Metabolic alterations in fiber layers of the CA 1 region of the gerbil hippocampus following short-term ischemia: high-energy phosphates, glucose-related metabolites, and amino acids.

The CA 1 neurons of the gerbil hippocampus die at 4 days following 5 min of bilateral ischemia. The fiber and somal layers of the CA 1 region of the gerbil hippocampus were analyzed for high-energy phosphates, glucose-related metabolites, and amino acids from 0.75 hr to 4 days of postischemia. The results were compared to those from two layers of the CA 3 region and the cerebral cortex. The metabolite changes in the fiber layers of the CA 1 region were qualitatively similar to those in the somal layer. The energy status of the tissues taken from the CA 1 region was never compromised for up to 2 days of recirculation, after which the ATP and P-creatine in the somal layer decreased to 43 and 56% of the control, respectively, whereas the average decreases in the CA 1 fiber layers were only 71 and 88% of the control, respectively. Thus, the high-energy phosphate response of the neuronal elements in the fiber layers was temporally similar to that found in the somal layer of the CA 1 region. The biphasic increases in glycogen, glucose, glucose-6-phosphate, and high-energy phosphates to values greater than the control indicated that the metabolic restoration following transient ischemia is a dynamic process which persists for up to 2 days of recirculation, even in resistant tissues. A similar pattern of delayed changes was observed in glutamate, gamma-aminobutyric acid (GABA), and glutamine, but the change in each amino acid appeared to be independent of the others despite their close metabolic relationship. The delayed decreases in GABA would favor a loss of inhibition to the CA 1 neurons and may be related to the phenomenon of delayed neuronal death.