Postischemic calmodulin gene expression in the rat hippocampus

The hippocampal calmodulin (CaM) gene expression was determined in the rat after transient forebrain ischemia. Ischemia was induced by the 4-vessel oc clusion model, and the hybridized mRNA copy numbers corresponding to the 3 CaM genes detected by phosphorimaging were determined by quantitative in si tu hybridization 24 h post-insult. A small, but significant upregulation (b y 8.8%) of the CaM I gene was observed in the CA1 pyramidal cell layer, whe reas other regions exhibited a maintained or slightly decreased CaM gene ex pression. The CaM mRNA levels decreased most markedly (by 10-15%) in the hi ppocampal molecular layers. No consistent correlation was found between the ischemic vulnerability and the CaM gene expression pattern. The results in dicate that the induction of delayed neuronal death is not incidental to th e transcriptional activation of the CaM genes in the ischemic rat hippocamp us in vivo. As the calcium-bound CaM content increases during the ischemic insult, downregulation of the CaM gene expression could be a homeostatic re sponse aimed at maintaining the intracellular level of the active CaM pool. (C) 2001 Elsevier Science Inc. All rights reserved.