Fetal transplantation following spinal contusion injury results in chronic alterations in CNS glucose metabolism.

Glucose utilization of the injured rat spinal cord was determined using the autoradiographic technique of Sokoloff et al. (33). Animals were analyzed chronically (2 and 3 months) after spinal contusion injury alone or when a spinal lesion was followed by subchronic (10-day) intraparenchymal fetal spinal transplantation. At 2 and 3 months postinjury, spinal glucose utilization was reduced in dorsal gray and white matter above and below the lesion site. In addition, sensory regions of the forebrain and brain stem (e.g., nucleus gracilis and ventral posterior medial nucleus of the thalamus) had a lower basal metabolic rate than control animals. Decreased metabolic rates in supraspinal regions were reversed by the presence of a spinal graft at 3 but not at 2 months postinjury. Furthermore, gray matter in animals receiving an intraspinal transplant had elevated glucose utilization rates for several spinal segments rostral and caudal to the lesion epicenter. Graft glucose utilization was higher at 2 months (80-90 mumol/100 g/min) than at 3 months (60-70 mumol/100 g/min) posttransplantation. These data are the first quantitative metabolic imaging of spinal and brain metabolism following spinal contusion injury and fetal transplantation. The study suggests that intraspinal transplants can become functionally integrated with adjacent host gray matter and can chronically alter specific postinjury metabolic patterns.