ArticleThe Journal of physiology2004
Physiological mechanisms of lysophosphatidylcholine-induced de-ramification of murine microglia.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 71 citations in OpenAlex.
- Lysophospholipids in Synucleinopathies: A Conceptual Framework Linking Proteostasis and Neuroinflammatory Signaling.Brain sciences · 2026Review
- Metabolomics-driven elucidation of the synergistic therapeutic mechanism of a novel SGLT-2/PPAR-γ dual receptor supramolecular system for treatment diabetes and obesity.Journal of pharmaceutical analysis · 2025Article
- Multi-omics reveal critical roles of phosphatidylcholine and sphingomyelin in antipsychotic efficacy for schizophrenia.Signal transduction and targeted therapy · 2025Article
- Impaired membrane lipids in ischemic stroke: a key player in inflammation and thrombosis.Journal of neuroinflammation · 2025Article
- Lysophosphatidylcholine induced by fat transplantation regulates hyperalgesia by affecting the dysfunction of ACC perineuronal nets.iScience · 2024Article
- Genetic Downregulation of GABACells · 2024Article
- Helicobacter pylori outer membrane vesicles directly promote Aβ aggregation and enhance Aβ toxicity in APP/PS1 mice.Communications biology · 2024Article
- Dried Blood Spot Metabolome Features of Ischemic-Hypoxic Encephalopathy: A Neonatal Rat Model.International journal of molecular sciences · 2024Article
- Identification of Metabolomic Signatures for Ischemic Hypoxic Encephalopathy Using a Neonatal Rat Model.Children (Basel, Switzerland) · 2023Article
- Maternal antibiotic administration during gestation can affect the memory and brain structure in mouse offspring.Frontiers in cellular neuroscience · 2023Article
- Microglial morphometric analysis: so many options, so little consistency.Frontiers in neuroinformatics · 2023Review
- Dynamic Responses of Microglia in Animal Models of Multiple Sclerosis.Frontiers in cellular neuroscience · 2020Article
- TRPM2 Channel in Microglia as a New Player in Neuroinflammation Associated With a Spectrum of Central Nervous System Pathologies.Frontiers in pharmacology · 2019Review
- NLR members NLRC4 and NLRP3 mediate sterile inflammasome activation in microglia and astrocytes.The Journal of experimental medicine · 2017Article
- IL-4 type 1 receptor signaling up-regulates KCNN4 expression, and increases the KCa3.1 current and its contribution to migration of alternative-activated microglia.Frontiers in cellular neuroscience · 2014Article
- Inhibition of microglia activation as a phenotypic assay in early drug discovery.Journal of biomolecular screening · 2014Review
- Differential response of macrophages to core-shell Fe3O4@Au nanoparticles and nanostars.Nanoscale · 2012Article
- Significance of brain tissue oxygenation and the arachidonic acid cascade in stroke.Antioxidants & redox signaling · 2011Review
- Lysophosphatidylcholine- and MCP-1-induced chemotaxis of monocytes requires potassium channel activity.Pflugers Archiv : European journal of physiology · 2009Article
- Lipopolysaccharide-induced down-regulation of Ca2+ release-activated Ca2+ currents (I CRAC) but not Ca2+-activated TRPM4-like currents (I CAN) in cultured mouse microglial cells.The Journal of physiology · 2008Article
Corrections and comments
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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
Activation of microglial cells, the resident macrophages of the brain, occurs rapidly following brain injury. De-ramification, i.e. transformation from ramified into amoeboid morphology is one of the earliest manifestations of microglial activation. In the present study, we identified the physiological mechanisms underlying microglial de-ramification induced by lysophosphatidylcholine (LPC). Patch-clamp experiments revealed activation of non-selective cation currents and Ca(2+)-dependent K(+) currents by extracellular LPC. LPC-activated non-selective cation channels were permeable for monovalent and divalent cations. They were inhibited by Gd(3+), La(3+), Zn(2+) and Grammostola spatulata venom, but were unaffected by diltiazem, LOE908MS, amiloride and DIDS. Ca(2+) influx through non-selective cation channels caused sustained increases in intracellular Ca(2+) concentration. These Ca(2+) increases were sufficient to elicit charybdotoxin-sensitive Ca(2+)-dependent K(+) currents. However, increased [Ca(2+)](i) was not required for LPC-induced morphological changes. In LPC-stimulated microglial cells, non-selective cation currents caused transient membrane depolarization, which was followed by sustained membrane hyperpolarization induced by Ca(2+)-dependent K(+) currents. Furthermore, LPC elicited K(+) efflux by stimulating electroneutral K(+)-Cl(-) cotransporters, which were inhibited by furosemide and DIOA. LPC-induced microglial de-ramification was prevented by simultaneous inhibition of non-selective cation channels and K(+)-Cl(-) cotransporters, suggesting their functional importance for microglial activation.
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