 pm-100 nm) blocks a medium afterhyperpolarization current but not an I(sAHP). In contrast to previous reports, the I(sAHP) observed in rat GnRH neurones was potently blocked by apamin. In addition, the GnRH neurones expressed transcripts for SK1-3 channels. The results indicate that rat GnRH neurones express all five subtypes of voltage-gated Ca(2+) channels and exhibit an apamin-sensitive I(sAHP), which may allow continuous firing in response to a relatively strong depolarizing input.
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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.