CALCIUM ACTIVITY AND POSTISCHEMIC SUPPRESSION OF PROTEIN-SYNTHESIS

Increase in intracellular calcium concentration is a prominent feature of ischemia and has been considered a major factor in the initiation of ischemic pathology, which involves inhibition of protein synthesis. A reduction of calcium ion activity during and immediately after in v itro ischemia did not prevent inhibition of protein synthesis in hippo campae slices. When slices were overloaded with calcium by NMDA recept or activation or by the calcium ionophore A23187, no significant inhib ition of protein synthesis was observed. We conclude that calcium over load plays only a limited role in ischemic inhibition of protein synth esis.