The hippocampal calmodulin (CaM) gene expression was determined in the rat after transient forebrain ischemia. Ischemia was induced by the 4-vessel occlusion model, and the hybridized mRNA copy numbers corresponding to the 3 CaM genes detected by phosphorimaging were determined by quantitative in situ hybridization 24 h post-insult. A small, but significant upregulation (by 8.8%) of the CaM I gene was observed in the CA1 pyramidal cell layer, whereas other regions exhibited a maintained or slightly decreased CaM gene expression. The CaM mRNA levels decreased most markedly (by 10-15%) in the hippocampal molecular layers. No consistent correlation was found between the ischemic vulnerability and the CaM gene expression pattern. The results indicate that the induction of delayed neuronal death is not incidental to the transcriptional activation of the CaM genes in the ischemic rat hippocampus in vivo. As the calcium-bound CaM content increases during the ischemic insult, downregulation of the CaM gene expression could be a homeostatic response aimed at maintaining the intracellular level of the active CaM pool.
- 4-Vessel occlusion model
- Calmodulin gene expression
- Forebrain ischemia
- Quantitative in situ hybridization
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Pharmacology, Toxicology and Pharmaceutics(all)