Recovery from muscarinic modulation of M current channels requires phosphatidylinositol 4,5-bisphosphate synthesis
Suppression of M current channels by muscarinic receptors enhances neuronal excitability. Little is known about the molecular mechanism of this inhibition except the requirement for a specific G protein and the involvement of an unidentified diffusible second messenger. We demonstrate here that intr...
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| Vydané v: | Neuron (Cambridge, Mass.) Ročník 35; číslo 3; s. 507 |
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| Hlavní autori: | , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
United States
01.08.2002
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| Predmet: | |
| ISSN: | 0896-6273 |
| On-line prístup: | Zistit podrobnosti o prístupe |
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| Abstract | Suppression of M current channels by muscarinic receptors enhances neuronal excitability. Little is known about the molecular mechanism of this inhibition except the requirement for a specific G protein and the involvement of an unidentified diffusible second messenger. We demonstrate here that intracellular ATP is required for recovery of KCNQ2/KCNQ3 current from muscarinic suppression, with an EC(50) of approximately 0.5 mM. Substitution of nonhydrolyzable ATP analogs for ATP slowed or prevented recovery. ADPbetaS but not ADP also prevented the recovery. Receptor-mediated inhibition was irreversible when recycling of agonist-sensitive pools of phosphatidylinositol-4,5-bisphosphate (PIP(2)) was blocked by lipid kinase inhibitors. Lipid phosphorylation by PI 4-kinase is required for recovery from muscarinic modulation of M current. |
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| AbstractList | Suppression of M current channels by muscarinic receptors enhances neuronal excitability. Little is known about the molecular mechanism of this inhibition except the requirement for a specific G protein and the involvement of an unidentified diffusible second messenger. We demonstrate here that intracellular ATP is required for recovery of KCNQ2/KCNQ3 current from muscarinic suppression, with an EC(50) of approximately 0.5 mM. Substitution of nonhydrolyzable ATP analogs for ATP slowed or prevented recovery. ADPbetaS but not ADP also prevented the recovery. Receptor-mediated inhibition was irreversible when recycling of agonist-sensitive pools of phosphatidylinositol-4,5-bisphosphate (PIP(2)) was blocked by lipid kinase inhibitors. Lipid phosphorylation by PI 4-kinase is required for recovery from muscarinic modulation of M current. Suppression of M current channels by muscarinic receptors enhances neuronal excitability. Little is known about the molecular mechanism of this inhibition except the requirement for a specific G protein and the involvement of an unidentified diffusible second messenger. We demonstrate here that intracellular ATP is required for recovery of KCNQ2/KCNQ3 current from muscarinic suppression, with an EC(50) of approximately 0.5 mM. Substitution of nonhydrolyzable ATP analogs for ATP slowed or prevented recovery. ADPbetaS but not ADP also prevented the recovery. Receptor-mediated inhibition was irreversible when recycling of agonist-sensitive pools of phosphatidylinositol-4,5-bisphosphate (PIP(2)) was blocked by lipid kinase inhibitors. Lipid phosphorylation by PI 4-kinase is required for recovery from muscarinic modulation of M current.Suppression of M current channels by muscarinic receptors enhances neuronal excitability. Little is known about the molecular mechanism of this inhibition except the requirement for a specific G protein and the involvement of an unidentified diffusible second messenger. We demonstrate here that intracellular ATP is required for recovery of KCNQ2/KCNQ3 current from muscarinic suppression, with an EC(50) of approximately 0.5 mM. Substitution of nonhydrolyzable ATP analogs for ATP slowed or prevented recovery. ADPbetaS but not ADP also prevented the recovery. Receptor-mediated inhibition was irreversible when recycling of agonist-sensitive pools of phosphatidylinositol-4,5-bisphosphate (PIP(2)) was blocked by lipid kinase inhibitors. Lipid phosphorylation by PI 4-kinase is required for recovery from muscarinic modulation of M current. |
| Author | Hille, Bertil Suh, Byung-Chang |
| Author_xml | – sequence: 1 givenname: Byung-Chang surname: Suh fullname: Suh, Byung-Chang organization: Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, WA 98195, USA – sequence: 2 givenname: Bertil surname: Hille fullname: Hille, Bertil |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/12165472$$D View this record in MEDLINE/PubMed |
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| Snippet | Suppression of M current channels by muscarinic receptors enhances neuronal excitability. Little is known about the molecular mechanism of this inhibition... |
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| SubjectTerms | 1-Phosphatidylinositol 4-Kinase - antagonists & inhibitors 1-Phosphatidylinositol 4-Kinase - metabolism Adenosine Diphosphate - metabolism Adenosine Diphosphate - pharmacology Adenosine Triphosphate - analogs & derivatives Adenosine Triphosphate - metabolism Adenosine Triphosphate - pharmacology Animals Cells, Cultured Enzyme Inhibitors - pharmacology Glucose - metabolism Glucose - pharmacology GTP-Binding Proteins - drug effects GTP-Binding Proteins - metabolism KCNQ2 Potassium Channel KCNQ3 Potassium Channel Male Membrane Potentials - drug effects Membrane Potentials - physiology Muscarinic Agonists - pharmacology Neural Inhibition - drug effects Neural Inhibition - physiology Neurons - cytology Neurons - drug effects Neurons - metabolism Phosphatidylinositol 4,5-Diphosphate - biosynthesis Phosphorylation Potassium Channels - drug effects Potassium Channels - genetics Potassium Channels - metabolism Potassium Channels, Voltage-Gated Rats Rats, Sprague-Dawley Receptors, Muscarinic - drug effects Receptors, Muscarinic - metabolism Superior Cervical Ganglion - cytology Superior Cervical Ganglion - drug effects Superior Cervical Ganglion - metabolism Synaptic Transmission - drug effects Synaptic Transmission - physiology Type C Phospholipases - antagonists & inhibitors Type C Phospholipases - metabolism |
| Title | Recovery from muscarinic modulation of M current channels requires phosphatidylinositol 4,5-bisphosphate synthesis |
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