Different expression of glycogen synthase kinase-3 beta between young and old rat brains after transient middle cerebral artery occlusion

Citation
C. Sasaki et al., Different expression of glycogen synthase kinase-3 beta between young and old rat brains after transient middle cerebral artery occlusion, NEUROL RES, 23(6), 2001, pp. 588-592
Citations number
16
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROLOGICAL RESEARCH
ISSN journal
01616412 → ACNP
Volume
23
Issue
6
Year of publication
2001
Pages
588 - 592
Database
ISI
SICI code
0161-6412(200109)23:6<588:DEOGSK>2.0.ZU;2-N
Abstract
Ischemia is a common stress to human brain and is difficult to cure in olde r individuals. To examine the differences of the response to cerebral ische mia between young and old rat brains, distributions of glycogen synthase ki nase-3 beta (GSK3 beta) and tau proteins were analyzed after 90 min of tran sient middle cerebral artery occlusion (MCAO) in young (10-11 weeks) and ol d (15 months) rats by immunohistochemical analyses. At 4 h of reperfusion, strong cytoplasmic and nuclear immunoreactivity for GSK3 beta was induced i n neurons of lamina I, II, V and VI of the cerebral cortex and dorsal cauda te in young brains, while the induction was not observed in lamina I and II of old cerebral cortex. The staining in lamina V and VI and dorsal caudate then gradually decreased until seven days of reperfusion in both animal gr oups. The staining of tau protein and terminal deoxynucleotidyl transferase -mediated dUTP-biotin in situ nick end labeling (TUNEL) did not show any po sitive signals in the control brain, but showed positive signals after isch emia with a peak at 24 h and 3 days, respectively. No significant differenc e was observed in the temporal and spatial patterns of tau and TUNEL staini ngs between these two groups. These data suggest that GSK3 beta may have a role in ischemic neuronal cell death, and that the different spatial expres sion of GSK3 beta between young and old rat brains may partly explain the v ulnerability of older neurons after ischemia.