On the mechanism of the inhibitory effect of potasium ions on amino acid incorporation into rat cerebral cortex proteins in vivo.
Earlier results on potassium ion inhibition of amino acid incorporation into the brain proteins in vivo (spreading cortical depression) led to the hypothesis that inhibition of protein synthesis is based on ATP deficiency. In the present study we tested various aspects of the aminocylation of tRNA, an ATP-dependent process, during spreading cortical depression produced by the topical application of 25% KCl. On using a 7-min interval between the subcutaneous injection of L-[U-14C] leucine and killing the rat, incorporation into the tRNA fraction was found to be reduced by 25%. Total amino acid radioactivity in the soluble fraction was unaltered. The acceptor capacity of tRNA, measured in vitro, and the proportion of non-acylated tRNA in vivo were likewise unchanged.
D000215:Acylation; D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism*; D013181:Cortical Spreading Depression; D007930:Leucine / Q000378:metabolism*; D008297:Male; D011188:Potassium / Q000494:pharmacology*; D012343:RNA, Transfer / Q000378:metabolism*; D051381:Rats
D012343:RNA, Transfer; D007930:Leucine; D011188:Potassium