ArticleASN neuro2013
The GluN3A subunit exerts a neuroprotective effect in brain ischemia and the hypoxia process.
Article in ASN neuro, 2013. 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, 20 citations in OpenAlex.
- Transcriptional regulation of NRF1 on metabotropic glutamate receptors in a neonatal hypoxic‑ischemic encephalopathy rat model.Pediatric research · 2023Article
- Clonidine ameliorates cerebral ischemia-reperfusion injury by up-regulating the GluN3 subunits of NMDA receptor.Metabolic brain disease · 2022Article
- The Development of Novel Drug Treatments for Stroke Patients: A Review.International journal of molecular sciences · 2022Review
- Review
- The pathogenic S688Y mutation in the ligand-binding domain of the GluN1 subunit regulates the properties of NMDA receptors.Scientific reports · 2020Article
- Phased Treatment Strategies for Cerebral Ischemia Based on Glutamate Receptors.Frontiers in cellular neuroscience · 2019Review
- Neonatal Clonazepam Administration Induces Long-Lasting Changes in Glutamate Receptors.Frontiers in molecular neuroscience · 2018Article
- A neuroprotective role of the NMDA receptor subunit GluN3A (NR3A) in ischemic stroke of the adult mouse.American journal of physiology. Cell physiology · 2015Article
- Inhibition of ACE Retards Tau Hyperphosphorylation and Signs of Neuronal Degeneration in Aged Rats Subjected to Chronic Mild Stress.BioMed research international · 2015Article
- In vitro ischemia triggers a transcriptional response to down-regulate synaptic proteins in hippocampal neurons.PloS one · 2014Article
- GluN3A: an NMDA receptor subunit with exquisite properties and functions.Neural plasticity · 2013Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NMDARs (N-methyl-D-aspartate receptors) mediate the predominantly excitatory neurotransmission in the CNS (central nervous system). Excessive release of glutamate and overactivation of NMDARs during brain ischemia and the hypoxia process are causally linked to excitotoxicity and neuronal damage. GluN3 subunits, the third member of the NMDAR family with two isoforms, GluN3A and GluN3B, have been confirmed to display an inhibitory effect on NMDAR activity. However, the effect of GluN3 subunits in brain ischemia and hypoxia is not clearly understood. In the present study, the influence of ischemia and hypoxia on GluN3 subunit expression was observed by using the 2VO (two-vessel occlusion) rat brain ischemia model and cell OGD (oxygen and glucose deprivation) hypoxia model. It was found that GluN3A protein expression in rat hippocampus and the prefrontal cortex was increased quickly after brain ischemia and remained at a high level for at least 24 h. However, the expression of the GluN3B subunit was not remarkably changed in both the animal and cell models. After OGD exposure, rat hippocampal neurons with GluN3A subunit overexpression displayed more viability than the wild-type neurons. NG108-15 cells overexpressing GluN3A presented pronounced resistance to glutamate insult. Blocking the increase of intracellular Ca2+ concentration may underlie the neuroprotective mechanism of up-regulated GluN3A subunit. Suppressing the generation of hydroxyl radicals and NO (nitric oxide) is probably also involved in the neuroprotection.
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