ArticleThe Journal of physiology2007
Regulation of M(Kv7.2/7.3) channels in neurons by PIP(2) and products of PIP(2) hydrolysis: significance for receptor-mediated inhibition.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 90 citations in OpenAlex.
- Physiological 17β-oestradiol inhibits KChannels (Austin, Tex.) · 2026Article
- Cholesterol and Cholesterol-Derived Molecules Differentially Modulate Neuronal Kv7.2/7.3 Channels.Archiv der Pharmazie · 2026Article
- Regulatory role of cholesterol in modulating actin dynamics and cell adhesive interactions in the trabecular meshwork.bioRxiv : the preprint server for biology · 2024Article
- G protein βγ regulation of KCNQ-encoded voltage-dependent K channels.Frontiers in physiology · 2024Review
- A muscarinic, GIRK channel-mediated inhibition of inspiratory-related XII nerve motor output emerges in early postnatal development in mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- KCNQ Potassium Channels as Targets of Botanical Folk Medicines.Annual review of pharmacology and toxicology · 2022Review
- The CD63 homologs, Tsp42Ee and Tsp42Eg, restrict endocytosis and promote neurotransmission through differential regulation of synaptic vesicle pools.Frontiers in cellular neuroscience · 2022Article
- KJournal of neurophysiology · 2021Article
- The KNeuroscience · 2021Article
- Physiology and Therapeutic Potential of SK, H, and M Medium AfterHyperPolarization Ion Channels.Frontiers in molecular neuroscience · 2021Review
- Phosphatidylinositol-4,5-Bisphosphate Binding to Amphiphysin-II Modulates T-Tubule Remodeling: Implications for Heart Failure.Frontiers in physiology · 2021Article
- Control of Neuronal Excitability by Cell Surface Receptor Density and Phosphoinositide Metabolism.Frontiers in pharmacology · 2021Article
- Kv7 Channels and Excitability Disorders.Handbook of experimental pharmacology · 2021Article
- Phosphoinositides: Roles in the Development of Microglial-Mediated Neuroinflammation and Neurodegeneration.Frontiers in cellular neuroscience · 2021Review
- Review of PIP2 in Cellular Signaling, Functions and Diseases.International journal of molecular sciences · 2020Review
- TwoFrontiers in physiology · 2020Article
- Nociceptor Signalling through ion Channel Regulation via GPCRs.International journal of molecular sciences · 2019Review
- Pore- and voltage sensor-targeted KCNQ openers have distinct state-dependent actions.The Journal of general physiology · 2018Article
- One drug-sensitive subunit is sufficient for a near-maximal retigabine effect in KCNQ channels.The Journal of general physiology · 2018Article
- Metabotropic Acetylcholine and Glutamate Receptors Mediate PI(4,5)PScientific reports · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
M-channels are voltage-gated K+ channels that regulate the excitability of many neurons. They are composed of Kv7 (KCNQ) family subunits, usually Kv7.2 + Kv7.3. Native M-channels and expressed Kv7.2 + 7.3 channels are inhibited by stimulating G(q/11)-coupled receptors - prototypically the M1 muscarinic acetylcholine receptor (M1-mAChR). The channels require membrane phosphatidylinositol-4,5-bisphosphate (PIP(2)) to open and the effects of mAChR stimulation result primarily from the reduction in membrane PIP(2) levels following G(q)/phospholipase C-catalysed PIP(2) hydrolysis. However, in sympathetic neurons, M-current inhibition by bradykinin appears to be mediated through the release and action of intracellular Ca(2)+ by inositol-1,4,5-trisphosphate (IP(3)), a product of PIP(2) hydrolysis, rather than by PIP(2) depletion. We have therefore compared the effects of bradykinin and oxotremorine-M (a muscarinic agonist) on membrane PIP(2) in sympathetic neurons using a fluorescently tagged mutated C-domain of the PIP(2) binding probe, 'tubby'. In concentrations producing equal M-current inhibition, bradykinin produced about one-quarter of the reduction in PIP(2) produced by oxotremorine-M, but equal reduction when PIP(2) synthesis was blocked with wortmannin. Likewise, wortmannin restored bradykinin-induced M-current inhibition when Ca(2)+ release was prevented with thapsigargin. Thus, inhibition by bradykinin can use product (IP(3)/Ca(2)+)-dependent or substrate (PIP(2)) dependent mechanisms, depending on Ca(2)+ availability and PIP(2) synthesis rates.
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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.