Calcium activity and post-ischemic 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 vitro ischemia did not prevent inhibition of protein synthesis in hippocampae slices. When slices were overloaded with calcium by NMDA receptor activation or by the calcium ionophore A23187, no significant inhibition of protein synthesis was observed. We conclude that calcium overload plays only a limited role in ischemic inhibition of protein synthesis.
Djuricic
B
B
Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Cologne, Germany.
Röhn
G
G
Paschen
W
W
Hossmann
K A
KA
D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D003620:Dantrolene / Q000494:pharmacology; D005260:Female; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism*; D066298:In Vitro Techniques; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D007700:Kinetics; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D051381:Rats; D011916:Rats, Inbred F344; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism*; D012430:Ruthenium Red / Q000494:pharmacology
D009419:Nerve Tissue Proteins; D016194:Receptors, N-Methyl-D-Aspartate; D012430:Ruthenium Red; D000001:Calcimycin; D003620:Dantrolene; D002118:Calcium