PROTEIN-SYNTHESIS IN THE HIPPOCAMPAL SLICE - TRANSIENT INHIBITION BY GLUTAMATE AND LASTING INHIBITION BY ISCHEMIA

Protein synthesis was measured in hippocampal slices which were expose d to glutamate (1 mM or 10 mM) or which were deprived of glucose and o xygen ('in vitro ischemia') for 15 min. Glutamate at 1 mM, a concentra tion estimated to occur during in vivo ischemia did not affect protein synthesis. Ten mM glutamate inhibited protein synthesis immediately a fter exposure (50% of control values) and reduced ATP levels to about 30% of the control. After two hours, slices fully recovered their prot ein synthesis and energy metabolism. The effect of 10 mM glutamate was not receptor-mediated, as NMDA, AMPA, or metabotropic receptor antago nists failed to block the glutamate effect. Immediately after ischemia , protein synthesis was reduced to 30% of control values, and 2 hours later it was still depressed to one-half of control values. Energy cha rge, however, recovered completely. Ischemic inhibition of protein syn thesis was not reversed by glutamate receptor antagonists. The data in dicate that inhibition of protein synthesis in hippocampal slices duri ng ischemia is not glutamate-dependent.