During early postischemic reperfusion, the vulnerable brain regions (e.g., hippocampal CA1) 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 CA1 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 CA1 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 CA3). 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 CA1 and sometimes CA3 showed a columnar pattern of high and low metabolism. CA1 and CA3 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. CA1 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.