ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Changes in intracellular chloride after oxygen-glucose deprivation of the adult hippocampal slice: effect of diazepam.
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 45 papers.
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Who cites it
45 citing papers in PubMed, 110 citations in OpenAlex.
- Oxytocin Exhibits Neuroprotective Effects on Hippocampal Cultures under Severe Oxygen-Glucose Deprivation Conditions.Current issues in molecular biology · 2024Article
- Hyperchloremia and Hypernatremia Decreased Microglial and Neuronal Survival during Oxygen-Glucose Deprivation/Reperfusion.Biomedicines · 2024Article
- Bumetanide Attenuates Cognitive Deficits and Brain Damage in Rats Subjected to Hypoxia-Ischemia at Two Time Points of the Early Postnatal Period.Neurotoxicity research · 2023Article
- The role ofJournal of pharmaceutical analysis · 2023Review
- Cerebrospinal Fluid Chloride Is Associated with Disease Activity of Relapsing-Remitting Multiple Sclerosis: A Retrospective Cohort Study.Brain sciences · 2023Article
- Role of NKCC1 and KCC2 during hypoxia-induced neuronal swelling in the neonatal neocortex.Neurobiology of disease · 2023Article
- Multi-target action of β-alanine protects cerebellar tissue from ischemic damage.Cell death & disease · 2022Article
- Recent advance in dual-functional luminescent probes for reactive species and common biological ions.Analytical and bioanalytical chemistry · 2022Review
- Drug development in targeting ion channels for brain edema.Acta pharmacologica Sinica · 2020Article
- Neuronal Transmembrane Chloride Transport Has a Time-Dependent Influence on Survival of Hippocampal Cultures to Oxygen-Glucose Deprivation.Brain sciences · 2019Article
- Alterations in GABAFrontiers in cellular neuroscience · 2019Article
- Chloride Homeostasis in Neurons With Special Emphasis on the Olivocerebellar System: Differential Roles for Transporters and Channels.Frontiers in cellular neuroscience · 2018Review
- Chloride Dysregulation, Seizures, and Cerebral Edema: A Relationship with Therapeutic Potential.Trends in neurosciences · 2017Review
- The K(+)-Cl(-) Cotransporter KCC2 and Chloride Homeostasis: Potential Therapeutic Target in Acute Central Nervous System Injury.Molecular neurobiology · 2016Review
- Expanding Spectrum of Sodium Potassium Chloride Co-transporters in the Pathophysiology of Diseases.Current neuropharmacology · 2015Review
- Prenatal Hypoxia-Ischemia Induces Abnormalities in CA3 Microstructure, Potassium Chloride Co-Transporter 2 Expression and Inhibitory Tone.Frontiers in cellular neuroscience · 2015Article
- 3-Nitropropionic acid-induced ischemia tolerance in the rat brain is mediated by reduced metabolic activity and cerebral blood flow.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Article
- Controversies and evolving new mechanisms in subarachnoid hemorrhage.Progress in neurobiology · 2014Article
- Bumetanide protects focal cerebral ischemia-reperfusion injury in rat.International journal of clinical and experimental pathology · 2014Article
- Characterization of inhibitory GABA-A receptor activation during spreading depolarization in brain slice.PloS one · 2014Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Ischemic injury to the CNS results in loss of ionic homeostasis and the development of neuronal death. An increase in intracellular Ca2+ is well established, but there are few studies of changes in intracellular Cl- ([Cl-]i) after ischemia. We used an in vitro model of cerebral ischemia (oxygen-glucose deprivation) to examine changes in [Cl-]i and GABA(A) receptor-mediated responses in hippocampal slices from adult rats. Changes in [Cl-]i were measured in area CA1 pyramidal neurons using optical imaging of 6-methoxy-N-ethylquinolinium chloride, a Cl--sensitive fluorescent indicator. Oxygen-glucose deprivation induced an immediate rise in [Cl-]i, which recovered within 20 min. A second and more prolonged rise in [Cl-]i occurred within the next hour, during which postsynaptic field potentials failed to recover. The sustained increase in [Cl-]i was not blocked by GABA(A) receptor antagonists. However, oxygen-glucose deprivation caused a progressive downregulation of the K+-Cl- cotransporter (KCC2), which may have contributed to the Cl- accumulation. The rise in [Cl-]i was accompanied by an inability of the GABA(A) agonist muscimol to cause Cl- influx. In vivo, diazepam is neuroprotective when given early after ischemia, although the mechanism by which this occurs is not well understood. Here, we added diazepam early after oxygen-glucose deprivation and prevented the downregulation of KCC2 and the accumulation of [Cl-]i. Consequently, both GABA(A) responses and synaptic transmission within the hippocampus were restored. Thus, after oxygen-glucose deprivation, diazepam may decrease neuronal excitability, thereby reducing the energy demands of the neuron. This may prevent the activation of downstream cell death mechanisms and restore Cl- homeostasis and neuronal function
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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.