Cerebral glucose metabolism in aging rodents: effects of co-dergocrine.

Because glucose is the primary substrate for oxidative metabolism of the adult brain, measurements of glucose utilization provide information on cerebral energy metabolism, which ultimately is linked to neuronal activity. Early studies utilized in vitro techniques to measure carbohydrate oxidation as well as glycolytic and citric acid cycle enzymatic activities as a function of age. Although the results of these studies are somewhat equivocal, they generally indicate a decline in cerebral carbohydrate metabolism in senescent rodents. More recently, local cerebral glucose utilization (LCGU) has been measured in awake, resting rats with the 2-deoxy-D[1-14C]glucose metabolic mapping technique. Using this technique, decrements in LCGU have been observed in rats by midlife. Co-dergocrine, an ergot alkaloid used extensively in geriatric psychopharmacology, reversed subcortical LCGU decrements in brain areas associated with motor function, motivation, and learning. In contrast, the drug decreased frontal cortical LCGU in middle-aged rats. Stimulatory effects of co-dergocrine on LCGU in brain areas associated with motivation and learning support the view that the drug may be useful against age-associated disorders of cognition. Furthermore, the co-dergocrine-induced decrease in cortical glucose utilization coupled with the drug's cerebral vasoconstrictive action may render cortical cells less susceptible to the sequelae of ischemia.