Figure 2.

Morphological context of metabolic activity in PCC in monkeys. A. 2-deoxy-D-glucose utilization coded for four levels of utilization and thalamic projections to RSC shown with a tritiated-amino acid injection (hatched) into the anterior thalamic nuclei and a coronal section through RSC areas 29 and 30. The close relationship between high glucose metabolism and thalamic afferents are obvious. Interestingly, high levels of the mitochondrial enzyme cytochrome c oxidase also occur in the granular layer of RSC and in layers III-IV of areas 30 and 23. The asterisk in B shows where the section through ACC in C. was taken. Notice that ACC has much less cytochrome c oxidase activity than does area 23 (shown with the pair of arrows delineating these areas). A midcingulotomy lesion (D.; at coronal level shown with “v” on medial surface in B.) that removes thalamic afferents to PCC/RSC as well as frontal lobe inputs shows a massive reduction of activity in the thalamoreceptive layers as predicted from selective thalamic lesions in rat. There is about a 20% volumetric reduction in the posterior cingulate gyrus and reductions in enzyme activity are emphasized with three arrows from layer III/IV in area 29 and layers III and IV in areas 30 and 23c. Thus, high metabolic activity in PCC, RSC, and PrCC is driven primarily by thalamic afferents.