Inhibited glutamate release by granulocyte-colony stimulating factor after experimental stroke

• Published in: Neuroscience letters 2008-02, Vol.432 (3), p.167-169
• Main Authors: Han, Jun-liang, Kollmar, Rainer, Tobyas, Blank, Schwab, Stefen
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Brain Infarction - etiology; Brain Infarction - metabolism; Brain Infarction - pathology; Brain Infarction - prevention & control; Corpus Striatum - drug effects; Corpus Striatum - metabolism; Corpus Striatum - pathology; Disease Models, Animal; Fundamental and applied biological sciences. Psychology; G-CSF; Glutamate; Glutamic Acid - metabolism; Granulocyte Colony-Stimulating Factor - drug effects; Infarction, Middle Cerebral Artery - complications; Infarction, Middle Cerebral Artery - drug therapy; Infarction, Middle Cerebral Artery - metabolism; Infarction, Middle Cerebral Artery - pathology; Ischemic stroke; Male; Rat; Rats; Rats, Wistar; Time Factors; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2007.07.056

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 μg/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±10 mm 3) at 24 hours after tMCAO. The result of present study show that G-CSF possess an ability to inhibit excitotoxicity after ischemic stroke.