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• W1601351641 endingPage "925" @default.
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• W1601351641 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 Gq/11-coupled receptors – prototypically the M1 muscarinic acetylcholine receptor (M1-mAChR). The channels require membrane phosphatidylinositol-4,5-bisphosphate (PIP2) to open and the effects of mAChR stimulation result primarily from the reduction in membrane PIP2 levels following Gq/phospholipase C-catalysed PIP2 hydrolysis. However, in sympathetic neurons, M-current inhibition by bradykinin appears to be mediated through the release and action of intracellular Ca2+ by inositol-1,4,5-trisphosphate (IP3), a product of PIP2 hydrolysis, rather than by PIP2 depletion. We have therefore compared the effects of bradykinin and oxotremorine-M (a muscarinic agonist) on membrane PIP2 in sympathetic neurons using a fluorescently tagged mutated C-domain of the PIP2 binding probe, ‘tubby’. In concentrations producing equal M-current inhibition, bradykinin produced about one-quarter of the reduction in PIP2 produced by oxotremorine-M, but equal reduction when PIP2 synthesis was blocked with wortmannin. Likewise, wortmannin restored bradykinin-induced M-current inhibition when Ca2+ release was prevented with thapsigargin. Thus, inhibition by bradykinin can use product (IP3/Ca2+)-dependent or substrate (PIP2) dependent mechanisms, depending on Ca2+ availability and PIP2 synthesis rates." @default.
• W1601351641 created "2016-06-24" @default.
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• W1601351641 creator A5027714194 @default.
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• W1601351641 date "2007-07-21" @default.
• W1601351641 modified "2023-09-23" @default.
• W1601351641 title "Regulation of M(Kv7.2/7.3) channels in neurons by PIP₂and products of PIP₂hydrolysis: significance for receptor-mediated inhibition" @default.
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• W1601351641 doi "https://doi.org/10.1113/jphysiol.2007.132498" @default.
• W1601351641 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2075249" @default.
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