ArticleHandbook of experimental pharmacology2021
Pharmacological Activation of Neuronal Voltage-Gated Kv7/KCNQ/M-Channels for Potential Therapy of Epilepsy and Pain.
Article in Handbook of experimental pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
- TWIK-1 plays distinct roles in spinal and peripheral sensory circuits controlling mechanical sensitivity and neuropathic hypersensitivity.Signal transduction and targeted therapy · 2026Article
- Synaptic Plasticity-Intrinsic Excitability and Antidepressant Discovery.Biomedicines · 2026Review
- Galangin, a novel Kv7 potassium channel opener, exerts potent antinociceptive effects in multiple chronic pain mouse models.Acta pharmacologica Sinica · 2026Article
- A novel role of the antidepressant paroxetine in inhibiting neuronal Kv7/M channels to enhance neuronal excitability.Translational psychiatry · 2025Article
- TET1 Participates in Complete Freund's Adjuvant-induced Trigeminal Inflammatory Pain by Regulating Kv7.2 in a Mouse Model.Neuroscience bulletin · 2024Article
- The binding and mechanism of a positive allosteric modulator of Kv3 channels.Nature communications · 2024Article
- Selective KCNQ2/3 Potassium Channel Opener ICA-069673 Inhibits Excitability in Mouse Vagal Sensory Neurons.The Journal of pharmacology and experimental therapeutics · 2024Article
- Circuit-based intervention corrects excessive dentate gyrus output in the fragile X mouse model.eLife · 2024Article
- Voltage-gated potassium channels and genetic epilepsy.Frontiers in neurology · 2024Review
- Circuit-based intervention corrects excessive dentate gyrus output in the Fragile X mouse model.bioRxiv : the preprint server for biology · 2023Article
- Investigating genotype-phenotype relationship of extreme neuropathic pain disorders in a UK national cohort.Brain communications · 2023Article
- Structural mechanisms for the activation of human cardiac KCNQ1 channel by electro-mechanical coupling enhancers.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Normalization of Neuroinflammation: A New Strategy for Treatment of Persistent Pain and Memory/Emotional Deficits in Chronic Pain.Journal of inflammation research · 2022Review
- Peripheral Voltage-Gated Cation Channels in Neuropathic Pain and Their Potential as Therapeutic Targets.Frontiers in pain research (Lausanne, Switzerland) · 2021Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Native M-current is a low-threshold, slowly activating potassium current that exerts an inhibitory control over neuronal excitability. The M-channel is primarily co-assembled by heterotetrameric Kv7.2/KCNQ2 and Kv7.3/KCNQ3 subunits that are specifically expressed in the brain and peripheral nociceptive and visceral sensory neurons in the spinal cord. Reduction of M-channel function leads to neuronal hyperexcitability that defines the fundamental mechanism of neurological disorders such as epilepsy and pain, indicating that pharmacological activation of Kv7/KCNQ/M-channels may serve the basis for the therapy. The well-known KCNQ opener retigabine (ezogabine or Potiga) was approved by FDA in 2011 as an anticonvulsant used for an adjunctive treatment of partial epilepsies. Unfortunately, retigabine was discontinued in 2017 due to its side effects of blue-colored appearance of the skin and eyes after prolonged intake. In addition, flupirtine, a structural derivative of retigabine and a centrally acting non-opioid analgesic, was also withdrawn in 2018 for liver toxicity. Fortunately, these side effects are compound-structures related and can be avoided. Thus, further identification and development of novel potent and selective Kv7 channel openers may lead to an effective therapy with improved safety window for anti-epilepsy and anti-nociception.
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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.