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ON THE MECHANISM OF ELECTROSHOCK‐INDUCED INHIBITION OF PROTEIN SYNTHESIS IN RABBIT CEREBRAL CORTEX
Author(s) -
Metafora. S.,
Persico Maria,
Felsani A.,
Ferraiuolo Rosa,
Giuditta A.
Publication year - 1977
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1977.tb12329.x
Subject(s) - polysome , protein biosynthesis , ribosome , cerebral cortex , ribonuclease , biochemistry , biology , messenger rna , cortex (anatomy) , chemistry , biophysics , endocrinology , rna , neuroscience , gene
— The mechanism of electroshock (ES)‐induced inhibition of protein synthesis in rabbit cerebral cortex has been investigated by using a cell‐free system. The protein biosynthetic activity of the post‐mitochondrial supernatant (PMS) obtained from the cerebral cortex of ES‐treated animals was found to be markedly lower than in controls (C). This inhibition was accompanied by a decrease of polysomes and an increase of monomers. In addition, a relative increase in light polysomes was evident at short intervals after ES treatment. No difference was found in the total soluble activity and in the activity of the elongation factors and ribonuclease present in the cell sap of C and ES animals. The biosynthetic activity of ES‐total. free and membrane‐bound ribosomes was approx 45% lower than that of the corresponding C fractions: polysome/monomer ratios were similarly reduced. The total content of cortical ribosomes was not affected by ES. Following ES treatment there was no change in the ribo‐somal ability to elongate, terminate and release polypeptide chains, nor a decrease in the polysomal content of poly(A)‐containing mRNA. These data strongly suggest that the ES‐induced inhibition of protein synthesis results from a defect in the initiation process. The possible mechanisms mediating this defect have been discussed.