ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Roles of volume-sensitive chloride channel in excitotoxic neuronal injury.
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 48 papers.
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Who cites it
48 citing papers in PubMed, 86 citations in OpenAlex.
- Mechanism of action of two potent LRRC8/VRAC channel inhibitors.Research square · 2026Article
- Boi-Ogi-To, a Traditional Japanese Kampo Medicine, Promotes Cellular Excretion of Chloride and Water by Activating Volume-Sensitive Outwardly Rectifying Anion Channels.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The SWELL1 Channel Promotes Ischemic Brain Damage by Mediating Neuronal Swelling and Glutamate Toxicity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Physiology of the volume-sensitive/regulatory anion channel VSOR/VRAC. Part 1: from its discovery and phenotype characterization to the molecular entity identification.The journal of physiological sciences : JPS · 2024Review
- Honey, I shrunk the extracellular space: Measurements and mechanisms of astrocyte swelling.Glia · 2022Review
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- Astrocytic Glutamatergic Transmission and Its Implications in Neurodegenerative Disorders.Cells · 2022Review
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- Time dependence in diffusion MRI predicts tissue outcome in ischemic stroke patients.Magnetic resonance in medicine · 2021Article
- Dysregulation of Astrocyte Ion Homeostasis and Its Relevance for Stroke-Induced Brain Damage.International journal of molecular sciences · 2021Review
- Properties, Structures, and Physiological Roles of Three Types of Anion Channels Molecularly Identified in the 2010's.Frontiers in physiology · 2021Review
- Cell Death Induction and Protection by Activation of Ubiquitously Expressed Anion/Cation Channels. Part 2: Functional and Molecular Properties of ASOR/PAC Channels and Their Roles in Cell Volume Dysregulation and Acidotoxic Cell Death.Frontiers in cell and developmental biology · 2021Review
- Viscoelasticity and Volume of Cortical Neurons under Glutamate Excitotoxicity and Osmotic Challenges.Biophysical journal · 2020Article
- LRRC8A-dependent volume-regulated anion channels contribute to ischemia-induced brain injury and glutamatergic input to hippocampal neurons.Experimental neurology · 2020Article
- Intracellular ClPflugers Archiv : European journal of physiology · 2020Review
- Ischemia-Triggered Glutamate Excitotoxicity From the Perspective of Glial Cells.Frontiers in cellular neuroscience · 2020Article
- Norcepharadione B attenuates HExperimental biology and medicine (Maywood, N.J.) · 2019Article
- The signaling role for chloride in the bidirectional communication between neurons and astrocytes.Neuroscience letters · 2019Review
- Blockade of the swelling-induced chloride current attenuates the mouse neonatal hypoxic-ischemic brain injury in vivo.Acta pharmacologica Sinica · 2018Article
- SWELL1 is a glucose sensor regulating β-cell excitability and systemic glycaemia.Nature communications · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Excitotoxicity is associated with stroke, brain trauma, and a number of neurodegenerative disorders. In the brain, during excitotoxic insults, neurons undergo rapid swelling in both the soma and dendrites. Focal swellings along the dendrites called varicosities are considered to be a hallmark of acute excitotoxic neuronal injury. However, it is not clear what pathway is involved in the neuronal anion flux that leads to the formation and resolution of excitotoxic varicosities. Here, we assessed the roles of the volume-sensitive outwardly rectifying (VSOR) Cl- channel in excitotoxic responses in mouse cortical neurons. Whole-cell patch-clamp recordings revealed that the VSOR Cl- channel in cultured neurons was activated by NMDA exposure. Moreover, robust expression of this channel on varicosities was confirmed by on-cell and nystatin-perforated vesicle patch techniques. VSOR channel blockers, but not blockers of GABA(A) receptors and Cl- transporters, abolished not only varicosity resolution after sublethal excitotoxic stimulation but also necrotic death after sustained varicosity formation induced by prolonged NMDA exposure in cortical neurons. The present slice-patch experiments demonstrated, for the first time, expression of the VSOR Cl- channels in somatosensory pyramidal neurons. NMDA-induced necrotic neuronal death in slice preparations was largely suppressed by a blocker of the VSOR Cl- channel but not of the GABA(A) receptor. These results indicate that VSOR Cl- channels exert dual, reciprocal actions on neuronal excitotoxicity by serving as major anionic pathways both for varicosity recovery after washout of an excitotoxic stimulant and for persistent varicosity formation under prolonged excitotoxic insults leading to necrosis in cortical neurons.
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