ArticleEuropean biophysics journal : EBJ2004
Phospholipid metabolism is required for M1 muscarinic inhibition of N-type calcium current in sympathetic neurons.
Article in European biophysics journal : EBJ, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Modulation of CaBMC research notes · 2018Article
- Article
- Actions and Mechanisms of Polyunsaturated Fatty Acids on Voltage-Gated Ion Channels.Frontiers in physiology · 2017Review
- Gα14 subunit-mediated inhibition of voltage-gated Ca2+ and K+ channels via neurokinin-1 receptors in rat celiac-superior mesenteric ganglion neurons.Journal of neurophysiology · 2016Article
- Phosphoinositides regulate ion channels.Biochimica et biophysica acta · 2015Review
- Biphasic modulation by mGlu5 receptors of TRPV1-mediated intracellular calcium elevation in sensory neurons contributes to heat sensitivity.British journal of pharmacology · 2015Article
- Characterization of ST14A Cells for Studying Modulation of Voltage-Gated Calcium Channels.PloS one · 2015Article
- Voltage-dependent regulation of CaV2.2 channels by Gq-coupled receptor is facilitated by membrane-localized β subunit.The Journal of general physiology · 2014Article
- The Ca2+ channel beta subunit determines whether stimulation of Gq-coupled receptors enhances or inhibits N current.The Journal of general physiology · 2009Article
- Molecular reconstruction of mGluR5a-mediated endocannabinoid signaling cascade in single rat sympathetic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Regulation of voltage-gated Ca2+ channels by lipids.Cell calcium · 2009Review
- Inhibition of transmitter release from rat sympathetic neurons via presynaptic M(1) muscarinic acetylcholine receptors.British journal of pharmacology · 2009Article
- The lipid connection-regulation of voltage-gated Ca(2+) channels by phosphoinositides.Pflugers Archiv : European journal of physiology · 2007Review
- Role of PIP2 in regulating versus modulating Ca2+ channel activity.The Journal of physiology · 2007Article
- M1 muscarinic receptors inhibit L-type Ca2+ current and M-current by divergent signal transduction cascades.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Inhibition of ligand binding to G protein-coupled receptors by arachidonic acid.Journal of molecular neuroscience : MN · 2005Article
- Phosphatidylinositol [correction] 4,5-bisphosphate signals underlie receptor-specific Gq/11-mediated modulation of N-type Ca2+ channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The signal transduction cascade mediating muscarinic receptor modulation of N-type Ca2+ channel activity by the slow pathway has remained incompletely characterized despite focused investigation. Recently we confirmed a role for the G-protein Gq and identified phospholipase C (PLC), phospholipase A2 (PLA2), and arachidonic acid (AA) as additional molecules involved in N-current inhibition in superior cervical ganglion (SCG) neurons by the slow pathway. We have further characterized this signal transduction cascade by testing whether additional molecules downstream of phosphatidylinositol-4,5-bisphosphate (PIP2) are required. The L-channel antagonist nimodipine was bath-applied to block L-current. Pretreating cells with pertussis toxin (PTX) minimized M2/M4 muscarinic receptor inhibition of N-current by the membrane-delimited pathway. Consistent with our previous studies, pharmacologically antagonizing M1 muscarinic receptors (M1Rs), Gqalpha, PLC, PLA2, and AA minimized N-current inhibition by the muscarinic agonist oxotremorine-M (Oxo-M). When cells were left untreated with PTX, leaving the membrane-delimited pathway intact and the same antagonists retested, Oxo-M decreased whole cell currents. Moreover, inhibited currents displayed slowed activation kinetics, indicating intact N-current inhibition by the membrane-delimited pathway. These findings indicate that the antagonists used to block the slow pathway acted selectively. PLA2 cleaves AA from phospholipids, generating additional metabolites. We tested whether the metabolite lysophosphatidic acid (LPA) mimicked the inhibitory actions of Oxo-M. In contrast to AA, applying LPA did not inhibit whole cell currents. Taken together, these findings suggest that the slow pathway requires M1Rs, Gqalpha, PLC, PIP2, PLA2, and AA for N-current inhibition.
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