Ischemia-induced upregulation of excitatory amino acid transport sites.
The response of excitatory amino acid transporter binding sites in the rat brain to 10 min of cerebral ischemia induced by bilateral common carotid occlusion combined with hypotension was examined. We observed a transient increase in the density of transporter binding sites that was first noticeable at 5 min post-recovery and persisted for 48 h. The increase in binding sites was found throughout the brain, but was most prevalent in hippocampus and other cortical regions. We conclude that delayed neuronal death following transient cerebral ischemia may not be due to a decrease in the number of excitatory amino acid transport sites.
Anderson
K J
KJ
Department of Physiological Sciences, University of Florida, Gainesville 32610-0144.
Nellgård
B
B
Wieloch
T
T
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism*; D001665:Binding Sites / Q000502:physiology; D001692:Biological Transport / Q000502:physiology; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D014316:Tritium; D015854:Up-Regulation / Q000502:physiology
D005971:Glutamates; D014316:Tritium; D001224:Aspartic Acid; D018698:Glutamic Acid