Calcium-dependent glutamate release concomitant with massive potassium flux during cerebral ischemia in vivo.
The changes in extracellular glutamate ([Glu]e) and potassium ([K+]e) in the rat hippocampus during cerebral ischemia were determined simultaneously by microdialysis in vivo. Biphasic increases in [Glu]e, i.e. an earlier rapid increase concomitant with an abrupt increase in [K+]e followed by a later slow increase, were observed. Dialysis with Ca(2+)-free perfusate containing Co2+ blocked the earlier rapid increase completely but the later slow increase only partially. These findings suggest that Ca(2+)-dependent exocytotic release from the presynaptic nerve terminals is involved predominantly in the earlier rapid increase in [Glu]d. The later slow increase in [Glu]d may be due in part to a breakdown of membrane function resulting from several causes, including a loss of the electrogenic component of the glutamate gradients across the plasma membrane, and a loss of function of the glutamate uptake system.
Katayama
Y
Y
Division of Neurosurgery, UCLA School of Medicine, University of California, Los Angeles 90024.
Kawamata
T
T
Tamura
T
T
Hovda
D A
DA
Becker
D P
DP
Tsubokawa
T
T
D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism*; D002118:Calcium / Q000494:pharmacology*; D003035:Cobalt / Q000494:pharmacology; D003956:Dialysis / Q000379:methods; D004305:Dose-Response Relationship, Drug; D005110:Extracellular Space / Q000378:metabolism; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D009994:Osmolar Concentration; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D005971:Glutamates; D003035:Cobalt; D018698:Glutamic Acid; D011188:Potassium; D002118:Calcium