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Postischemic Glucose Metabolism is Modified in the Hippocampal CA 1 Region Depleted of Excitatory Input or Pyramidal Cells

1990; SAGE Publishing; Volume: 10; Issue: 2 Linguagem: Inglês

10.1038/jcbfm.1990.41

1559-7016

Martin Balslev Jørgensen, Donald C. Wright, Nils Henrik Diemer,

Memory and Neural Mechanisms

During early postischemic reperfusion, the vulnerable brain regions (e.g., hippocampal CA 1 ) show a relatively high deoxyglucose accumulation. To investigate if this accumulation is a marker for the later-occurring regional cell death and to determine its cellular localization, we studied the glucose metabolism in the CA 1 region post ischemia after removal of its pre- or postsynaptic components. A 20-min period of cerebral ischemia was used for selective removal of the main postsynaptic component in CA 1 pyramidal cells, and a bilateral intraventricular injection of kainic acid for removal of the majority of presynaptic axon terminals in this region (and postsynaptic terminals and cell bodies in CA 3 ). The glucose metabolism was studied in these two lesion types and in sham-operated animals before and after a period of ischemia. There was a 60% reduction of metabolism after ischemia in the nonvulnerable regions, whereas CA 1 and sometimes CA 3 showed a columnar pattern of high and low metabolism. CA 1 and CA 3 devoid of the postsynaptic component showed increased postischemic metabolism. The latter was due to the presence of macrophages, as demonstrated by an enzyme histochemical stain for nonspecific esterase. CA 1 with no presynaptic component showed a postischemic depression of the glucose metabolism similar to the rest of the brain. It is suggested that the level of the postischemic glucose metabolism in the ischemia-vulnerable regions is determined by the presence of both synaptic components. The presence of macrophages in a region gives rise to apparently normal values of glucose metabolism.