ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Inositol triphosphate-mediated Ca2+ signals direct purinergic P2Y receptor regulation of neuronal ion channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
47 citing papers in PubMed, 71 citations in OpenAlex.
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- Ticagrelor Can Regulate the Ion Channel Characteristics of Superior Cervical Ganglion Neurons after Myocardial Infarction.Journal of cardiovascular development and disease · 2023Article
- Biophysical physiology of phosphoinositide rapid dynamics and regulation in living cells.The Journal of general physiology · 2022Article
- Kv7 Channels and Excitability Disorders.Handbook of experimental pharmacology · 2021Article
- Phosphatidylinositol 4,5-bisphosphate is regenerated by speeding of the PI 4-kinase pathway during long PLC activation.The Journal of general physiology · 2020Article
- PIPInternational journal of molecular sciences · 2020Article
- Pharmacological Manipulation of KFrontiers in physiology · 2020Review
- 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
- Phosphatidylinositol 4,5-bisphosphate (PIPThe Journal of biological chemistry · 2018Article
- Neuronal heterogeneity and stereotyped connectivity in the auditory afferent system.Nature communications · 2018Article
- Metabotropic Acetylcholine and Glutamate Receptors Mediate PI(4,5)PScientific reports · 2018Article
- Calmodulin: A Multitasking Protein in Kv7.2 Potassium Channel Functions.Biomolecules · 2018Review
- M-type KBritish journal of pharmacology · 2018Review
- A Calcium-Dependent Chloride Current Increases Repetitive Firing in Mouse Sympathetic Neurons.Frontiers in physiology · 2018Article
- Glia-derived ATP inversely regulates excitability of pyramidal and CCK-positive neurons.Nature communications · 2017Article
- Differential Regulation of PI(4,5)PFrontiers in molecular neuroscience · 2017Article
- P2Y Receptors Sensitize Mouse and Human Colonic Nociceptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Dynamics of Phosphoinositide-Dependent Signaling in Sympathetic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- KCNQ potassium channels in sensory system and neural circuits.Acta pharmacologica Sinica · 2016Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Purinergic P2Y receptors are one of four types of G(q/11)-coupled receptors in rat superior cervical ganglia (SCG) sympathetic neurons. In cultured SCG neurons, purinergic and bradykinin suppression of I(M) were similar in magnitude and somewhat less than that by muscarinic agonists. The effects of the P2Y receptor agonist UTP on neuronal excitability and discharge properties were studied. Under current clamp, UTP increased action potential (AP) firing in response to depolarizing current steps, depolarized the resting potential, decreased the threshold current required to fire an AP, and decreased spike-frequency adaptation. These effects were very similar to those resulting from bradykinin stimulation and not as profound as from muscarinic stimulation or full M-current blockade. We then examined the P2Y mechanism of action. Like bradykinin, but unlike muscarinic, purinergic stimulation induced rises in intracellular [Ca(2+)](i). Tests using expression of IP(3)"sponge" or IP(3) phosphatase constructs implicated IP(3) accumulation as necessary for purinergic suppression of I(M). Overexpression of wild-type or dominant-negative calmodulin (CaM) implicated Ca(2+)/CaM in the purinergic action. Both sets of results were similar to bradykinin, and opposite to muscarinic, suppression. We also examined modulation of Ca(2+) channels. As for bradykinin, purinergic stimulation did not suppress I(Ca), unless neuronal calcium sensor-1 (NCS-1) activity was blocked by a dominant-negative NCS-1 construct. Our results indicate that P2Y receptors modulate M-type channels in SCG cells via IP(3)-mediated [Ca(2+)](i) signals in concert with CaM and not by depletion of phosphatidylinositol-4, 5-biphosphate. We group purinergic P2Y and bradykinin B(2) receptors together as having a common mode of action.
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Registered trials
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.