Abstract
Induction of heat shock protein (HSP) 70 and heat shock cognate protein (HSC) 70 mRNAs, and immunoreactivity for HSP70 were investigated in rat hippocampus after transient global ischemia with in situ hybridization and immunohistochemistry. In sham control brain, HSP70 mRNA was scarcely present, while HSC70 mRNA was expressed in most neuronal cells. After 20 min of transient four-vessel occlusion (4VO), ischemia-resistant hippocampal CA3 cells consistently induced HSP70 mRNA along with further HSC70 mRNA. The resistant dentate granule (DG) cells continuously induced HSC70 mRNA even after the great reduction of HSP70 mRNA. In contrast, in ischemia-vulnerable CA1 cells, a relatively lower level of HSC70 mRNA induction than the level of HSP70 mRNA induction was observed. The vulnerable CA1 cells produced a prominent HSP70 immunoreactivity. These results suggest that the vulnerability of the CA1 cells after transient ischemia may not be explained only by the ability of HSP70 induction, but may be related to the imbalance of HSP70 and HSC70 mRNA inductions.
| Original language | English |
|---|---|
| Pages (from-to) | 165-168 |
| Number of pages | 4 |
| Journal | Neuroscience Letters |
| Volume | 153 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Apr 30 1993 |
| Externally published | Yes |
Keywords
- Cerebral ischemia
- Heat shock cognate protein
- Heat shock protein
- In situ hybridization
- Rat
- Selective vulnerability
ASJC Scopus subject areas
- Neuroscience(all)