ArticleProceedings of the National Academy of Sciences of the United States of America2003
Arachidonic acid mediates muscarinic inhibition and enhancement of N-type Ca2+ current in sympathetic neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 68 citations in OpenAlex.
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- The HOOK region of voltage-gated Ca2+ channel β subunits senses and transmits PIP2 signals to the gate.The Journal of general physiology · 2017Article
- Eag1 KOxidative medicine and cellular longevity · 2017Review
- Actions and Mechanisms of Polyunsaturated Fatty Acids on Voltage-Gated Ion Channels.Frontiers in physiology · 2017Review
- Constitutive and ghrelin-dependent GHSR1a activation impairs CaV2.1 and CaV2.2 currents in hypothalamic neurons.The Journal of general physiology · 2015Article
- cAMP/PKA Pathways and S56 Phosphorylation Are Involved in AA/PGE2-Induced Increases in rNaV1.4 Current.PloS one · 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
- Arachidonic acid activation of BKCa (Slo1) channels associated to the β1-subunit in human vascular smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014Article
- Regulation of Ca(V)2 calcium channels by G protein coupled receptors.Biochimica et biophysica acta · 2013Review
- Membrane-localized β-subunits alter the PIP2 regulation of high-voltage activated Ca2+ channels.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Differential modulation of N-type calcium channels by micro-opioid receptors in oxytocinergic versus vasopressinergic neurohypophysial terminals.Journal of cellular physiology · 2010Article
- Modulation of high-voltage activated Ca(2+) channels by membrane phosphatidylinositol 4,5-bisphosphate.Neuron · 2010Article
- Orientation of palmitoylated CaVbeta2a relative to CaV2.2 is critical for slow pathway modulation of N-type Ca2+ current by tachykinin receptor activation.The Journal of general physiology · 2009Article
- The Ca2+ channel beta subunit determines whether stimulation of Gq-coupled receptors enhances or inhibits N current.The Journal of general physiology · 2009Article
- An oily competition: role of beta subunit palmitoylation for Ca2+ channel modulation by fatty acids.The Journal of general physiology · 2009Article
- Inhibition of N and PQ calcium channels by calcium entry through L channels in chromaffin cells.Pflugers Archiv : European journal of physiology · 2009Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
N-type Ca(2+) channels participate in acute activity-dependent processes such as regulation of Ca(2+)-activated K(+) channels and in more prolonged events such as gene transcription and long-term depression. A slow postsynaptic M(1) muscarinic receptor-mediated modulation of N-type current in superior cervical ganglion neurons may be important in regulating these processes. This slow pathway inhibits N-type current by using a diffusible second messenger that has remained unidentified for more than a decade. Using whole-cell patch-clamp techniques, which isolate the slow pathway, we found that the muscarinic agonist oxotremorine methiodide not only inhibits currents at positive potentials but enhances N-type current at negative potentials. Enhancement was also observed in cell-attached patches. These findings provide evidence for N-type Ca(2+)-current enhancement by a classical neurotransmitter. Moreover, enhancement and inhibition of current by oxotremorine methiodide mimics modulation observed with direct application of a low concentration of arachidonic acid (AA). Although no transmitter has been reported to use AA as a second messenger to modulate any Ca(2+) current in either neuronal or nonneuronal cells, we nevertheless tested whether a fatty acid signaling cascade was involved. Blocking phospholipase C, phospholipase A(2), or AA but not AA metabolism minimized muscarinic modulation of N-type current, supporting the participation of these molecules in the slow pathway. A role for the G protein G(q) was also confirmed by blocking muscarinic modulation of Ca(2+) currents with anti-G(qalpha) antibody. Our finding that AA participates in the slow pathway strongly suggests that it may be the previously unknown diffusible second messenger.
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