Increased calcium accumulation and decreased protein synthesis activity are sensitive indicators of brain damage after ischemia that provide insight into distinct components in the evolution of the injury process. Protein synthesis, largely reflecting neuronal elements, is lost immediately and uniformly in global ischemia models, recovers within hours in regions that are resistant to injury, but remains low in vulnerable regions such CA1 of hippocampus. Accumulation of 45Ca is a later component that occurs in surviving cells in regions where neuronal loss has already occurred. Calcium uptake studies have identified the GABAergic reticular nucleus of the thalamus as a particularly early site of injury in a rat cardiac arrest model. Detailed quantitative comparisons of these two indicators in this rat model will continue. This project is currently in a suspended state, and will be completed upon return of the principal investigator.