[Changes in protein and RNA synthesis following acute hindbrain ischemia]

Protein and RNA synthesis of the brain is affected by focal transient ischemia. Protein synthesis is depressed by the depletion of energy metabolism during ischemia, and its recovery following recirculation is slower than restoration of energy metabolism. On the other hand, RNA synthesis is more tolerable to ischemia than protein synthesis. Present study has designed to evaluate changes of protein and RNA synthesis of the brain after ischemia. We used a hindbrain ischemia model of gerbils, and quantitative autoradiography was applied for estimation of regional protein and RNA synthesis. The model was made by occluding the basilar artery for 15 minutes and recirculating afterwards. 14C-valine was used as a tracer for protein synthesis. In the ischemic group, protein synthesis was inhibited extremely in the medial thalamus, inferior colliculus, gray matter of the pons and midbrain, and cerebellum, RNA synthesis by salvage pathway was evaluated using tracer doses of 14C-uridine. It increased 1.6-2.4 folds of sham controls in the thalamus, and gray matter of the pons and midbrain. De novo synthesis of RNA was evaluated using 14C-carbamoylphosphate and 14C-NaHCO3. 14C-NaHCO3 antoradiogram showed inhibition of tracer incorporation into RNA and protein fraction in the ischemic lesions. 14C-carbamoylphosphate autoradiogram showed no significant change. These results indicate that protein synthesis is inhibited after ischemia but response of RNA synthesis to ischemia is not uniform. De novo synthesis of RNA is inhibited following ischemia, but RNA synthesis by salvage pathway increases in the ischemic lesion.(ABSTRACT TRUNCATED AT 250 WORDS)