The concentration dependence of the neuroprotective effect of the GM1 ganglioside for the neuronal-like PC12 cell line following the cytotoxic action of hydrogen peroxide was studied. An increase in GM1 concentration in the ranges 1-50μ and 1-10 nM resulted in increased neuroprotection. However, no significant differences in the effects of GM1 in doses of 10 nM, 100 nm, and 1μM were found. This fact could be associated with GM1 transition from a monomeric to a micellar form. GM1 decreased the generation of active oxygen metabolites and the accumulation of malone dialdehyde that were induced by the action of hydrogen peroxide, and protected Na+, K+-ATPase from oxidative inactivation. The effect of GM1 was shown to depend on modulation of the signal transduction system. Inhibitors of tyrosine kinase of Trk-receptors or tyrosine kinases were able to prevent or decrease the effects of GM1. Micromolar GM1 concentrations were more effective in comparison with nanomolar concentrations in PC12 cells. In contrast, nanomolar GM1 concentrations were more efficient in brain nerve endings without nuclei. These differences in the mechanism of action of low concentrations of GM1 were probably associated with its ability to operate without the activation of nuclear processes.