Effects of a restricted unilateral neocortical lesion upon cerebral glucose and oxidative metabolisms in fetal and neonatal cats.
The present study was designed to measure cerebral glucose and oxidative metabolisms and to assess relationships with previously identified morphological changes in adult cats with a unilateral, restricted neocortical lesion sustained either during fetal life or neonatally. Local cerebral metabolic rates for glucose (LCMR(glc)) were measured using the [14C]2-deoxy-D-glucose (2 DG) autoradiography method and oxidative capacity was determined using cytochrome oxidase histochemistry (C.O.). Only glucose metabolism in the fetal-lesioned cats was affected substantially. There was a global decrease (31.0% relative to controls) of the LCMR(glc) for both cerebral hemispheres while focal decreases were seen mainly in thalamic and neostriatal nuclei (and reaching declines of over 50%). Cats with a neonatal lesion showed only a tendency to such declines (19.5% and 22.0% for the right and left hemispheres, respectively). C.O. values were not affected significantly either globally or locally in any of the age-at-lesion groups. In previous work using fetal animals with similar lesions, morphological evidence of subcortical neuropile degeneration was not observed; instead, a marked decrease in size of the ipsilateral remaining neocortex and a pronounced distortion of gyri and sulci patterns bilaterally were found. In this context, we propose that in the fetal-lesioned cats, there was a widespread lesion-induced decrease in corticofugal (and transcortical) synaptic inputs which was responsible for a decline in functional (synaptic) activities, and that this, in turn, caused a downturn in glucose utilization. In the neonatal cats minor degeneration, coupled with lack of reinnervation, would account for the tendency to 2 DG declines. These results indicate that the long-term metabolic response of the fetal brain to injury is also less adaptive than that of the neonatal brain. Since standard methods are available to measure cerebral metabolism in humans, our studies in animal models may help understanding the long term physiological consequences of developmental focal brain damage in patients as well as to predict the relationships between cerebral metabolism and the underlying long-term morphological effects of such lesions.
Villablanca
J R
JR
Department of Psychiatry and Biobehavioral Sciences, Department of Neurobiology, Mental Retardation Research Center and Brain Research Institute, University of California, Los Angeles, CA, USA. jvillablanca@mednet.ucla.edu
Schmanke
T D
TD
Hovda
D A
DA
D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D001921:Brain / Q000196:embryology / Q000378:metabolism*; D002415:Cats; D002541:Cerebral Decortication; D003847:Deoxyglucose / Q000378:metabolism; D005260:Female; D005333:Fetus / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008297:Male; D019579:Neocortex / Q000196:embryology / Q000378:metabolism*; D010084:Oxidation-Reduction
D003847:Deoxyglucose; D005947:Glucose