ArticleThe Journal of general physiology2004
Mechanism of arachidonic acid modulation of the T-type Ca2+ channel alpha1G.
Article in The Journal of general physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 55 citations in OpenAlex.
- The anticonvulsant phytocannabinoids CBGVA and CBDVA inhibit recombinant T-type channels.Frontiers in pharmacology · 2022Article
- Neuronal Cav3 channelopathies: recent progress and perspectives.Pflugers Archiv : European journal of physiology · 2020Review
- A compartmentalized mathematical model of mouse atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2020Article
- Actions and Mechanisms of Polyunsaturated Fatty Acids on Voltage-Gated Ion Channels.Frontiers in physiology · 2017Review
- Effects of unsaturated fatty acids on the kinetics of voltage-gated proton channels heterologously expressed in cultured cells.The Journal of physiology · 2016Article
- Putative binding sites for arachidonic acid on the human cardiac Kv 1.5 channel.British journal of pharmacology · 2015Article
- 5,6-EET potently inhibits T-type calcium channels: implication in the regulation of the vascular tone.Pflugers Archiv : European journal of physiology · 2014Article
- Modulation of T-type calcium channels by bioactive lipids.Pflugers Archiv : European journal of physiology · 2014Review
- Low-voltage-activated T-type Ca2+ channel inhibitors as new tools in the treatment of glioblastoma: the role of endostatin.Pflugers Archiv : European journal of physiology · 2014Review
- Inhibition of human recombinant T-type calcium channels by N-arachidonoyl 5-HT.British journal of pharmacology · 2012Article
- T-type voltage-gated calcium channels as targets for the development of novel pain therapies.British journal of pharmacology · 2011Review
- The Ca2+ channel beta subunit determines whether stimulation of Gq-coupled receptors enhances or inhibits N current.The Journal of general physiology · 2009Article
- Regulation of voltage-gated Ca2+ channels by lipids.Cell calcium · 2009Review
- Arachidonic acid inhibition of L-type calcium (CaV1.3b) channels varies with accessory CaVbeta subunits.The Journal of general physiology · 2009Article
- Inhibition of human recombinant T-type calcium channels by the endocannabinoid N-arachidonoyl dopamine.British journal of pharmacology · 2009Article
- Arachidonic acid and ion channels: an update.British journal of pharmacology · 2008Review
- Activation of protein kinase C augments T-type Ca2+ channel activity without changing channel surface density.The Journal of physiology · 2006Article
- 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
- Evidence for common structural determinants of activation and inactivation in T-type Ca2+ channels.Pflugers Archiv : European journal of physiology · 2006Article
- The antiarrhythmic effect of n-3 polyunsaturated fatty acids: modulation of cardiac ion channels as a potential mechanism.The Journal of membrane biology · 2005Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arachidonic acid (AA) modulates T-type Ca(2+) channels and is therefore a potential regulator of diverse cell functions, including neuronal and cardiac excitability. The underlying mechanism of modulation is unknown. Here we analyze the effects of AA on the T-type Ca(2+) channel alpha(1G) heterologously expressed in HEK-293 cells. AA inhibited alpha(1G) currents within a few minutes, regardless of preceding exposure to inhibitors of AA metabolism (ETYA and 17-ODYA). Current inhibition was also observed in cell-free inside-out patches, indicating a membrane-delimited interaction of AA with the channel. AA action was consistent with a decrease of the open probability without changes in the size of unitary currents. AA shifted the inactivation curve to more negative potentials, increased the speed of macroscopic inactivation, and decreased the extent of recovery from inactivation at -80 mV but not at -110 mV. AA induced a slight increase of activation near the threshold and did not significantly change the deactivation kinetics or the rectification pattern. We observed a tonic current inhibition, regardless of whether the channels were held in resting or inactivated states during AA perfusion, suggesting a state-independent interaction with the channel. Model simulations indicate that AA inhibits T-type currents by switching the channels into a nonavailable conformation and by affecting transitions between inactivated states, which results in the negative shift of the inactivation curve. Slow-inactivating alpha(1G) mutants showed an increased affinity for AA with respect to the wild type, indicating that the structural determinants of fast inactivation are involved in the AA-channel interaction.
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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.