The infusion of NMDA induced degeneration of hippocampal principal cells.
Neurodegeneration was accompanied with progressive and severe neuroinflammation.
The lesion did not induce loss of GABAergic interneurons.
GluN1 and GluN2B subunits of NMDA receptor were upregulated at early time points.
GABAA receptor α5 subunit was downregulated at 30 days after the lesion.