SEIZURE-RELATED CHANGES IN THE GLUTAMATE R2 AND R5 RECEPTOR GENES EXPRESSION IN THE RAT HIPPOCAMPAL-FORMATION

The expression of mRNA coding for AMPA selective glutamate (Glu) R2 re ceptor and kainate selective GluR5 receptor was studied in the rat hip pocampal formation in two animal models of limbic seizures evoked by s ystemic administration of pilocarpine (400 mg/kg ip) or kainate (15 mg /kg ip). As shown by an in situ hybridization study, pilocarpine decre ased the GluR2 flip mRNA level in CA1 and CA3 areas of the hippocampus after 3h and kainate after 24h, e.g. at the time preceding neuronal d egeneration. No changes in the GluR2 flop or GluR5 mRNA level were fou nd in those regions. In the dentate gyrus, resistant to neurodegenerat ion, pilocarpine and kainate differentialy affected the expression of GluR2 and GluR5 mRNAs. After 72h pilocarpine, but not kainate, increas ed the GluR2 flop mRNA level and decreased the flip one, which suggest s attenuation of the GluR2 sensitivity. On the other hand, kainate, el evated the GluR2 flip and GluR5 mRNA level in the dentate gyrus after 72h. All in all the above data suggest that changes in the GluR2 gene expression may play some role in the neuronal damage to vulnerable are as (CA1, CA3). However, differences in the kainate- and pilocarpine-in duced changes in the dentate gyrus at the late time points indicate th at alterations in the stoichiometry of GluR2 forms or GluR5 gene expre ssion in this brain region are not a common causal factor responsible for delayed neuronal hyperexcitability.