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Mesial temporal lobe epilepsy (MTLE) is associ-ated with severe neuronal death and reactive gliosis in hipocampus. However, the molecular mechanisms underlying these pathological chan-ges remain unanswered. ERK has been reported chronically activated in reactive glia of human epil-eptic hipocampus. In the present study, we in-vestigated which of the downstream signaling mol-ecules of ERK would be involved in MTLE. Wes-tern blot analysis demonstrated that CREB and Increase in the active forms of CREB and p90RSK resulted not only from the increase in their phos-phorylation levels but also from the increase in the protein levels. Activation of CREB and p90RSK was noted in the whole subfields of hippocampus with Amon's horn sclerosis (AHS) representing a distinctive cellular distribution. However, the comon major change was present in proliferating reactive astrocytes. In contrast, their activation spite the presence of a number of astrocytes ex-pressing high levels of GFAP. Our results demon-strate that chronic activation CREB and p90RSK in the epileptic hipocampus may be closely as-sociated with the histopathological changes of AHS.

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