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 damage caused by an approximately 10-min intra-ischemic period. Numerous studies have suggested that the extracellular glutamate concentration ([Glu] e) in the intra-ischemic period and the initial postischemia period is strongly implicated in such damage. In this study, the effects of intra-ischemic brain temperature (32, 37, 39°C) on [Glu] e were investigated utilizing 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 postischemic glutamate re-uptake in ischemia–reperfusion models. The biphasic [Glu] e elevation in the intra-ischemic period did not differ markedly among intra-ischemic brain temperatures ranging from 32 to 39°C. Intra-ischemic normothermia (37°C) and mild hyperthermia (39°C) markedly inhibited [Glu] e re-uptake during the postischemic period, although the intra-ischemic [Glu] e elevation did not differ from that during intra-ischemic hypothermia (32°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 directly modulating intra-ischemic [Glu] e dynamics.