[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address Please contact the publisher to request reinstatement.
Sign In
Individual Sign In
Create an Account
Institutional Sign In
OpenAthens Shibboleth
[Skip to Content Landing]
Citations 0
American Society for Experimental Neurotherapeutics Abstracts
August 2000

Dose-Dependent Neuroprotection of Taigabine After 2-Hour Middle Cerebral Artery Embolization in the Rat

Arch Neurol. 2000;57(8):1239. doi:

γ-Aminobutyric acid (GABA) is a potent and ubiquitous inhibitor in the central neuronal system (CNS), and enhancement of its inhibitory activity may protect ischemic neurons. In a current study, we evaluate the neuroprotective effect of a novel GABA agonist, taigabine, in a reversible focal cerebral ischemia model of rats subjected to 2-hour middle cerebral artery embolization with a filament. Taigabine was given at 10, 20, and 40 mg/kg intraperitoneally at 1 hour after the onset of reperfusion. Neurobehavioral outcome was examined at 1 hour and 24 hours, respectively, after reperfusion. The percentage of brain infarction volume was calculated from the coronal brain sections, which were stained with 2,3,5-triphenyltetrazolium chloride (TTC) at 72 hours after cerebral ischemia. Significant neurological improvement was observed only in animals treated with taigabine at a dose of 20 or 40 mg/kg (both P<.05). Postischemic treatment of taigabine displayed a dose-dependent reduction in brain infarct size, but only taigabine given at 20 and 40 mg/kg showed significant differences when compared with that of the control group (control, 28.7 ± 11.0; 10 mg/kg, 19.5 ± 10.8, P = .07; 20 mg/kg, 12.3 ± 9.7, P = .006; and 40 mg/kg, P<.001). The results from this study suggest that postischemic administration of taigabine is neuroprotective in the focal cerebral ischemia model.