DEVELOPMENTAL REGULATION OF GLUTAMATE AND GABA(A) RECEPTOR GENE-EXPRESSION IN RAT HIPPOCAMPUS FOLLOWING KAINATE-INDUCED STATUS EPILEPTICUS

In adult rats, kainic acid-induced status epilepticus markedly reduces GluR2 (the pha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid, A MPA subunit that limits Ca2+ permeability), receptor mRNA in the vulne rable CA3 and may contribute to delayed neurodegeneration. In rat pups resistant to kainate seizure-induced hippocampal neurodegeneration by silver impregnation, glutamate or GABA(A) alpha 1-receptor mRNAs were unaltered in CA3 neurons 24 h after status epilepticus. In the dentat e gyrus, GluR1 and GluR2 mRNAs were transiently increased in P14 but n ot P5 pups. Immunocytochemistry revealed no apparent differences in th e distribution patterns of GluR1, GluR2, or GluR2/3 receptor proteins in the CA3 or dentate gyrus of P14 pups. Status epilepticus-induced al terations in receptor GluR2 and GABA(A) alpha 1 mRNAs and AMPA protein expression vary with developmental age. Sustained expression at young ages may contribute to the resistance of developing hippocampal neuro ns to seizure-induced damage.