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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.

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