Quantitative evaluation of extracellular glutamate concentration in postischemic glutamate re-uptake, dependent on brain temperature, in the rat following severe global brain ischemia

Changes in brain temperature are known to modulate the marked neuronal dama ge caused by an approximately 10-min intra-ischemic period. Numerous studie s have suggested that the extracellular glutamate concentration ([Glu](e)) in the intra-ischemic period and the initial postischemia period is strongl y implicated in such damage. In this study, the effects of intra-ischemic b rain temperature (32, 37, 39 degrees C) on [Glu](e) were investigated utili zing a dialysis electrode combined with ferrocene bovine serum albumin (BSA ), which allows oxygen-independent real-time measurement of [Glu](e). This system allowed separate quantitative evaluation of intra-ischemic biphasic glutamate release from the neurotransmitter and metabolic pools, and of pos tischemic glutamate re-uptake in ischemia-reperfusion models. The biphasic [Glu](e) elevation in the intra-ischemic period did not differ markedly amo ng intra-ischemic brain temperatures ranging from 32 to 39 degrees C. Intra -ischemic normothermia (37 degrees C) and mild hyperthermia (39 degrees C) markedly inhibited [Glu](e) re-uptake during the postischemic period, altho ugh the intra-ischemic [Glu](e) elevation did not differ from that during i ntra-ischemic hypothermia (32 degrees C). It was assumed that normothermia or mild hyperthermia in the intra-ischemic period influences intracellular functional abnormalities other than the intra-ischemic [Glu](e) elevation, thereby inhibiting glutamate re-uptake after reperfusion rather than direct ly modulating intra-ischemic [Glu](e) dynamics. (C) 2000 Elsevier Science B .V. All rights reserved.