Protein synthesis in the hippocampal slice: transient inhibition by glutamate and lasting inhibition by ischemia.
Protein synthesis was measured in hippocampal slices which were exposed to glutamate (1 mM or 10 mM) or which were deprived of glucose and oxygen ('in vitro ischemia') for 15 min. Glutamate at 1 mM, a concentration estimated to occur during in vivo ischemia did not affect protein synthesis. Ten mM glutamate inhibited protein synthesis immediately after exposure (50% of control values) and reduced ATP levels to about 30% of the control. After two hours, slices fully recovered their protein synthesis and energy metabolism. The effect of 10 mM glutamate was not receptor-mediated, as NMDA, AMPA, or metabotropic receptor antagonists 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 charge, however, recovered completely. Ischemic inhibition of protein synthesis was not reversed by glutamate receptor antagonists. The data indicate that inhibition of protein synthesis in hippocampal slices during ischemia is not glutamate-dependent.
Department of Experimental Neurology, Max-Planck-Institute for Neurological Research, Cologne, Germany.
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Djuricic
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Röhn
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Paschen
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Hossmann
D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism*; D018698:Glutamic Acid / Q000494:pharmacology*; D006624:Hippocampus / Q000098:blood supply / Q000378:metabolism*; D066298:In Vitro Techniques; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D051381:Rats; D011916:Rats, Inbred F344
D009419:Nerve Tissue Proteins; D018698:Glutamic Acid