SEIZURES-EVOKED ACTIVATION OF TRANSCRIPTION FACTORS

Chemically provoked seizures have proved to serve as useful model to i nvestigate long term neuronal responses collectively termed as neurona l plasticity. In particular, rapid, transient activation of immediate early gene expression induced by such chemoconvulsants like pentylenet etrazole (PTZ) and kainic acid (KA) drew a great attention. These gene s code for transcription factors, known to influence gene expression, and therefore able to orchestrate genomic responses to extracellular s timuli. In our studies reviewed herein and reported in detail eslewher e, we have investigated PTZ- and KA-dependent activation of a function al feature of transcription factors i.e. their DNA-binding activity. W e have found that only AP-1 DNA-binding activity was elevated in the r at hippocampus, entorhinal and sensory cortices 2-6 h after the PTZ ad ministration, and only in the hippocampus and entorhinal cortex at sim ilar times following KA injection. The AP-1 response to PTZ was striki ngly enhanced in aged (18-24 months old) animals when compared to youn g (3 months old) ones. KA, apart from this early phase of AP-1 DNA-bin ding activity increase, evoked also the late one (reaching a peak valu e at 72 h). The protein composition of the latter differed from the fo rmer mostly by substitution of Jun B with Jun D protein and lack of c- Fos. Because the KA treatment leads not only to the seizures but to ap optosis (programmed cell death) as well, our results indicate that var ious AP-1 complexes may be involved in both of these phenomenona.