Focal protein synthesis inhibition in a model of neonatal hypoxic-ischemic brain injury.
Cerebral hypoxia-ischemia was produced in 1-week-old rats by exposing them to 8% O2-92% N2 commencing 4 to 6 h after unilateral carotid artery ligation. Protein synthesis rates were measured in cerebral cortex, caudate-putamen, thalamus, and lateral septal nuclei during 2 h of hypoxia and at three times (15 min, 10 h, and 18 h) after a 3.5-h hypoxic exposure. Protein synthesis was inhibited in the ipsilateral but not contralateral forebrain during the brief hypoxic exposure, and in both hemispheres during early recovery after a 3.5 h exposure, which was sufficient to produce brain injury in the ipsilateral hemisphere. At 10 h after hypoxia, protein synthesis rates in the contralateral forebrain had recovered to control values, but in vulnerable structures of the ipsilateral forebrain, recovery of protein synthesis was transient and incomplete (cerebral cortex) or remained at the low values found immediately after hypoxia (caudate-putamen). The early development of abnormal patterns of protein synthesis in vulnerable brain regions during hypoxia and its persistence in some rats during recovery when irreversible cell injury becomes manifest suggests a possible role for abnormal protein metabolism in the evolution of irreversible brain cell damage.
D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D001345:Autoradiography; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism*; D004195:Disease Models, Animal; D002534:Hypoxia, Brain / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D051381:Rats; D011919:Rats, Inbred Strains; D014633:Valine / Q000378:metabolism
D009419:Nerve Tissue Proteins; D014633:Valine