ArticleThe Journal of physiology2012
Transcompartmental reversal of single fibre hyperexcitability in juxtaparanodal Kv1.1-deficient vagus nerve axons by activation of nodal KCNQ channels.
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Sex-specific differences in mortality and neurocardiac interactions in the Kv1.1 knockout mouse model of sudden unexpected death in epilepsy (SUDEP).The Journal of physiology · 2026Article
- LGI3/2-ADAM23 interactions cluster Kv1 channels in myelinated axons to regulate refractory period.The Journal of cell biology · 2023Article
- Kcnq2/Kv7.2 controls the threshold and bi-hemispheric symmetry of cortical spreading depolarization.Brain : a journal of neurology · 2021Article
- Kv1.1 subunits localize to cardiorespiratory brain networks in mice where their absence induces astrogliosis and microgliosis.Molecular and cellular neurosciences · 2021Article
- Kv1.1 potassium channel subunit deficiency alters ventricular arrhythmia susceptibility, contractility, and repolarization.Physiological reports · 2021Article
- Neuron-specific Kv1.1 deficiency is sufficient to cause epilepsy, premature death, and cardiorespiratory dysregulation.Neurobiology of disease · 2020Article
- Kv1.1 channel subunits in the control of neurocardiac function.Channels (Austin, Tex.) · 2019Review
- Cardiorespiratory profiling reveals primary breathing dysfunction in Kcna1-null mice: Implications for sudden unexpected death in epilepsy.Neurobiology of disease · 2019Article
- Pharmacogenetics of KCNQ channel activation in 2 potassium channelopathy mouse models of epilepsy.Epilepsia · 2018Article
- p53-Sensitive Epileptic Behavior and Inflammation inFrontiers in genetics · 2018Article
- Article
- Precision physiology and rescue of brain ion channel disorders.The Journal of general physiology · 2017Review
- M-currents (Kv7.2-7.3/KCNQ2-KCNQ3) Are Responsible for Dysfunctional Autonomic Control in Hypertensive Rats.Frontiers in physiology · 2016Article
- Spontaneous seizures in Kcna1-null mice lacking voltage-gated Kv1.1 channels activate Fos expression in select limbic circuits.Journal of neurochemistry · 2015Article
- Expression and function of Kv1.1 potassium channels in human atria from patients with atrial fibrillation.Basic research in cardiology · 2015Article
- Genomic biomarkers of SUDEP in brain and heart.Epilepsy & behavior : E&B · 2014Review
- High-resolution molecular genomic autopsy reveals complex sudden unexpected death in epilepsy risk profile.Epilepsia · 2014Article
- Sudden unexpected death in Dravet syndrome: respiratory and other physiological dysfunctions.Respiratory physiology & neurobiology · 2013Review
- Antisense reduction of tau in adult mice protects against seizures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Sudden unexpected death in a mouse model of Dravet syndrome.The Journal of clinical investigation · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Kv1.1 channels cluster at juxtaparanodes of myelinated axons in the vagus nerve, the primary conduit for parasympathetic innervation of the heart. Kcna1-null mice lacking these channels exhibit neurocardiac dysfunction manifested by atropine-sensitive atrioventricular conduction blocks and bradycardia that may culminate in sudden death. To evaluate whether loss of Kv1.1 channels alters electrogenic properties within the nerve, we compared the intrinsic excitability of single myelinated A- and Aδ-axons from excised cervical vagus nerves of young adult Kcna1-null mice and age-matched, wild-type littermate controls. Although action potential shapes and relative refractory periods varied little between genotypes, Kv1.1-deficient large myelinated A-axons showed a fivefold increase in susceptibility to 4-aminopyridine (4-AP)-induced spontaneous ectopic firing. Since the repolarizing currents of juxtaparanodal Kv1 channels and nodal KCNQ potassium channels both act to dampen repetitive activity, we examined whether augmenting nodal KCNQ activation could compensate for Kv1.1 loss and reverse the spontaneous hyperexcitability in Kv1.1-deficient A-axons. Application of the selective KCNQ opener flupirtine raised A-axon firing threshold while profoundly suppressing 4-AP-induced spontaneous firing, demonstrating a functional synergy between the two compartments. We conclude that juxtaparanodal Kv1.1-deficiency causes intrinsic hyperexcitability in large myelinated axons in vagus nerve which could contribute to autonomic dysfunction in Kcna1-null mice, and that KCNQ openers reveal a transcompartmental synergy between Kv1 and KCNQ channels in regulating axonal excitability.
Indexed as
Identifiers
What 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.