ReviewBritish journal of pharmacology2009
Neural KCNQ (Kv7) channels.
Review in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 403 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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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
403 citing papers in PubMed, 653 citations in OpenAlex.
- Identification of a Ste20-like kinase-dependent signaling network orchestrating cytoskeletal and synaptic development of cortical neurons.Cell communication and signaling : CCS · 2026Article
- Impacts of Kv3.1 Channels on Action Potentials in Fusiform Neurons From the Dorsal Cochlear Nucleus of Mice Before and After Hearing Onset.Journal of the Association for Research in Otolaryngology : JARO · 2026Article
- Sustained Ion Imbalances Enhance Ferroptosis.bioRxiv : the preprint server for biology · 2026Article
- Multi-omics analysis of ion channels expressed by chicken embryo vestibular type I and type II hair cells.Experimental physiology · 2026Article
- Discovery of Novel Bicyclic Pyrazole Amides as Potent Neuronal KACS medicinal chemistry letters · 2026Article
- μ-Opioid receptor signalling enhances Kir3 currents in glutamatergic preBötzinger complex neurons in mice.The Journal of physiology · 2026Article
- Multibehavioral Phenotyping in Early-Life-Stage Zebrafish for Identifying Disruptors of Nonassociative Learning.Environmental health perspectives · 2026Article
- A prefrontal cortex-nucleus accumbens circuit attenuates cocaine-conditioned place preference memories.Molecular psychiatry · 2026Article
- Ionic Homeostasis Failure in Major Depressive Disorder: Ion Channel Mechanisms, Excitation-Inhibition Imbalance, and Precision Therapeutics.International journal of molecular sciences · 2026Review
- Therapeutic potential of small molecules that block receptor-induced Kv7/M-current suppression in neuroprotection, seizures, and pain.British journal of pharmacology · 2026Article
- Article
- Synaptic Plasticity-Intrinsic Excitability and Antidepressant Discovery.Biomedicines · 2026Review
- Robust activity-dependent mitochondrial calcium dynamics at the AIS is dispensable for action potential generation.The Journal of physiology · 2026Article
- Pharmacological manipulation of nested oscillations in human iPSC-derived 2D neuronal networks.Neurobiology of disease · 2026Article
- Bidirectional Modulation of Beam Traversal Performance by Acetylcholine in the Cerebellar Nuclei.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- The Kv4.3 channel on c-low threshold mechanoreceptors in DRG is a key mediator transforming tactile stimuli into nociceptive signals in chemotherapy-induced neuropathy.Acta pharmaceutica Sinica. B · 2026Article
- Shaping the Action Potential in Dorsal Root and Trigeminal Ganglia Neurons: Relevance to Pain Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Review
- Multi-Omics Analysis Reveals Nono-Kcnq2 Regulation of Neuronal Excitability in Chronic Constriction Injury-Induced Neuropathic Pain.Research (Washington, D.C.) · 2026Article
- The rise and deceleration of neuronal excitability in aging and Alzheimer's disease: Mechanisms, implications, and therapeutic targets.Ageing research reviews · 2026Review
- CRISPR/Cas9-mediatedFrontiers in physiology · 2026Article
343 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
KCNQ genes encode five Kv7 K(+) channel subunits (Kv7.1-Kv7.5). Four of these (Kv7.2-Kv7.5) are expressed in the nervous system. Kv7.2 and Kv7.3 are the principal molecular components of the slow voltage-gated M-channel, which widely regulates neuronal excitability, although other subunits may contribute to M-like currents in some locations. M-channels are closed by receptors coupled to Gq such as M1 and M3 muscarinic receptors; this increases neuronal excitability and underlies some forms of cholinergic excitation. Muscarinic closure results from activation of phospholipase C and consequent hydrolysis and depletion of membrane phosphatidylinositol-4,5-bisphosphate, which is required for channel opening. Some effects of M-channel closure, determined from transmitter action, selective blocking drugs (linopirdine and XE991) and KCNQ2 gene disruption or manipulation, are as follows: (i) in sympathetic neurons: facilitation of repetitive discharges and conversion from phasic to tonic firing; (ii) in sensory nociceptive systems: facilitation of A-delta peripheral sensory fibre responses to noxious heat; and (iii) in hippocampal pyramidal neurons: facilitation of repetitive discharges, enhanced after-depolarization and burst-firing, and induction of spontaneous firing through a reduction of action potential threshold at the axon initial segment. Several drugs including flupirtine and retigabine enhance neural Kv7/M-channel activity, principally through a hyperpolarizing shift in their voltage gating. In consequence they reduce neural excitability and can inhibit nociceptive stimulation and transmission. Flupirtine is in use as a central analgesic; retigabine is under clinical trial as a broad-spectrum anticonvulsant and is an effective analgesic in animal models of chronic inflammatory and neuropathic pain.
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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.