ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Glutamate release through volume-activated channels during spreading depression.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 147 citations in OpenAlex.
- Mechanistic insight into the initiation of spreading depolarizations: Is it really all about potassium?The Journal of physiology · 2025Article
- Pharmacological inhibition of all known major inward cationic currents does not block the induction of spreading depolarizations.Frontiers in cellular neuroscience · 2025Article
- Glutamate load fosters spreading depolarization under osmotic stress in brain slices.Frontiers in cellular neuroscience · 2025Article
- Spreading depolarizations pose critical energy challenges in acute brain injury.Journal of neurochemistry · 2024Review
- Astrocyte β-Adrenergic Receptor Activity Regulates NMDA Receptor Signaling of Medial Prefrontal Cortex Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Pharmacological modulation of chloride channels as a therapeutic strategy for neurological disorders.Frontiers in physiology · 2023Review
- Extracellular Alterations in pH and K+ Modify the Murine Brain Endothelial Cell Total and Phospho-Proteome.Pharmaceutics · 2022Article
- Malignant astrocyte swelling and impaired glutamate clearance drive the expansion of injurious spreading depolarization foci.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- Astrocytic Glutamatergic Transmission and Its Implications in Neurodegenerative Disorders.Cells · 2022Review
- Cortical spreading depression: culprits and mechanisms.Experimental brain research · 2022Review
- Glia as a key factor in cell volume regulation processes of the central nervous system.Frontiers in cellular neuroscience · 2022Review
- Dysregulation of the peripheral glutamatergic system: A key player in migraine pathogenesis?Cephalalgia : an international journal of headache · 2021Review
- Sex hormones regulate NHE1 functional expression and brain endothelial proteome to control paracellular integrity of the blood endothelial barrier.Brain research · 2021Article
- Article
- Mechanisms of the negative potential associated with Leão's spreading depolarization: A history of brain electrogenesis.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Review
- 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
- CysLT1 receptor antagonists pranlukast and zafirlukast inhibit LRRC8-mediated volume regulated anion channels independently of the receptor.American journal of physiology. Cell physiology · 2019Article
- Striatal spreading depolarization: Possible implication in levodopa-induced dyskinetic-like behavior.Movement disorders : official journal of the Movement Disorder Society · 2019Article
- Physiology of Astroglia.Physiological reviews · 2018Review
- The role of glutamate in neuronal ion homeostasis: A case study of spreading depolarization.PLoS computational biology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Volume-sensitive organic anion channels (VSOACs) in astrocytes are activated by cell swelling and are permeable to organic anions, such as glutamate and taurine. We have examined the release of glutamate through VSOACs during the propagation of spreading depression (SD). SD was induced by bath application of ouabain in hippocampal brain slices and was monitored by imaging intrinsic optical signals, a technique that provides a measure of cellular swelling. The onset of SD was associated with increased light transmittance, confirming previous studies that cellular swelling occurs during SD. NMDA receptor antagonists, either noncompetitive (MK-801, 10-50 microM) or competitive (CGS-17355, 100 microM), reduced the rate of propagation of SD, indicating that glutamate release contributes to SD onset. SD still occurred in zero Ca(2+)-EGTA (0-Ca(2+)-EGTA) solution, a manipulation that depresses synaptic transmission. HPLC measurements indicated that, even in this solution, there was significant glutamate release. Two lines of experiments indicated that glutamate was released through VSOACs during SD. First, 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB), a blocker of VSOACs, depressed the rate of propagation of SD in a manner similar to NMDA antagonists. Second, NPPB inhibited the release of glutamate during SD in 0-Ca(2+)-EGTA external solution. These results indicate that cellular swelling during SD causes the activation of VSOACs and the release of glutamate by permeation through this channel. Cellular swelling is a result of neuronal activity and is observed during excitotoxicity. Therefore, glutamate release from VSOAC activation could occur under conditions of cell swelling and contribute to excitotoxic damage.
Indexed as
Identifiers
10414972PMC6782824W2135877388What OpenQuestion holds
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.