Neural KCNQ (Kv7) channels
Open accessAbstract
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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Closure of Kv7 via Gq-coupled receptor pathways or direct blockers like paroxetine and linopirdine depolarizes neurons and increases release probability.
“Conversely, closure via Gq-coupled receptor pathways or direct blockers like paroxetine and linopirdine depolarizes neurons and increases release probability, a double-edged mechanism that can enhance cognition yet risk hyperexcitability when unchecked [245,246,247].”
From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [246]
The overview (p. 1) says Gq-coupled receptors close M-channels and increase neuronal excitability; Pharmacological implications (p. 7) reports that the blocker XE991 depolarizes hippocampal neurons. The paper identifies linopirdine as a blocker and discusses its attempted use as a cognition enhancer and its pro-epileptic side effects (p. 5). Our copy does not identify paroxetine as a Kv7 blocker or show that channel closure increases release probability. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMolecular studies show that PIP2 and small-molecule openers such as retigabine bias the Kv7 pore toward the open state.
“Molecular studies show that phosphatidylinositol-4,5-bisphosphate and small-molecule openers such as retigabine bias the pore toward the open state, offering a structural rationale for pharmacologic control of excitability [246].”
From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [246]
Kv7 channels formed by KCNQ2-5 subunits generate the M-current, a non-inactivating conductance that opens near resting membrane potential, stabilizes membrane potential, and raises the threshold for spike initiation.
“Kv7 channels formed by potassium voltage-gated channel subfamily Q member 2–5 (KCNQ2–5) subunits generate the M-current (muscarinic-sensitive potassium current), a non-inactivating conductance that opens near resting membrane potential, stabilizes membrane potential, and raises the threshold for spike initiation [246,247,248].”
From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [246]
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- Authors
- Brown, D. A., & Passmore, G. M.
- Affiliations
- University College London (GB)
- Corresponding author
- Brown, David A
- ORCID
- Brown, David A
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2009-04
- Volume
- 156
- Issue
- 8
- Pages
- 1185-1195
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- PMC
- PMC2697739
- OpenAlex
- W1736719008
- Cited by
- 676
- References
- 82
- Citations by year
- 2026: 26 · 2025: 40 · 2024: 48 · 2023: 30 · 2022: 47 · 2021: 43 · 2020: 41 · 2019: 39 · 2018: 36 · 2017: 46 · 2016: 42 · 2015: 41 · 2014: 37 · 2013: 47 · 2012: 41
- FWCI
- 2.88
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Wellcome Trust
- European Commission
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Keywords
- Kv7 potassium channels, KCNQ channels, M-channels, neuronal excitability, phosphatidylinositol 4,5-bisphosphate, linopirdine, XE991, KCNQ2, sympathetic neurons, nociceptors, hippocampal pyramidal neurons, flupirtine, retigabine, analgesia, antiepileptic drugs, neuropathic pain, chronic inflammatory pain, voltage-dependent gating
- MeSH terms
- Acetylcholine, Action Potentials, Adrenergic Fibers, Analgesics, Animals, Anticonvulsants, Humans, Synaptic Transmission, Neurons, Potassium, Receptors, Muscarinic, Sensory Receptor Cells, Ion Channel Gating, Pyramidal Cells, Muscarinic Agonists, Potassium Channel Blockers, KCNQ Potassium Channels, CA1 Region, Hippocampal
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