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- Title
Transient Cerebral Ischemia Alters GSK-3β and p-GSK-3β Immunoreactivity in Pyramidal Neurons and Induces p-GSK-3β Expression in Astrocytes in the Gerbil Hippocampal CA1 Area.
- Authors
Chen, Bai; Ahn, Ji; Park, Joon; Shin, Bich; Lee, Yun; Kang, Il; Hong, Seongkweon; Kim, Yang; Jeon, Yong; Kim, In; Cho, Jeong; Lee, Tae-Kyeong; Lee, Jae; Won, Moo-Ho; Cho, Jun; Moon, Joong
- Abstract
Glycogen synthase kinase 3β (GSK-3β) is a key downstream protein in the PI3K/Akt pathway. Phosphorylation of serine 9 of GSK-3β (GSK-3β activity inhibition) promotes cell survival. In this study, we examined changes in expressions of GSK-3β and phosphorylation of GSK-3β (p-GSK-3β) in the gerbil hippocampal CA1 area after 5 min of transient cerebral ischemia. GSK-3β immunoreactivity in the CA1 area was increased in pyramidal cells at 6 h after ischemia-reperfusion. It was decreased in CA1 pyramidal cells from 12 h after ischemia-reperfusion, and hardly detected in the CA1 pyramidal cells at 5 days after ischemia-reperfusion. p-GSK-3β immunoreactivity was slightly decreased in CA1 pyramidal cells at 6 and 12 h after ischemia-reperfusion. It was significantly increased in these cells at 1 and 2 days after ischemia-reperfusion. Five days after ischemia-reperfusion, p-GSK-3β immunoreactivity was hardly found in CA1 pyramidal cells. However, p-GSK-3β immunoreactivity was strongly expressed in astrocytes primarily distributed in strata oriens and radiatum. In conclusion, GSK-3β and p-GSK-3β were significantly changed in pyramidal cells and/or astrocytes in the gerbil hippocampal CA1 area following 5 min of transient cerebral ischemia. This finding indicates that GSK-3β and p-GSK-3β are closely related to delayed neuronal death.
- Subjects
TRANSIENT ischemic attack; GLYCOGEN synthase kinase-3; PHOSPHORYLATION; SERINE; PYRAMIDAL neurons; ASTROCYTES
- Publication
Neurochemical Research, 2017, Vol 42, Issue 8, p2305
- ISSN
0364-3190
- Publication type
Article
- DOI
10.1007/s11064-017-2245-5