EN
The common effects of epileptic seizures are aberrant plastic changes in synaptic connectivity and morphological rearrangements in hippocampal mossy fi bers. This phenomenon is believed to be a basis of facilitation of further epileptic episodes, however its molecular mechanism remains elusive. mTOR kinase is crucial for rearrangements of neuronal morphology and for long term synaptic plasticity. Overactivation of mTOR was reported in brain pathologies associated with seizures (tuberous sclerosis, cortical dysplasia). Experimental evidence supports causative role of mTOR in these forms of epilepsy. So far, however, links of mTOR signaling pathway to other types of epilepsy are unknown. To address this issue we investigated activation of mTOR and its downstream effectors in rat brain after kainic acid (KA) induced epilepsy. Animals were sacrifi ced 2, 6, 12, 24 and 72 hours after KA administration and levels of phosphorylated mTOR and S6 has been examined. Both, biochemical methods and immunohistochemistry proved S6 activation in hippocampus and cerebral cortex at all time points after KA. Immunohistochemical analysis additionally revealed that 2 h after KA, activities of mTOR and S6 are upregulated mainly in neurons while after 6 h there was also enhancement of glial S6 immunoreactivity. Our data suggest that KA induced seizures activate mTOR signaling in various cell types with specifi c spatio-temporal pattern. This work has been fi nanced by PNRF-96-AI-1/07 grant.