Expression of beta-actin and alpha-tubulin mRNA in gerbil brain following transient ischemia and reperfusion up to 1 month.

The time course of mRNA expressions of two cytoskeletal proteins, beta-actin and alpha-tubulin, was studied by Northern blot analysis and in situ hybridization in the same gerbil brains at various periods of recirculation following 10 min of forebrain ischemia. On Northern blot analysis, beta-actin mRNA in the forebrain showed increase after 6 h and 24 h recirculation. There was wide variation in its expression 3 days postischemia (PI), and by 7 days PI it had returned to control. The alpha-tubulin mRNA in the forebrain was shown to be reduced 6 h PI in our previous study. In the present analysis of Northern blots of delayed postischemic periods, there was no significant change in its expression even though there were variations. In situ hybridization revealed a decline in the mRNA expressions of both alpha-tubulin and beta-actin in the CA1 region as early as 6-24 h PI with the reductions being prominent at 3 days PI. By 7 days PI, beta-actin was only faintly visible while alpha-tubulin was completely absent in the CA1 region. Neither RNA was detectable in CA1 1 month PI. The heat shock-70 protein was expressed by 1 h PI, and it continued to be expressed up to 24 h, returning to control by 3 days PI. These results indicate that ischemia inhibits mRNA expressions of cytoskeletal protein in the selectively vulnerable region of the brain, i.e. CA1. The time course of the reduction of the two mRNAs coincides with delayed neuronal death suggesting that the cytoskeletal proteins may play important roles in selective postischemic neuronal injury.