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 degrees 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 degrees C. Intra-ischemic normothermia (37 degrees C) and mild hyperthermia (39 degrees 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 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 directly modulating intra-ischemic [Glu](e) dynamics.
Asai
S
S
Department of Pharmacology, Nihon University School of Medicine, Oyaguchi-Kami Machi, Itabashi-ku, Tokyo, Japan. satoshi@med.nihon-u.ac.jp
Zhao
H
H
Kohno
T
T
Takahashi
Y
Y
Nagata
T
T
Ishikawa
K
K
D000818:Animals; D001831:Body Temperature / Q000502:physiology*; D001921:Brain / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D003593:Cytoplasm / Q000378:metabolism; D004195:Disease Models, Animal; D005110:Extracellular Space / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism*; D020925:Hypoxia-Ischemia, Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000502:physiology; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*
D018698:Glutamic Acid