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Brain Res. 2019 Oct 1;1720:146297. doi: 10.1016/j.brainres.2019.06.016. Epub 2019 Jun 21.

The temporal and spatial changes of actin cytoskeleton in the hippocampal CA1 neurons following transient global ischemia.

Author information

1
Department of Histology and Embryology, College of Basic Medical Sciences, Norman Bethune Health Science Center of Jilin University, Jilin Province 130021, PR China.
2
Laboratory Teaching Center of Basic Medicine, Norman Bethune Health Science Center of Jilin University, Jilin Province 130021, PR China.
3
Department of Geriatrics and General Medicine, The Second Hospital of Jilin University, Changchun, Jilin, PR China.
4
Department of Histology and Embryology, College of Basic Medical Sciences, Norman Bethune Health Science Center of Jilin University, Jilin Province 130021, PR China. Electronic address: liyanchao@jlu.edu.cn.

Abstract

Transient global ischemia usually results in delayed neuronal death in selective brain regions, prior to which a rapid loss of dendritic spines has been widely reported in these regions. Dendritic spines are characterized by a highly branched meshwork of actin cytoskeleton (F-actin), which is extremely vulnerable to the ATP-depleted conditions such as hypoxia/ischemia. However, the ischemia-induced changes of F-actin are still not clarified in the vulnerable brain areas. This study was designed to examine the temporal and spatial alterations of F-actin in the CA1 subfield of rat hippocampus following reperfusion after global cerebral ischemia. Phalloidin staining and confocal microscopic examination showed that F-actin disappeared from the dentritic spines in the CA1 stratum radiatum, but aggregated into thread- or fiber-like structures on days 1.5-2 after ischemia. This was followed by a nearly complete loss of F-actin in the CA1 subfield on days 3-7 after ischemia. Colocalization analysis demonstrated that the F-actin threads or fibers were located mainly within the dentritic trunks. As revealed by Nissl and Fluoro-Jade B staining, the decrease of F-actin proceeded concurrently with the evolution of ischemic damage. Consistently, western blots detected a significant decrease of F-/G-actin ratio in the dissected CA1 subfield after ischemia. To our knowledge, this is the first report on the change of F-actin in the ischemic brain. Although the underlying mechanisms remain to be elucidated, our findings may provide an important structural clue for the neuronal dysfunction induced by ischemia.

KEYWORDS:

Dendritic spine; F-actin; Hippocampus; Transient cerebral ischemia

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