• E Titova, R P Ostrowski, J H Zhang, and J Tang.
• Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA 92354, USA.
• Acta Neurochir. Suppl. 2008 Jan 1;105:119-21.

AbstractRecent studies have shown that amantadine, an uncompetitive N-methyl-d-aspartate receptor antagonist and dopamine agonist, is effective for the treatment of various cerebral disorders and causes relatively mild side effects. In this study, we investigated whether administration of amantadine will provide a neuroprotective effect in the intracerebral hemorrhage (ICH) rat model. A total of 15 male Sprague Dawley rats (300-380 g) were divided into sham, ICH-untreated, and ICH-treated with amantadine sulphate groups. ICH was induced by collagenase injection. Total dose 6 mg/kg of amantadine sulphate was divided into 3 injections and administered intraperitoneally at 1, 8, and 16 h after ICH. Brain injury was evaluated by investigating neurological function and brain edema at 24 h after ICH. Our data demonstrates that ICH caused significant neurological deficit associated with marked brain edema. Amantadine did not reduce brain injury after ICH; neurological function and brain edema in the treated group were not different from those of the untreated group. We conclude that amantadine sulphate does not offer neuroprotection in acute stage of experimental ICH-induced brain injury.

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