ArticleThe Journal of physiology2007
Decrease in PIP(2) channel interactions is the final common mechanism involved in PKC- and arachidonic acid-mediated inhibitions of GABA(B)-activated K+ current.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- PKC isoform-specific targeting of the phosphorylation site SerinePflugers Archiv : European journal of physiology · 2026Article
- Membrane-associated estrogen receptor α prevents the amyloid β-induced suppression of GIRK channel activity in hippocampal neurons from female mice.Biology of sex differences · 2025Article
- Amyloid-β oligomers trigger sex-dependent inhibition of GIRK channel activity in hippocampal neurons in mice.Science signaling · 2024Article
- Angiotensin receptors and αPflugers Archiv : European journal of physiology · 2024Article
- Involvement of CaCellular and molecular neurobiology · 2023Article
- Neuronal G protein-gated KAmerican journal of physiology. Cell physiology · 2022Review
- Kir Channel Molecular Physiology, Pharmacology, and Therapeutic Implications.Handbook of experimental pharmacology · 2021Review
- Gq-Coupled Muscarinic Receptor Enhancement of KCNQ2/3 Channels and Activation of TRPC Channels in Multimodal Control of Excitability in Dentate Gyrus Granule Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- A Critical Gating Switch at a Modulatory Site in Neuronal Kir3 Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Rescue of homeostatic regulation of striatal excitability and locomotor activity in a mouse model of Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Role of TRP channels in the cardiovascular system.American journal of physiology. Heart and circulatory physiology · 2015Review
- Article
- A genetically encoded tool kit for manipulating and monitoring membrane phosphatidylinositol 4,5-bisphosphate in intact cells.PloS one · 2011Article
- Regulation of Adenosine-activated GIRK Channels by Gq-coupled Receptors in Mouse Atrial Myocytes.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2010Article
- Substance P inhibits GABAB receptor signalling in the ventral tegmental area.The Journal of physiology · 2010Article
- Cholesterol inhibits M-type K+ channels via protein kinase C-dependent phosphorylation in sympathetic neurons.The Journal of biological chemistry · 2010Article
- Tibolone rapidly attenuates the GABAB response in hypothalamic neurones.Journal of neuroendocrinology · 2008Article
- Arachidonic acid and ion channels: an update.British journal of pharmacology · 2008Review
- Regulation of ion channels and transporters by phosphatidylinositol 4,5-bisphosphate.The Journal of physiology · 2007Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We showed in our previous study that in hippocampal CA1 neurons the stimulation of muscarinic receptors inhibited the GIRK current (I(GIRK)) via a PLC/PKC pathway, whereas group I metabotropic glutamate receptors (mGluR) inhibited I(GIRK) via a PLA(2)/arachidonic acid pathway. In this study, we present evidence that receptor-mediated signalling pathways activated by the two G(q)-coupled receptors (G(q)PCRs) converge on the inhibition of GIRK channel-PIP(2) interaction. I(GIRK) was activated in acutely isolated hippocampal CA1 neurons by repetitive application of baclofen, a GABA(B) receptor agonist, with a 2-3 min interval. When both CCh and DHPG were pretreated before the second I(GIRK) activation, the magnitude of the second I(GIRK) was 52.2 +/- 2.5% of the first I(GIRK), which was not significantly different from the magnitude of inhibition by CCh or DHPG alone. This result shows that the effects of muscarinic receptor and group I mGluR stimulation on I(GIRK) are not additive but occlusive, suggesting that each pathway may converge to a common mechanism that finally regulates I(GIRK). To test the involvement of PIP(2) in this mechanism, the effect of CCh and DHPG on I(GIRK) was tested in cells loaded with exogenous PIP(2). The inhibition of I(GIRK) by CCh or DHPG was almost completely abolished in PIP(2)-loaded cells. We confirmed that the inhibition of I(GIRK) by direct application of phorbol ester or arachidonic acid was also completely reversed in PIP(2)-loaded cells. These results indicate that the decrease in PIP(2)-channel interactions is the final common mechanism responsible for G(q)PCR-induced inhibitions of I(GIRK) mediated by PKC and arachidonic acid.
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