ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Sequential release of GABA by exocytosis and reversed uptake leads to neuronal swelling in simulated ischemia of hippocampal slices.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 126 citations in OpenAlex.
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- Cerebrovascular miRNAs Track Early Development of Alzheimer's Disease and Target Molecular Markers of Angiogenesis and Blood Flow Regulation.Journal of Alzheimer's disease : JAD · 2024Article
- Low Temperature Delays the Effects of Ischemia in Bergmann Glia and in Cerebellar Tissue Swelling.Biomedicines · 2023Article
- Conditioned-medium of stem cells from human exfoliated deciduous teeth prevent apoptosis of neural progenitors.The Saudi dental journal · 2022Article
- Selective block of adenosine ABritish journal of pharmacology · 2022Article
- Questioning Glutamate Excitotoxicity in Acute Brain Damage: The Importance of Spreading Depolarization.Neurocritical care · 2022Article
- The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention.Neurocritical care · 2022Review
- The Relationship Between Seizures and Spreading Depolarizations in Patients with Severe Traumatic Brain Injury.Neurocritical care · 2022Observational
- Migraine Aura, Transient Ischemic Attacks, Stroke, and Dying of the Brain Share the Same Key Pathophysiological Process in Neurons Driven by Gibbs-Donnan Forces, Namely Spreading Depolarization.Frontiers in cellular neuroscience · 2022Review
- Pharmacological and Biophysical Characteristics of Picrotoxin-Resistant, δSubunit-Containing GABAFrontiers in synaptic neuroscience · 2021Article
- Review
- The Neurology of Death and the Dying Brain: A Pictorial Essay.Frontiers in neurology · 2020Review
- Neuronal Transmembrane Chloride Transport Has a Time-Dependent Influence on Survival of Hippocampal Cultures to Oxygen-Glucose Deprivation.Brain sciences · 2019Article
- Age-Dependency of Levetiracetam Effects on Exocytotic GABA Release from Nerve Terminals in the Hippocampus and Cortex in Norm and After Perinatal Hypoxia.Cellular and molecular neurobiology · 2019Article
- Mannitol decreases neocortical epileptiform activity during early brain development via cotransport of chloride and water.Neurobiology of disease · 2019Article
- The Roles of GABA in Ischemia-Reperfusion Injury in the Central Nervous System and Peripheral Organs.Oxidative medicine and cellular longevity · 2019Review
- Article
- Understanding Spreading Depression from Headache to Sudden Unexpected Death.Frontiers in neurology · 2018Review
- Effects of interleukin-1ß on cortical spreading depolarization and cerebral vasculature.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
GABA release during cerebral energy deprivation (produced by anoxia or ischemia) has been suggested either to be neuroprotective, because GABA will hyperpolarize neurons and reduce release of excitotoxic glutamate, or to be neurotoxic, because activation of GABA(A) receptors facilitates Cl- entry into neurons and consequent cell swelling. We have used the GABA(A) receptors of hippocampal area CA1 pyramidal cells to sense the rise of [GABA](o) occurring in simulated ischemia. Ischemia evoked, after several minutes, a large depolarization to approximately -20 mV. Before this "anoxic depolarization," there was an increase in GABA release by exocytosis (spontaneous IPSCs). After the anoxic depolarization, there was a much larger, sustained release of GABA that was not affected by blocking action potentials, vesicular release, or the glial GABA transporter GAT-3 but was inhibited by blocking the neuronal GABA transporter GAT-1. Blocking GABA(A) receptors resulted in a more positive anoxic depolarization but decreased cell swelling at the time of the anoxic depolarization. The influence of GABA(A) receptors diminished in prolonged ischemia because glutamate release evoked by the anoxic depolarization inhibited GABA(A) receptor function by causing calcium entry through NMDA receptors. These data show that ischemia releases GABA initially by exocytosis and then by reversal of GAT-1 transporters and that the resulting Cl- influx through GABA(A) receptor channels causes potentially neurotoxic cell swelling.
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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.