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Examination of Anatomical Features of Retinal Ganglion Cells Under N-methyl-D-aspartic Acid (NMDA)-induced Excitotoxicity
Published on: September 19, 2025
Expression of NMDA neuroreceptors in experimental ischemia
M U Gappoeva1, G A Izykenova, O K Granstrem
1Department of Neurology and Neurosurgery, Pavlov State Medical University, ul. Tolstogo 6/8, St. Petersburg, Russia. gappoeva@mail.ru
Abstract:
The role of NMDA receptors in molecular mechanisms of neurotoxicity was investigated using rat models of global and focal cerebral ischemia. Expression of NR2A and NR2B receptor mRNAs up-regulated in cortex after 3 h of reperfusion following middle cerebral artery occlusion (MCAo). This effect was accompanied by an increase in NR2A and NR2B immunoreactivity. At six hours of reperfusion, drastic activation of NR2A mRNA expression was observed in the penumbra that returned to the control level at 24 h of reperfusion. The monitoring of NR2A autoantibodies in the blood of the experimental rats showed its reliable increase to the 5-6th day of reperfusion that maintained elevated to the 20th day of the experiment. The data indicate that NR2A and 2B receptor subunits and NR2A autoantibodies are biochemical markers of the neurotoxicity underlying cerebral ischemia.
Insights
This study identifies NR2A and NR2B receptor subunits and NR2A autoantibodies as key biochemical markers for neurotoxicity following cerebral ischemia in rat models. These findings offer insights into the molecular mechanisms of brain injury and potential diagnostic indicators.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- NMDA receptors play a critical role in neuronal function and excitotoxicity.
- Cerebral ischemia, a condition of reduced blood flow to the brain, triggers complex molecular events leading to neurotoxicity.
- Understanding the specific receptor subunits involved in ischemia-induced neurotoxicity is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the role of NMDA receptor subunits (NR2A and NR2B) in the molecular mechanisms of neurotoxicity.
- To identify potential biochemical markers for neurotoxicity in rat models of cerebral ischemia.
- To examine the temporal expression patterns of NR2A and NR2B and the presence of NR2A autoantibodies.
Main Methods:
- Utilized rat models of global and focal cerebral ischemia, including middle cerebral artery occlusion (MCAo).
- Analyzed the expression of NR2A and NR2B receptor mRNAs and immunoreactivity in cortical and penumbra regions.
- Monitored NR2A autoantibodies in the blood serum of experimental rats over a 20-day period.
Main Results:
- NR2A and NR2B receptor mRNAs and immunoreactivity were upregulated in the cortex post-MCAo.
- A significant increase in NR2A mRNA expression was observed in the penumbra at six hours of reperfusion.
- Elevated levels of NR2A autoantibodies were detected from day 5-6 to day 20 of reperfusion.
Conclusions:
- NR2A and NR2B receptor subunits are implicated in the neurotoxicity associated with cerebral ischemia.
- NR2A autoantibodies emerge as reliable biochemical markers for neurotoxicity.
- These findings contribute to understanding the molecular pathology of ischemic brain injury and suggest potential biomarkers.
