ArticlePflugers Archiv : European journal of physiology1993
Protein kinase C as mediator of arachidonic acid-induced decrease of neuronal M current.
Article in Pflugers Archiv : European journal of physiology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 24 citations in OpenAlex.
- Protein kinase C shifts the voltage dependence of KCNQ/M channels expressed in Xenopus oocytes.The Journal of physiology · 2005Article
- Cholinergic inhibition of neocortical pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Arachidonic acid plays a role in rat vomeronasal signal transduction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Cannabinoids decrease the K(+) M-current in hippocampal CA1 neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Separation of M-like current and ERG current in NG108-15 cells.British journal of pharmacology · 1999Article
- Inhibition of rat neuronal kainate receptors by cis-unsaturated fatty acids.The Journal of physiology · 1998Article
- Roles of arachidonic acid, lipoxygenases and phosphatases in calcium-dependent modulation of M-current in bullfrog sympathetic neurons.The Journal of physiology · 1995Article
- Modulation of neuronal calcium channels by arachidonic acid and related substances.The Journal of membrane biology · 1995Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The M current, IM, of NG108-15 neuroblastoma x glioma hybrid cells, a non-inactivating K+ current, is decreased by arachidonic acid (5-25 microM), often after an initial transitory increase. To test the possibility that the decrease is caused by activation of protein kinase C (PKC) we used the PKC 19-31 peptide, which is an effective inhibitor of PKC. With 1 microM peptide in the pipette solution the normally observed strong reduction of IM by 1 microM phorbol 12,13-dibutyrate (PDB) was almost totally prevented, indicating that PKC is completely inhibited; also the voltage dependence of the M conductance, gM(V), was shifted to more negative membrane potentials. In the presence of 1 microM peptide the effect of 25 microM arachidonic acid on IM was significantly reduced, suggesting that the effect, or at least a large part of it, is mediated by PKC.
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