Increased NR1-NR2A/B coassembly as a mechanism for rat chronic hippocampal epilepsy.

The N-methyl-D-aspartate receptors (NMDAR) produce physiologically functional channels for enhanced excitatory neurotransmission when they exist as heteromeric complexes containing the NMDAR1 subunit combined with NMDAR2. We examined the expressions of NMDAR1 and 2A/B protein in the kainic acid induced rat chronic epileptic hippocampus. Immunoreactivities of both NMDAR1 and NDMAR2A/B were increased in the inner molecular layer of the dentate gyrus, while they were decreased in the hilar and CA3/4 pyramidal zones. Immunoblot analysis demonstrated that the overall level of NMDAR1-2A/B coassembly was increased in the whole hippocampus. These results indicate that the increase of the NMDAR1-2A/B complex in the inner molecular layer is a significant cellular mechanism that contributes to focal hyperexcitability in rat chronic hippocampal epilepsy.