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 oxi dative capacity following cerebral hemineodecortication, adult cats wh ich had undergone surgery early postnatally (mean age: 11.4 days) or d uring adulthood were studied using cytochrome oxidase histochemistry. A total of 18 animals were employed and 50 brain regions were quantifi ed bilaterally using optical densitometry. Although many subcortical r egions exhibiting extensive degenerative features revealed lower level s of cytochrome oxidase (C.O.) activity, this reduction was relatively unremarkable compared to intact controls. Nevertheless, it was intere sting that this decrease (down to 66-89%) of normal was more pronounce d in neonatal-lesioned cats, reaching significance in a number of ipsi lateral thalamic nuclei, compared to adult-lesioned animals (91-100% o f normal), suggesting a contribution of glial cells to the density of C.O. staining in the latter cats. Regions of the brain spared from deg eneration exhibited a bilateral increase in C.O. activity which may re flect 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, reachi ng significance in four ipsilateral and nine contralateral areas with the density of the reaction attaining levels over 125% of control. Thi s may indicate different demands for oxidative metabolism in the adult -lesioned cats. These results enhance our understanding of the mechani sm(s) underlying the greater extent of functional sparing or recovery in cats sustaining injury to the cerebral cortex early vs, late in lif e. In addition, the findings complement our previous companion report on glucose metabolism supporting the concept of energy compartmentaliz ation, which reflects the dynamic interaction between anatomical and f unctional changes in this age-at-lesion model of recovery. (C) 1998 El sevier Science B.V. All rights reserved.