2005•Journal of Apoplexy and Nervous DiseasesRequires access

Alterations in protein expression of NMDA receptor subunits NR2A and NR2B during reperfusion after ischemia in the rat brain

Yuan Fan

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Abstract

Objective By immunohistochemistry and compute-assisted image analysis,We investigated the changes in protein expression of NMDA receptor subunits NR2A and NR2B levels in rat brain area 1 of parietal cortex during reperfusion after ischemia. Methods 70 male wistar rats were randomly divided into 3 groups:normal control group(n= 10),sham-ischemia group(n=30),cerebral ischemia-reperfusion group(n=30). Temporary cerebral ischemia-reperfusion injury model was established by using common carotid artery blood drainage method. Brain section was obtained by cryostat sectioning. The section was prepared for NR2A/B immunohistochemistry staining and was observed by optical microscope. Quantitate analysis was carried out for NR2A/B immunoreactive matter and stain area. Results (1)The expression of NR2A and NR2B protein in area of parietal cortex transitory and lightly increased after narcosis and sham-operated, but came back to the normal control level at 24h. (2)Dur-ing ischemia-reperfusion,the expression of NR2A and NR2B protein in area of parietal cortex is increased sharply at 6h, and fall back to the control level at 24h,then it reduced sharply at 72h. Conclusion The present results demonstrate that the sharply expression of NR2A and NR2B protein in brain at early reperfusion might be one of the mechanism for delayed brain ischemia reperfusion injury.

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Objective By immunohistochemistry and compute-assisted image analysis,We investigated the changes in protein expression of NMDA receptor subunits NR2A and NR2B levels in rat brain area 1 of parietal cortex during reperfusion after ischemia. Methods 70 male wistar rats were randomly divided into 3 groups:normal control group(n= 10),sham-ischemia group(n=30),cerebral ischemia-reperfusion group(n=30). Temporary cerebral ischemia-reperfusion injury model was established by using common carotid artery blood drainage method. Brain section was obtained by cryostat sectioning. The section was prepared for NR2A/B immunohistochemistry staining and was observed by optical microscope. Quantitate analysis was carried out for NR2A/B immunoreactive matter and stain area. Results (1)The expression of NR2A and NR2B protein in area of parietal cortex transitory and lightly increased after narcosis and sham-operated, but came back to the normal control level at 24h. (2)Dur-ing ischemia-reperfusion,the expression of NR2A and NR2B protein in area of parietal cortex is increased sharply at 6h, and fall back to the control level at 24h,then it reduced sharply at 72h. Conclusion The present results demonstrate that the sharply expression of NR2A and NR2B protein in brain at early reperfusion might be one of the mechanism for delayed brain ischemia reperfusion injury.

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Available abstract

Objective By immunohistochemistry and compute-assisted image analysis,We investigated the changes in protein expression of NMDA receptor subunits NR2A and NR2B levels in rat brain area 1 of parietal cortex during reperfusion after ischemia. Methods 70 male wistar rats were randomly divided into 3 groups:normal control group(n= 10),sham-ischemia group(n=30),cerebral ischemia-reperfusion group(n=30). Temporary cerebral ischemia-reperfusion injury model was established by using common carotid artery blood drainage method. Brain section was obtained by cryostat sectioning. The section was prepared for NR2A/B immunohistochemistry staining and was observed by optical microscope. Quantitate analysis was carried out for NR2A/B immunoreactive matter and stain area. Results (1)The expression of NR2A and NR2B protein in area of parietal cortex transitory and lightly increased after narcosis and sham-operated, but came back to the normal control level at 24h. (2)Dur-ing ischemia-reperfusion,the expression of NR2A and NR2B protein in area of parietal cortex is increased sharply at 6h, and fall back to the control level at 24h,then it reduced sharply at 72h. Conclusion The present results demonstrate that the sharply expression of NR2A and NR2B protein in brain at early reperfusion might be one of the mechanism for delayed brain ischemia reperfusion injury.

Key concepts: Ischemia, NMDA receptor, Immunohistochemistry, Cortex (anatomy), Reperfusion injury, Glutamate receptor, Cerebral cortex, H&E stain

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Alterations in protein expression of NMDA receptor subunits NR2A and NR2B during reperfusion after ischemia in the rat brain — Research Paper | ScholarLens