ArticleChannels (Austin, Tex.)
Swelling activated Cl- channels in microglia: Biophysics, pharmacology and role in glutamate release.
Article in Channels (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
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- Excitotoxic Storms of Ischemic Stroke: A Non-neuronal Perspective.Molecular neurobiology · 2024Review
- Trends in volume-regulated anion channel (VRAC) research: visualization and bibliometric analysis from 2014 to 2022.Frontiers in pharmacology · 2023Article
- A SWELL time to develop the molecular pharmacology of the volume-regulated anion channel (VRAC).Channels (Austin, Tex.) · 2022Review
- Ion channels as a therapeutic target for renal fibrosis.Frontiers in physiology · 2022Review
- The NKCC1 ion transporter modulates microglial phenotype and inflammatory response to brain injury in a cell-autonomous manner.PLoS biology · 2022Article
- Article
- Roles of Microglial Ion Channel in Neurodegenerative Diseases.Journal of clinical medicine · 2021Review
- Cell Death Induction and Protection by Activation of Ubiquitously Expressed Anion/Cation Channels. Part 1: Roles of VSOR/VRAC in Cell Volume Regulation, Release of Double-Edged Signals and Apoptotic/Necrotic Cell Death.Frontiers in cell and developmental biology · 2020Review
- Substrate Elasticity Exerts Functional Effects on Primary Microglia.Frontiers in cellular neuroscience · 2020Article
- Metabolic constraints of swelling-activated glutamate release in astrocytes and their implication for ischemic tissue damage.Journal of neurochemistry · 2019Article
- Involvement of extrasynaptic glutamate in physiological and pathophysiological changes of neuronal excitability.Cellular and molecular life sciences : CMLS · 2018Review
- ATP release during cell swelling activates a CaScientific reports · 2017Article
- Volume-regulated anion channel--a frenemy within the brain.Pflugers Archiv : European journal of physiology · 2016Review
- Roles of microglia in brain development, tissue maintenance and repair.Brain : a journal of neurology · 2015Review
- The central role of aquaporins in the pathophysiology of ischemic stroke.Frontiers in cellular neuroscience · 2015Review
- Aquaporin and brain diseases.Biochimica et biophysica acta · 2014Review
- Article
- Flufenamic acid as an ion channel modulator.Pharmacology & therapeutics · 2013Review
- Microglial SK3 and SK4 currents and activation state are modulated by the neuroprotective drug, riluzole.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013Article
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Microglia have a swelling-activated Cl- current (which we call IClswell), and while some of its biophysical properties and functional roles have been elucidated, its molecular identity is unknown. To relate this current to cell functions and determine whether it is regulated by mechanisms other than cell swelling, it is important to establish both biophysical and pharmacological fingerprints. Here, we used rat microglia and a cell line derived from them (MLS-9) to study biophysical, regulatory and pharmacological properties of IClswell. The whole-cell current was activated in response to a hypo-osmotic bath solution, but not by voltage, and was time-independent during long voltage steps. The halide selectivity sequence was I->Br->Cl- (Eisenman sequence I) and importantly, the excitatory amino acid, glutamate was permeant. Current activation required internal ATP, and was not affected by the guanine nucleotides, GTPS or GDPS, or physiological levels of internal Mg2+. The same current was activated by a low intracellular ionic strength solution without an osmotic gradient. IClswell was reversibly inhibited by known Cl- channel blockers (NPPB, flufenamic acid, glibenclamide, DCPIB), and by the glutamate release inhibitor, riluzole. Cell swelling evoked glutamate release from primary microglia and MLS-9 cells, and this was inhibited by the blockers (above), and by IAA-94, but not by tamoxifen or the Na+/K+/Cl- symport inhibitor, bumetanide. Together, these results confirm the similarity of IClswell in the two cell types, and point to a role for this channel in inflammation-mediated glutamate release in the CNS.
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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.