Cerebral metabolism following neonatal or adult hemineodecortication in cats: effect on oxidative capacity using cytochrome oxidase histochemistry.
In order to determine the degree and extent of changes in cerebral oxidative capacity following cerebral hemineodecortication, adult cats which had undergone surgery early postnatally (mean age: 11.4 days) or during adulthood were studied using cytochrome oxidase histochemistry. A total of 18 animals were employed and 50 brain regions were quantified bilaterally using optical densitometry. Although many subcortical regions exhibiting extensive degenerative features revealed lower levels of cytochrome oxidase (C.O.) activity, this reduction was relatively unremarkable compared to intact controls. Nevertheless, it was interesting that this decrease (down to 66-89%) of normal was more pronounced in neonatal-lesioned cats, reaching significance in a number of ipsilateral thalamic nuclei, compared to adult-lesioned animals (91-100% of normal), suggesting a contribution of glial cells to the density of C.O. staining in the latter cats. Regions of the brain spared from degeneration exhibited a bilateral increase in C.O. activity which may reflect the demands for energy to support the anatomical reorganization which is prevalent in these animals. Surprisingly, such increases were more robust within spared regions of the adult-lesioned brain, reaching significance in four ipsilateral and nine contralateral areas with the density of the reaction attaining levels over 125% of control. This may indicate different demands for oxidative metabolism in the adult-lesioned cats. These results enhance our understanding of the mechanism(s) underlying the greater extent of functional sparing or recovery in cats sustaining injury to the cerebral cortex early vs. late in life. In addition, the findings complement our previous companion report on glucose metabolism supporting the concept of energy compartmentalization, which reflects the dynamic interaction between anatomical and functional changes in this age-at-lesion model of recovery.
Hovda
D A
DA
Department of Surgery, UCLA School of Medicine, Los Angeles, CA 90095-7039, USA. hovda@surgery.medsch.ucla.edu
Villablanca
J R
JR
D000375:Aging; D000818:Animals; D000831:Animals, Newborn; D001479:Basal Ganglia / Q000378:metabolism; D001921:Brain / Q000254:growth & development / Q000378:metabolism*; D001933:Brain Stem / Q000378:metabolism; D002415:Cats; D002531:Cerebellum / Q000378:metabolism; D002540:Cerebral Cortex / Q000254:growth & development / Q000378:metabolism / Q000502:physiology*; D003576:Electron Transport Complex IV / Q000378:metabolism*; D007839:Functional Laterality; D006651:Histocytochemistry; D008032:Limbic System / Q000378:metabolism; D009410:Nerve Degeneration; D009928:Organ Specificity; D012016:Reference Values; D013788:Thalamus / Q000378:metabolism
D003576:Electron Transport Complex IV