ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
The alpha subunit of Gq contributes to muscarinic inhibition of the M-type potassium current in sympathetic neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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Who cites it
41 citing papers in PubMed, 82 citations in OpenAlex.
- Kv7 Channels in Lung Diseases.Frontiers in physiology · 2020Review
- Pharmacological Manipulation of KFrontiers in physiology · 2020Review
- One drug-sensitive subunit is sufficient for a near-maximal retigabine effect in KCNQ channels.The Journal of general physiology · 2018Article
- The actions of Pasteurella multocida toxin on neuronal cells.Neuropharmacology · 2014Article
- Gq rather than G11 preferentially mediates nociceptor sensitization.Molecular pain · 2013Article
- Differential PKC-dependent and -independent PKD activation by G protein α subunits of the Gq family: selective stimulation of PKD Ser⁷⁴⁸ autophosphorylation by Gαq.Cellular signalling · 2012Article
- Regulation of voltage-gated Ca2+ channels by lipids.Cell calcium · 2009Review
- GPR55 is a cannabinoid receptor that increases intracellular calcium and inhibits M current.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- PIP(2)-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of PIP(2) depletion by Gq-coupled receptors in single living neurons.Pflugers Archiv : European journal of physiology · 2007Article
- Dual control of cardiac Na+ Ca2+ exchange by PIP(2): electrophysiological analysis of direct and indirect mechanisms.The Journal of physiology · 2007Article
- An M2-like muscarinic receptor enhances a delayed rectifier K+ current in rat sympathetic neurones.British journal of pharmacology · 2006Article
- Angiotensin II regulates neuronal excitability via phosphatidylinositol 4,5-bisphosphate-dependent modulation of Kv7 (M-type) K+ channels.The Journal of physiology · 2006Article
- Functions of neuronal P2Y receptors.Pflugers Archiv : European journal of physiology · 2006Review
- Probing the regulation of M (Kv7) potassium channels in intact neurons with membrane-targeted peptides.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Protein kinase C shifts the voltage dependence of KCNQ/M channels expressed in Xenopus oocytes.The Journal of physiology · 2005Article
- Relationship between membrane phosphatidylinositol-4,5-bisphosphate and receptor-mediated inhibition of native neuronal M channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Regulation of neuronal ion channels via P2Y receptors.Purinergic signalling · 2004Article
- Muscarinic modulation of erg potassium current.The Journal of physiology · 2004Article
- Regulation of KCNQ2/KCNQ3 current by G protein cycling: the kinetics of receptor-mediated signaling by Gq.The Journal of general physiology · 2004Article
- Why biophysicists make models: quantifying modulation of the M current.The Journal of general physiology · 2004Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Rat superior cervical ganglion (SCG) neurons express low-threshold noninactivating M-type potassium channels (IK(M)), which can be inhibited by activation of M1 muscarinic receptors. This inhibition occurs via pertussis toxin-insensitive G-proteins belonging to the Galphaq family (Caulfield et al., 1994 ). We have used DNA plasmids encoding antisense sequences against the 3' untranslated regions of Galpha subunits (antisense plasmids) to investigate the specific G-protein subunits involved in muscarinic inhibition of IK(M). These antisense plasmids specifically reduced levels of the target G-protein 48 hr after intranuclear injection. In cells depleted of Galphaq, muscarinic inhibition of IK(M) was attenuated compared both with uninjected neurons and with neurons injected with an inappropriate GalphaoA antisense plasmid. In contrast, depletion of Galpha11 protein did not alter IK(M) inhibition. To determine whether the alpha or beta gamma subunits of the G-protein mediated this inhibition, we have overexpressed the C terminus of beta adrenergic receptor kinase 1 (betaARK1), which binds free beta gamma subunits. betaARK1 did not reduce muscarinic inhibition of IK(M) at a concentration of plasmid that can reduce beta gamma-mediated inhibition of calcium current (). Also, expression of beta1gamma2 dimers did not alter the IK(M) density in SCG neurons. In contrast, IK(M) was virtually abolished in cells expressing GTPase-deficient, constitutively active forms of Galphaq and Galpha11. These data suggest that Galphaq is the principal mediator of muscarinic IK(M) inhibition in rat SCG neurons and that this more likely results from an effect of the alpha subunit than the beta gamma subunits of the Gq heterotrimer.
Indexed as
Identifiers
9614229PMC6792692W2164458919What OpenQuestion holds
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.