ArticleDevelopmental neurobiology2013
Arachidonic acid closes innexin/pannexin channels and thereby inhibits microglia cell movement to a nerve injury.
Article in Developmental neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 37 citations in OpenAlex.
- Pericyte pannexin1 controls cerebral capillary diameter and supports memory function.Nature communications · 2025Article
- Unnexin is a protein subunit of a large-pore channel expressed by unicellular organisms.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Integrated Metabolomics and Network Pharmacology to Reveal the Mechanisms of Gandouling Tablets Against Copper-Overload-Induced Neuronal Injury in Rats with Wilson's Disease.Drug design, development and therapy · 2023Article
- Mechanisms of Pannexin 1 (PANX1) Channel Mechanosensitivity and Its Pathological Roles.International journal of molecular sciences · 2022Review
- Review
- Structure versus function: Are new conformations of pannexin 1 yet to be resolved?The Journal of general physiology · 2021Article
- In focus in HCB.Histochemistry and cell biology · 2020Article
- PUFAs supplementation affects the renal expression of pannexin 1 and connexins in diabetic kidney of rats.Histochemistry and cell biology · 2020Article
- Gap Junction Channels of Innexins and Connexins: Relations and Computational Perspectives.International journal of molecular sciences · 2019Review
- Innexins: Expression, Regulation, and Functions.Frontiers in physiology · 2018Review
- Inhibitors of connexin and pannexin channels as potential therapeutics.Pharmacology & therapeutics · 2017Review
- Regulation of Connexin-Based Channels by Fatty Acids.Frontiers in physiology · 2017Review
- Connexins and Pannexins: New Insights into Microglial Functions and Dysfunctions.Frontiers in molecular neuroscience · 2016Review
- ATP release through pannexon channels.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Review
- Hypothalamic innate immune reaction in obesity.Nature reviews. Endocrinology · 2015Review
- Mechanosensitive unpaired innexin channels in C. elegans touch neurons.American journal of physiology. Cell physiology · 2014Article
- Inhibitors of the 5-lipoxygenase pathway activate pannexin1 channels in macrophages via the thromboxane receptor.American journal of physiology. Cell physiology · 2014Article
- Regulation of hemichannels and gap junction channels by cytokines in antigen-presenting cells.Mediators of inflammation · 2014Review
- Regulation of cellular communication by signaling microdomains in the blood vessel wall.Pharmacological reviews · 2014Review
- The pannexins: past and present.Frontiers in physiology · 2014Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pannexons are membrane channels formed by pannexins and are permeable to ATP. They have been implicated in various physiological and pathophysiological processes. Innexins, the invertebrate homologues of the pannexins, form innexons. Nerve injury induces calcium waves in glial cells, releasing ATP through glial pannexon/innexon channels. The ATP then activates microglia. More slowly, injury releases arachidonic acid (ArA). The present experiments show that ArA itself reduced the macroscopic membrane currents of innexin- and of pannexin-injected oocytes; ArA also blocked K(+) -induced release of ATP. In leeches, whose large glial cells have been favorable for studying control of microglia migration, ArA blocked glial dye-release and, evidently, ATP-release. A physiological consequence in the leech was block of microglial migration to nerve injuries. Exogenous ATP (100 µM) reversed the effect, for ATP causes activation and movement of microglia after nerve injury, but nitric oxide directs microglia to the lesion. It was not excluded that metabolites of ArA may also inhibit the channels. But for all these effects, ArA and its non-metabolizable analog eicosatetraynoic acid (ETYA) were indistinguishable. Therefore, ArA itself is an endogenous regulator of pannexons and innexons. ArA thus blocks release of ATP from glia after nerve injury and thereby, at least in leeches, stops microglia at lesions.
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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.