Ongoing studies continue to focus on the role of altered gene expression in postischemic pathophysiology. Specifically, transcriptional and translational expression of the stress protein, hsp7O, and transcription factors, Fos and Jun, are evaluated by comparison of in situ hybridization and immunocytochemistry. Perhaps the most significant result has been the observation that threshold ischemic , resulting in an induced tolerance to subsequent challenges, are correlated with hsp7O and Jun expression in the vulnerable CA l neurons that are protected. Protein synthesis deficits that follow severe initial insults apparently result in the failure to translate mRNAs even though they may be induced. Since Jun in turn functions to regulate the transcriptional expression of other genes, this finding begins to indicate the complexity of genetic reprogramming that must be associated with induced tolerance phenomena. Other changes in gene expression have been evaluated after ischemia, notably that of microtubule-associated protein 2 (MAP -2). An mRNA encoding a truncated protein, MAP-2c, is induced in cortex and hippocampal CA1 regions that show delayed damage in a rat cardiac arrest model. In contrast to stress protein and proto-oncogene expression that largely occur in surviving neurons, MAP-2c appears to constitute a selective marker for severely injured neurons after ischemia.
