ArticleCurrent neuropharmacology2006
The action of prostaglandins on ion channels.
Article in Current neuropharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 51 citations in OpenAlex.
- Article
- Inflammation and vasopressin hypersecretion in aging.Frontiers in endocrinology · 2025Review
- Schwann cell-secreted PGECell · 2024Article
- Crosstalk between P2Y receptors and cyclooxygenase activity in inflammation and tissue repair.Purinergic signalling · 2024Review
- The Role of Neuro-Immune Interactions in Chronic Pain: Implications for Clinical Practice.Journal of pain research · 2022Review
- Prostaglandin ERespiratory research · 2021Article
- Novel Analgesics with Peripheral Targets.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- Impairment of electroneutral NaAmerican journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Promiscuous G-Protein-Coupled Receptor Inhibition of Transient Receptor Potential Melastatin 3 Ion Channels by Gβγ Subunits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Enriched Chicken Bone Broth as a Dietary Supplement Reduces Nociception and Sensitization Associated with Prolonged Jaw Opening.Journal of oral & facial pain and headache · 2018Article
- A new role of growth hormone and insulin growth factor receptor type 1 in neonatal inflammatory nociception.Pain reports · 2017Article
- Current and Future Issues in the Development of Spinal Agents for the Management of Pain.Current neuropharmacology · 2017Review
- PnPP-19, a spider toxin peptide, induces peripheral antinociception through opioid and cannabinoid receptors and inhibition of neutral endopeptidase.British journal of pharmacology · 2016Article
- Bromoenol Lactone, an Inhibitor of Calcium-Independent Phospholipase A2, Suppresses Carrageenan-Induced Prostaglandin Production and Hyperalgesia in Rat Hind Paw.Mediators of inflammation · 2015Article
- Oxidative-stress induced increase in circulating fatty acids does not contribute to phospholipase A2-dependent appetitive long-term memory failure in the pond snail Lymnaea stagnalis.BMC neuroscience · 2014Article
- Exenatide induces aortic vasodilation increasing hydrogen sulphide, carbon monoxide and nitric oxide production.Cardiovascular diabetology · 2014Article
- Possible role of hemichannels in cancer.Frontiers in physiology · 2014Article
- Effect of chloride channel inhibitors on cytosolic Ca2+ levels and Ca2+-activated K+ (Gardos) channel activity in human red blood cells.The Journal of membrane biology · 2013Article
- Change in prostaglandin expression levels and synthesizing activities in dry eye disease.Ophthalmology · 2012Article
- Fish oil concentrate delays sensitivity to thermal nociception in mice.Pharmacological research · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostaglandins, in particular PGE(2) and prostacyclin PGI(2) have diverse biological effects. Most importantly, they are involved in inflammation and pain. Prostaglandins in nano- and micromolar concentrations sensitize nerve cells, i.e. make them more sensitive to electrical or chemical stimuli. Sensitization arises from the effect of prostaglandins on ion channels and occurs both at the peripheral terminal of nociceptors at the site of tissue injury (peripheral sensitization) and at the synapses in the spinal cord (central sensitization). The first step is the binding of prostaglandins to receptors in the cell membrane, mainly EP and IP receptors. The receptors couple via G proteins to enzymes such as adenylate cyclase and phospholipase C (PLC). Activation of adenylate cyclase leads to increase of cAMP and subsequent activation of protein kinase A (PKA) or PKA-independent effects of cAMP, e.g. mediated by Epac (=exchange protein activated by cAMP). Activation of PLC causes increase of inositol phosphates and increase of cytosolic calcium. This article summarizes the effects of PGE(2), PGE(1), PGI2 and its stable analogues on non-selective cation channels and sodium, potassium, calcium and chloride channels. It describes the mechanism responsible for the facilitatory or inhibitory prostaglandin effects on ion channels. Understanding these mechanisms is essential for the development of useful new analgesics.
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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.