ArticleThe Journal of physiology1998
Inhibition of rat neuronal kainate receptors by cis-unsaturated fatty acids.
Article in The Journal of physiology, 1998. 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, 34 citations in OpenAlex.
- Beyond Genes: Metabolomic Evidence Indicates Potential Species-Level Differentiation in European Wild Rabbits.Journal of experimental zoology. Part A, Ecological and integrative physiology · 2026Article
- Kainate Receptor Antagonists: Recent Advances and Therapeutic Perspective.International journal of molecular sciences · 2023Review
- Structural basis of AMPA receptor inhibition by trans-4-butylcyclohexane carboxylic acid.British journal of pharmacology · 2022Article
- Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.Pharmacological reviews · 2021Review
- AMPA receptor structure and auxiliary subunits.The Journal of physiology · 2021Review
- Clinical concentrations of chemically diverse general anesthetics minimally affect lipid bilayer properties.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Chimeric Glutamate Receptor Subunits Reveal the Transmembrane Domain Is Sufficient for NMDA Receptor Pore Properties but Some Positive Allosteric Modulators Require Additional Domains.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Purine receptors are required for DHA-mediated neuroprotection against oxygen and glucose deprivation in hippocampal slices.Purinergic signalling · 2015Article
- Glutamate receptor pores.The Journal of physiology · 2015Review
- Radial symmetry in a chimeric glutamate receptor pore.Nature communications · 2014Article
- Q/R site interactions with the M3 helix in GluK2 kainate receptor channels revealed by thermodynamic mutant cycles.The Journal of general physiology · 2013Article
- Fatty acid modulation and polyamine block of GluK2 kainate receptors analyzed by scanning mutagenesis.The Journal of general physiology · 2010Article
- Glutamate receptor ion channels: structure, regulation, and function.Pharmacological reviews · 2010Review
- Amino acid substitutions in the pore helix of GluR6 control inhibition by membrane fatty acids.The Journal of general physiology · 2008Article
- Docosahexaenoic acid alters bilayer elastic properties.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Q/R site editing controls kainate receptor inhibition by membrane fatty acids.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Effect of derivatives of docosahexaenoic acid on AMPA receptors in Purkinje neurons.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sectionsArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
1. Whole-cell recordings from cultured rat hippocampal neurons, from freshly dissociated dorsal root ganglion (DRG) neurons and from human embryonic kidney (HEK) 293 cells expressing the glutamate receptor GluR6 subunit were used to study the modulation of kainate receptor channels by long chain fatty acids. 2. In all three cell types, application of cis-unsaturated fatty acids caused a dose-dependent reduction in whole-cell currents evoked by kainate. Docosahexaenoic acid (DHA), arachidonic acid (AA), linolenic acid and linoleic acid all produced substantial inhibition at a concentration of 50 microM, whereas inhibition by linolenelaidic acid and linolelaidic acid was significantly weaker. Fully saturated fatty acids were essentially inactive. 3. With continuous exposure to active fatty acids, the peak current elicited by kainate declined over a time course of several minutes to reach a steady-state level less than 50 % of the initial amplitude. Recovery was slow in control solution, but was speeded up by exposure to bovine serum albumin (0.5 mg ml-1), a protein that binds fatty acids with submicromolar affinity. The inhibition in neurons was half-maximal with 5-15 microM AA or DHA, but potency was at least 10-fold greater at GluR6 in HEK 293 cells. 4. Inhibition by AA or DHA was unaffected by extracellular nordihydroguaiaretic acid (10 microM), indomethacin (10 microM), 17-octadecynoic acid (30 microM) or 1-(5-isoquinolinylsulphonyl)-2-methylpiperazine dihydrochloride (H-7; 10 microM). Furthermore, inclusion of H-7 (100 microM), BAPTA (10 mM), AA (50 microM), antioxidants, or the protein kinase C inhibitor PKC19-36 (20 microM) in the internal solution had little effect on whole-cell currents and did not prevent inhibition of currents by extracellular application of AA or DHA. 5. We conclude that the inhibition produced by cis-unsaturated fatty acids does not require conversion to oxidized metabolites or activation of PKC. Instead, active compounds may interact directly with an extracellular, or intramembraneous, site on kainate receptors.
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