Dynamic changes in cytoskeletal elements following acute cerebral ischemia and reperfusion in rats
- Author:
Yong ZHANG
1
;
Xue-Qin FU
2
;
Xu-Huan ZOU
2
;
Man-Man WANG
2
;
Wei-Wei WANG
2
;
Rui LAN
3
Author Information
- Publication Type:Journal Article
- Keywords: brain damage; cerebral ischemia and reperfusion; cytoskeletal elements; dynamic changes; middle cerebral artery occlusion; neuron
- From: Chinese Pharmacological Bulletin 2024;40(2):263-272
- CountryChina
- Language:Chinese
- Abstract: Aim To investigate the dynamic time-course changes in neuronal cytoskeleton after acute ischemia and reperfusion in rats. Methods Reperfusion was performedin rats by blocking the middle cerebralarteryfor 90 min, then therats wereobserved and collected at different time points. The brain damage wasobserved by Nissl staining,and neurobehavioural function was evaluated with neurological deficit score and forelimb placement test. The cellular changes in the alternations of cytoskeletal elements including microtubule associated protein 2 (MAP2) and neurofilament heavy chain (NF-H) were observed by immunohistochemistry staining and Western blot. Impaired axons, dendrites and cytoskeletal alternations were detected by electron microscope. Results Brain damage and neurobehavioural function were gradually aggravated with the prolongation of reperfusion. Brain damage appeared earlier and more severe in striatum than in cortex. Moreover, decreased MAP2-related and increased NF-H-related immunoreactive intensities were found in the ischemic areas. Impaired cytoskeletal arrangement and reduced dense were indicated. Damaged cytoskeletal components such as microtubules and neurofilament arrangement, decreased axonal filament density, and swelled dendrites were observed after cerebral ischemia reperfusion by ultrastructural observations. Conclusions Different brain regions have diverse tolerance to ischemia-reperfusion injury. Major elements of neuronal cytoskeleton show dynamic responses to ischemia and reperfusion, which may further contribute to brain damage and neurological impairment following MCAO and reperfusion.
