CREB is required for acquisition of ischemic tolerance in gerbil hippocampal CA1 region
Version of Record online: 21 JUL 2003
Journal of Neurochemistry
Volume 86, Issue 4, pages 805–814, August 2003
How to Cite
Hara, T., Hamada, J.-i., Yano, S., Morioka, M., Kai, Y. and Ushio, Y. (2003), CREB is required for acquisition of ischemic tolerance in gerbil hippocampal CA1 region. Journal of Neurochemistry, 86: 805–814. doi: 10.1046/j.1471-4159.2003.01847.x
- Issue online: 21 JUL 2003
- Version of Record online: 21 JUL 2003
- Received February 20, 2003; revised manuscript received April 8, 2003; accepted April 8, 2003.
- CRE decoy oligonucleotide;
- cyclic AMP responsive element binding protein;
- ischemic tolerance
Ischemic tolerance is well known as a neuroprotective effect of pre-conditioning ischemia against delayed neuronal death, however, the mechanism or mechanisms underlying this effect are not fully understood. We investigated the relationship between CREB and ischemic tolerance in gerbil hippocampal CA1 neurons using CRE decoy oligonucleotide. Sublethal ischemia led to an increase in the level of CREB phosphorylation in CA1 regions while lethal ischemia did not. Experiments with NG108-15 cells showed that adding CRE decoy oligonucleotide to culture media significantly inhibited the cell growth rate. The administration of CRE decoy oligonucleotide into gerbil cerebral ventricle decreased CREB-DNA binding activity to 38% of the control. Pre-treatment with CRE decoy oligonucleotide 24 h before the induction of ischemic tolerance decreased CA1 neuronal cell survival to 21% of the control. The present findings suggest that a CREB-mediated transcription system is necessary for the induction of ischemic tolerance.