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Some derivatives more lipophylic than creatine, thus theoretically being capable to better cross the blood-brain barrier, were studied for their neuroprotective effect in mouse hippocampal slices. In mouse hippocampal slices we found that EM2 I is ineffective, EM"" weakly increased the latency to population spike disapperance during anoxia. Creatine, Creatine-MG-complex (acetate) and Phosphocreatine-Mg-complex (acetate) increased more effectively the latency to population spike disappearance during anoxia. Moreover, Phosphocreatine-Mg-complex (acetate) significantly reduced neuronal hyperexcitability during anoxia, an effect that no other compound (including creatine itself) showed. Summing up, EM2 I is not useful for brain protection, while EM22 and cgelates of both creatine and phosphocreatine di replicate some of the knownn protective effects of creatine. In addition, Phosphocreatine-Mg-complex (acetate) also reduced neuronal hyperexcitability during anoxia.