Inhibited glutamate release by granulocyte-colony stimulating factor after experimental stroke.
We investigated the ability of granulocyte-colony stimulating factor (G-CSF) on inhibiting glutamate release by microdialysis in a rat stroke model. Male Wistar rats (n=15) were treated with either intravenous saline or G-CSF (60 microg/kg) 30 min after temporary middle cerebral artery occlusion (MCAO). G-CSF significantly attenuated the release of glutamate in the infarcted striatum from 30 minutes to 180 minutes after tMCAO compared with control (p<0.05). Infarct volume in G-CSF treated group (135+/-13 mm(3)) reduced significantly compared to control (181+/-10mm(3)) at 24 hours after tMCAO. The result of present study show that G-CSF possess an ability to inhibit excitotoxicity after ischemic stroke.
Han
Jun-liang
JL
Department of Neurology, University of Heidelberg, 69120 Heidelberg, Germany.
Blank
Tobias
T
Tobyas
Blank
B
Schwab
Stefan
S
Kollmar
Rainer
R
D000818:Animals; D020520:Brain Infarction / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D018698:Glutamic Acid / Q000378:metabolism*; D016179:Granulocyte Colony-Stimulating Factor / Q000187:drug effects*; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
D016179:Granulocyte Colony-Stimulating Factor; D018698:Glutamic Acid