ReviewNeuropharmacology2013
HCN and KV7 (M-) channels as targets for epilepsy treatment.
Review in Neuropharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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.
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Who cites it
21 citing papers in PubMed, 47 citations in OpenAlex.
- H- and m-channel overexpression promotes seizure-like events by impairing the ability of inhibitory neurons to process correlated inputs.PLoS computational biology · 2025Article
- ICA-27243 improves neuromuscular function and preserves motoneurons in the transgenic SOD1Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- KCNQ Channels Enable Reliable Presynaptic Spiking and Synaptic Transmission at High Frequency.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Rational design of a mutation to investigate the role of the brain protein TRIP8b in limiting the cAMP response of HCN channels in neurons.The Journal of general physiology · 2020Article
- Dynamic interplay between H-current and M-current controls motoneuron hyperexcitability in amyotrophic lateral sclerosis.Cell death & disease · 2019Article
- Endogenous HCN Channels Modulate the Firing Activity of Globus Pallidus Neurons in Parkinsonian Animals.Frontiers in aging neuroscience · 2019Article
- ERG3 potassium channel-mediated suppression of neuronal intrinsic excitability and prevention of seizure generation in mice.The Journal of physiology · 2018Article
- Developmental Changes in HCN Channel Modulation of Neocortical Layer 1 Interneurons.Frontiers in cellular neuroscience · 2018Article
- A Loss-of-FunctionFrontiers in molecular neuroscience · 2018Article
- Influence of Ivabradine on the Anticonvulsant Action of Four Classical Antiepileptic Drugs Against Maximal Electroshock-Induced Seizures in Mice.Neurochemical research · 2017Article
- Disturbed Processing of Contextual Information in HCN3 Channel Deficient Mice.Frontiers in molecular neuroscience · 2017Article
- Contrasting roles of Ih and the persistent sodium current at subthreshold voltages during naturalistic stimuli.Journal of neurophysiology · 2016Review
- Dysfunctional HCN ion channels in neurological diseases.Frontiers in cellular neuroscience · 2015Article
- Homeostasis or channelopathy? Acquired cell type-specific ion channel changes in temporal lobe epilepsy and their antiepileptic potential.Frontiers in physiology · 2015Review
- Article
- The effect of hyperpolarization-activated cyclic nucleotide-gated ion channel inhibitors on the vagal control of guinea pig airway smooth muscle tone.British journal of pharmacology · 2014Article
- Effects of SKF83959 on the excitability of hippocampal CA1 pyramidal neurons: a modeling study.Acta pharmacologica Sinica · 2014Article
- Novel role of KT5720 on regulating hyperpolarization-activated cyclic nucleotide-gated channel activity and dorsal root ganglion neuron excitability.DNA and cell biology · 2013Article
- Ion channels in genetic and acquired forms of epilepsy.The Journal of physiology · 2013Review
- TRIP8b-independent trafficking and plasticity of adult cortical presynaptic HCN1 channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Voltage-gated ion channels are important determinants of cellular excitability. The Hyperpolarization-activated Cyclic Nucleotide-gated (HCN) and KV7 (M-) channels are voltage-gated ion channels. Both channels are activated at sub-threshold potentials and have biophysical properties that mirror each other. KV7 channels inhibit neuronal excitability. Thus, mutations in KV7 channels that are associated with Benign Familial Neonatal Convulsions (BFNC) are likely to be epileptogenic. Mutations in HCN channels have also been associated with idiopathic epilepsies such as GEFS+. In addition, HCN channel expression and function are modulated during symptomatic epilepsies such as temporal lobe epilepsy. It is, though, unclear as to whether the changes in HCN channel expression and function associated with the various forms of epilepsy promote epileptogenesis or are adaptive. In this review, we discuss this as well as the potential for KV7 and HCN channels as drug targets for the treatment of epilepsy. This article is part of the Special Issue entitled 'New Targets and Approaches to the Treatment of Epilepsy'.
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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.