Excitotoxicity induces changes in rat brain gangliosides.

The patterns of major gangliosides in the rat hippocampi and olfactory bulbs was examined in vivo after microinjections of Ibotenic acid and L-BOAA (NMDA and AMPA receptor agonists, respectively) which were given under free-movement conditions. The excitotoxicity induced by injections of Ibotenic acid promoted transient ganglioside changes in olfactory bulbs and permanent changes in hippocampus. Four days after injections, the amount of gangliosides in the hippocampus increased significantly for GQ1b, GT1b and GD1b and decreased in the olfactory bulb for GQ1b, GT1b, GD1b, GD1a and GM1 compared to normal ganglioside levels. The alterations of gangliosides were minimal 1 day after injections. After 5 weeks, the amounts of GQ1b, GT1b and GD1b dramatically decreased in the hippocampus while in the olfactory bulbs gangliosides recovered to normal levels. The results obtained with L-BOAA 4 days after injections strengthen the results observed in the experiments using Ibotenic acid and corroborate our suggestion that gangliosides have an active role in the compensatory mechanism to maintain the number of glutamate receptors during the excitotoxicity.