ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Triple cysteine module within M-type K+ channels mediates reciprocal channel modulation by nitric oxide and reactive oxygen species.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- Physiological oxygen levels reset KRedox biology · 2026Article
- Migraine is a dysfunction of neuronal potassium ion channels.Frontiers in neurology · 2025Review
- Article
- Therapeutic role of voltage-gated potassium channels in age-related neurodegenerative diseases.Frontiers in cellular neuroscience · 2024Review
- Nitrergic modulation of ion channel function in regulating neuronal excitability.Channels (Austin, Tex.) · 2021Article
- Alteration of Mesopontine Cholinergic Function by the Lack of KCNQ4 Subunit.Frontiers in cellular neuroscience · 2021Article
- The S2-S3 Loop of Kv7.4 Channels Is Essential for Calmodulin Regulation of Channel Activation.Frontiers in physiology · 2020Article
- Redox Regulation of Ion Channels and Receptors in Pulmonary Hypertension.Antioxidants & redox signaling · 2019Review
- The dual role of KCNQ/M channels upon OGD or OGD/R insults in cultured cortical neurons of mice: Timing is crucial in targeting M-channels against ischemic injur ies.Journal of cellular physiology · 2019Article
- Activation of KBritish journal of pharmacology · 2019Article
- A mutually induced conformational fit underlies CaThe Journal of biological chemistry · 2019Article
- Kv7.4 Channel Contribute to Projection-Specific Auto-Inhibition of Dopamine Neurons in the Ventral Tegmental Area.Frontiers in cellular neuroscience · 2019Article
- M-type KBritish journal of pharmacology · 2018Review
- Intracellular zinc activates KCNQ channels by reducing their dependence on phosphatidylinositol 4,5-bisphosphate.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- An Extract from Shrimp Processing By-Products Protects SH-SY5Y Cells from Neurotoxicity Induced by AβMarine drugs · 2017Article
- Stimulation of calcium-sensing receptors induces endothelium-dependent vasorelaxations via nitric oxide production and activation of IKCa channels.Vascular pharmacology · 2016Article
- Getting to NO Alzheimer's Disease: Neuroprotection versus Neurotoxicity Mediated by Nitric Oxide.Oxidative medicine and cellular longevity · 2016Review
- Nitric Oxide-Mediated Posttranslational Modifications: Impacts at the Synapse.Oxidative medicine and cellular longevity · 2016Review
- Ziram, a pesticide associated with increased risk for Parkinson's disease, differentially affects the presynaptic function of aminergic and glutamatergic nerve terminals at the Drosophila neuromuscular junction.Experimental neurology · 2016Article
- Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels.Biomolecules · 2015Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
We have identified a new signaling role for nitric oxide (NO) in neurons from the trigeminal ganglia (TG). We show that in rat sensory neurons from the TG the NO donor, S-nitroso-N-acetyl-dl-penicillamine, inhibited M-current. This inhibitory effect was blocked by NO scavenging, while inhibition of NO synthases increased M-current, suggesting that tonic NO levels inhibit M-current in TG neurons. Moreover NO increased neuronal excitability and calcitonin gene-related peptide (CGRP) release and these effects could be prevented by perturbing M-channel function. First, NO-induced depolarization was prevented by pre-application of the M-channel blocker XE991 and second, NO-induced increase in CGRP release was prevented by incubation with the M-channel opener retigabine. We investigated the mechanism of the effects of NO on M-channels and identified a site of action of NO to be the redox modulatory site at the triplet of cysteines within the cytosolic linker between transmembrane domains 2 and 3, which is also a site of oxidative modification of M-channels by reactive oxygen species (ROS). NO and oxidative modifications have opposing effects on M-current, suggesting that a tightly controlled local redox and NO environment will exert fine control over M-channel activity and thus neuronal excitability. Together our data have identified a dynamic redox sensor within neuronal M-channels, which mediates reciprocal regulation of channel activity by NO and ROS. This sensor may play an important role in mediating excitatory effects of NO in such trigeminal disorders as headache and migraine.
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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 Socratic graph.