POSTISCHEMIC NEURONAL DAMAGE CAUSES ASTROGLIAL ACTIVATION AND INCREASE IN LOCAL CEREBRAL GLUCOSE-UTILIZATION OF RAT HIPPOCAMPUS

The purpose of the present study was to determine the consequences of postischemic neuronal damage on CMR(glc). Forebrain ischemia of 10 min duration was induced in male Wistar rats. The extent of neuronal damage and the numbers of immunocytochemically detected astrocytes in the hippocampal CA1 subfield as well as CMR(glc) were determined 2, 5, 7, and 14 days after ischemia. CBF was additionally measured 7 days postischemia. CMR(glc) was decreased in cortical and thalamic structures up to 5 days postischemia, and was normalized again on day 7 after ischemia. In the hippocampal areas, CMR(glc) was decreased only on day 2 after ischemia, was normalized after 5 days, and increased in the stratum oriens and pyramidale of the CA1 subfield from postischemic day 7 onward. Neuronal damage was clearly demonstrable 5 days after ischemia and further increased up to day 7. The number of GFAP-reactive astrocytes increased markedly at day 7 postischemia. It is assumed that the activation of astrocytes in induced by neuronal damage, and that the astroglial metabolism is responsible for the increase in CMR(glc) of the CA1 subfield 7 days after ischemia. The decrease in CBF of the CA1 subfield 7 days after ischemia could be caused by a reduced density of perfused capillaries.