ArticleThe Journal of physiology2015
Nitric oxide selectively suppresses IH currents mediated by HCN1-containing channels.
Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- The Contribution of HCN Channelopathies in Different Epileptic Syndromes, Mechanisms, Modulators, and Potential Treatment Targets: A Systematic Review.Frontiers in molecular neuroscience · 2022Pooled it
- A comprehensive review of HCN channel expression and IJournal of neurophysiology · 2025Review
- Distinct cell classes in the superior paraolivary nucleus (SPN) region in the gerbil auditory brainstem revealed by in vivo physiological and anatomical characterization.Hearing research · 2025Article
- Cellular and synaptic specializations for sub-millisecond precision in the mammalian auditory brainstem.Frontiers in cellular neuroscience · 2025Review
- Selective Vulnerability of GABAergic Inhibitory Interneurons to Bilirubin Neurotoxicity in the Neonatal Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Cerebellar interneurons control fear memory consolidation via learning-induced HCN plasticity.Cell reports · 2023Article
- Article
- Interferon-γ augments GABA release in the developing neocortexFrontiers in cellular neuroscience · 2022Article
- IProgress in biophysics and molecular biology · 2021Review
- Nitric Oxide Signaling in the Auditory Pathway.Frontiers in neural circuits · 2021Review
- Nitric oxide regulates the firing rate of neuronal subtypes in the guinea pig ventral cochlear nucleus.The European journal of neuroscience · 2020Review
- Nitric Oxide-Mediated Plasticity of Interconnections Between T-Stellate cells of the Ventral Cochlear Nucleus Generate Positive Feedback and Constitute a Central Gain Control in the Auditory System.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Effects of Non-traumatic Noise and Conductive Hearing Loss on Auditory System Function.Neuroscience · 2019Review
- Puncta of Neuronal Nitric Oxide Synthase (nNOS) Mediate NMDA Receptor Signaling in the Auditory Midbrain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Physiology and anatomy of neurons in the medial superior olive of the mouse.Journal of neurophysiology · 2016Article
- Serotonin modulates spike probability in the axon initial segment through HCN channels.Nature neuroscience · 2016Article
- Hyperpolarization-activated, cyclic nucleotide-gated cation channels in Aplysia: Contribution to classical conditioning.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Hyperpolarization-activated non-specific cation-permeable channels (HCN) mediate I(H) currents, which are modulated by cGMP and cAMP and by nitric oxide (NO) signalling. Channel properties depend upon subunit composition (HCN1-4 and accessory subunits) as demonstrated in expression systems, but physiological relevance requires investigation in native neurons with intact intracellular signalling. Here we use the superior olivary complex (SOC), which exhibits a distinctive pattern of HCN1 and HCN2 expression, to investigate NO modulation of the respective I(H) currents, and compare properties in wild-type and HCN1 knockout mice. The medial nucleus of the trapezoid body (MNTB) expresses HCN2 subunits exclusively, and sends inhibitory projections to the medial and lateral superior olives (MSO, LSO) and the superior paraolivary nucleus (SPN). In contrast to the MNTB, these target nuclei possess an I(H) with fast kinetics, and they express HCN1 subunits. NO is generated in the SOC following synaptic activity and here we show that NO selectively suppresses HCN1, while enhancing IH mediated by HCN2 subunits. NO hyperpolarizes the half-activation of HCN1-mediated currents and slows the kinetics of native IH currents in the MSO, LSO and SPN. This modulation was independent of cGMP and absent in transgenic mice lacking HCN1. Independently, NO signalling depolarizes the half-activation of HCN2-mediated I(H) currents in a cGMP-dependent manner. Thus, NO selectively suppresses fast HCN1-mediated I(H) and facilitates a slow HCN2-mediated I(H) , so generating a spectrum of modulation, dependent on the local expression of HCN1 and/or HCN2.
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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.