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The influence on hippocampal glucose utilization of a transient 10-min forebrain ischemia was quantified in male Wistar rats after 2 and 3 weeks as well as after 3 months by application of the [14C]2-deoxyglucose technique. Ischemia was induced by occlusion of the carotid arteries and simultaneous lowering of the blood pressure to 40 mm Hg. For identification of the hippocampal architecture, sections were stained for perikarya (cresyl violet) and for acetylcholinesterase. The hippocampal regions clearly showed different responses to the ischemic insult. The necrotic pyramidal cells being almost completely removed, significant increases in glucose utilization occurred in most layers of the CA1 sector at 2 and 3 weeks post ischemia, while widespread reductions prevailed in all other sectors and the dentate gyrus. At 3 months after the ischemic insult, glucose utilization was reduced in all hippocampal structures including the CA1 region. The increases in glucose utilization in the CA1 sector are suggested to indicate long-lasting presynaptic hyperexcitation, while the widespread reductions in glucose utilization demonstrate that neuronal activity is also altered in hippocampal areas that do not show major histological damage.

Glucose Utilization in Rat Hippocampus after Long-Term Recovery from Ischemia