Induction of alphaB-crystallin in the hippocampus of KA-treated mouse brain.
- Author:
Yongzhe CHE
1
;
Ja Kyeong LEE
Author Information
1. Department of Anatomy, Inha University School of Medicine, Inchon, Korea.
- Publication Type:Original Article
- Keywords:
alphaB-crystallin;
kainic acid;
astrocytes;
gliosis
- MeSH:
Animals;
Antibodies;
Astrocytes;
Brain*;
Central Nervous System;
Crystallins;
Gliosis;
Heat-Shock Proteins;
Hippocampus*;
Humans;
Kainic Acid;
Mice*;
Myocardium;
Neuroglia;
Neurons;
Oligodendroglia;
Vertebrates
- From:Korean Journal of Anatomy
2001;34(2):123-130
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The alphaB-crystallin, which is a member of small heat shock protein (sHSP), was initially identified as a component of a vertebrate eye lens protein, and also shown to be expressed in non-lenticular tissues including cardiac muscles and the central nervous system. Recently, it was demonstrated that alphaB-crystallin expression was increased in the brain of patients suffering various neurological diseases including Alzheimers disease. In the current study, we examined in detail the time-course of alphaB-crystallin expression in the region of neuronal loss and in activated glia cells in hippocampus of the KA-treated mouse brain. The alphaB-crystallin was expressed in pyramidal layer and in oligodendrocytes of hippocampus 1 day after KA-treatment, which was similar to that in normal mice. The alphaB-crystallin expression began to be increased 2 days after KA-treatment and reached peak induction, especially in astrocytes in the CA3 area of hippocampus 4 days after KA-treatment. Immunofluorescent staining with anti-alphaB-crystallin and anti-GFAP antibodies revealed that the induction of alphaB-crystallin was localized in the activated astrocytes, prominently in the CA3 region of hippocampus where a severe neuronal death was undergoing. The results suggested that alphaB-crystallin might play a role in reactive gliosis and/or in delayed neuronal death proceeded in KA-induced epileptic brain.