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Neuron FUNCTIONAL MATURATION OF LIMBIC SYSTEM. Harry T. Chugani, Departments of Pediatrics, Neurology and Radiology, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan.

Using positron emission tomography (PET) and the tracer 2-deoxy-2(18F)fluoro-D-glucose (FDG), we have shown that the pattern of glucose metabolism in the human newborn brain is fairly consistent, with the highest degree of activity in primary sensory and motor cortex, cingulate cortex, medial temporal region, thalamus, brainstem and cerebellar vermis. Increases of glucose utilization are seen by two to three months in the parietal, temporal and primary visual cortex, basal ganglia, and cerebellar hemispheres. These changes in glucose metabolism coincide with improved skills involving visuo-spatial and visuo-sensorimotor integration, the disappearance or reorganization of brainstem reflex neonatal behaviors, and increasing cortical contribution to the electroencephalogram. Starting between 6 and 8 months, lateral and inferior portions of frontal cortex become more functionally active and eventually, between 8 and 12 months, the dorsal and med ial frontal regions also show increased glucose utilization. These changes of frontal cortex metabolism come at a time when cognitively-related behaviors, such as the phenomenon of stranger anxiety, and improved performance on the delayed response task begin to appear. Increased glucose requirement in frontal cortex also coincides with the expansion of dendritic fields and the increased capillary density observed in frontal cortex during the same period of development. By approximately one year of age, the infant's pattern of glucose utilization resembles qualitatively that of the adult.

At birth, the regional or local cerebral metabolic rates of glucose utilization (LCMRglc) are about 30% lower than those seen in adults. Between birth and approximately 3 years, the cerebral cortex shows a dramatic increase in LCMRglc to reach levels that exceed adult rates by over two-fold. Such changes in LCMRglc are not observed in brainstem, but a less dramatic increase is seen in basal ganglia and thalamus. Between 3 years and about 10 years, the LCMRglc for cerebral cortex is essentially at a high plateau of over two-fold the glucose utilization seen in adults. Subsequently, LCMRglc for cerebral cortex begins to decline and gradually reaches adult values by 16-18 years. Based on the temporal relationship between these developmental changes of LCMRglc and synaptogenesis in humans, as well as on similar studies performed in our laboratory on developing cat and monkey, we believe that the ontogenetic changes of LCMRglc described above provide an indirect measure of synaptogenesis in the human brain.

[Abstract Titles] [Anderson] [Bolz] [Olson] [Levitt] [Zhou]

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