Abstract
Dysfunction of the gene for the NR1 subunit of NMDA receptor has been implicated in the pathogenesis of schizophrenia. In support of this hypothesis are psychosis-like behavioral abnormalities in 50-day-old rat males with attenuated specific synaptosomal binding of (3H) glutamate to NMDA receptor in their brains.
Quantitative internally standardized RT-PCR assay did not reveal any significant changes in mRNA levels of NR1 subunit in left and right hippocampii of naive rats and controls as well as in young adult males treated with quinolinic acid (QUIN; 250 nmol/0.25 uL buffered saline into each lateral cerebral ventricle) on postnatal day 12. In contrast, quantitative Western blotting disclosed increased protein levels of NR1 subunit in the left hippocampus of naive young adults.
The laterality disappeared in animals with psychosis-like behavior together with significant decrease of NR1 protein in their left hippocampi. These results suggest that protein expression of NR1 subunit exhibits changes comaparable to those observed in patients with schizophrenia.