ArticleOxidative medicine and cellular longevity2021
Pretreatment with mGluR2 or mGluR3 Agonists Reduces Apoptosis Induced by Hypoxia-Ischemia in Neonatal Rat Brains.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Molecular mechanisms of excitotoxicity and their relevance to the pathogenesis of neurodegenerative diseases-an update.Acta pharmacologica Sinica · 2025Review
- A Case Series of Anti-Metabotropic Glutamate Receptor 2 Antibody-Related Diseases with Distinct Neurological Involvement.ImmunoTargets and therapy · 2025Article
- Metabotropic glutamate receptors-guardians and gatekeepers in neonatal hypoxic-ischemic brain injury.Pharmacological reports : PR · 2024Review
- Mechanisms of glutamate metabolic function and dysfunction in vascular dementia.Neuroprotection (Chichester, England) · 2024Review
- Exploring the Neuroprotective Effects of Lithium in Ischemic Stroke: A literature review.International journal of medical sciences · 2024Review
- Transcriptional regulation of NRF1 on metabotropic glutamate receptors in a neonatal hypoxic‑ischemic encephalopathy rat model.Pediatric research · 2023Article
- Group II Metabotropic Glutamate Receptors Reduce Apoptosis and Regulate BDNF and GDNF Levels in Hypoxic-Ischemic Injury in Neonatal Rats.International journal of molecular sciences · 2022Article
- DNA Methylation-Dependent Gene Expression Regulation of Glutamate Transporters in Cultured Radial Glial Cells.Molecular neurobiology · 2022Article
- Review
- Molecular Mechanism of Tetramethylpyrazine Ameliorating Neuroexcitotoxicity through Activating the PKA/CREB Signaling Pathway.BioMed research international · 2022Article
- The Mechanism of the Neuroprotective Effect of Kynurenic Acid in the Experimental Model of Neonatal Hypoxia-Ischemia: The Link to Oxidative Stress.Antioxidants (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia-ischemia (HI) in an immature brain results in energy depletion and excessive glutamate release resulting in excitotoxicity and oxidative stress. An increase in reactive oxygen species (ROS) production induces apoptotic processes resulting in neuronal death. Activation of group II mGluR was shown to prevent neuronal damage after HI. The application of agonists of mGluR3 (N-acetylaspartylglutamate; NAAG) or mGluR2 (LY379268) inhibits the release of glutamate and reduces neurodegeneration in a neonatal rat model of HI, although the exact mechanism is not fully recognized. In the present study, the effects of NAAG (5 mg/kg) and LY379268 (5 mg/kg) application (24 h or 1 h before experimental birth asphyxia) on apoptotic processes as the potential mechanism of neuroprotection in 7-day-old rats were investigated. Intraperitoneal application of NAAG or LY379268 at either time point before HI significantly reduced the number of TUNEL-positive cells in the CA1 region of the ischemic brain hemisphere. Both agonists reduced expression of the proapoptotic Bax protein and increased expression of Bcl-2. Decreases in HI-induced caspase-9 and caspase-3 activity were also observed. Application of NAAG or LY379268 24 h or 1 h before HI reduced HIF-1
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