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Brief N-methyl-D-aspartate (NMDA) receptor blockade in neonatal rats has been reported to increase neuronal apoptosis. We replicated this finding using MK-801 (0.5 mg/kg) administered twice on postnatal day 7, and then studied the long-term consequences. In adulthood, treated rats showed reduced volume and neuronal number within the hippocampus, and altered hippocampal NMDA receptor (NR1 subunit) expression. Synaptophysin mRNA was decreased in the thalamus (laterodorsal nucleus). Adult MK-801-treated females had prepulse inhibition deficits and increased locomotor activity. The data show that a transient and limited glutamatergic intervention during development can have chronic behavioural, structural and molecular effects. The effects are reminiscent of alterations reported in schizophrenia and, as such, are consistent with hypotheses advocating a role for NMDA receptor hypofunction, and aberrant apoptosis, in the neurodevelopmental pathogenesis of the disorder.


Journal article


Eur J Neurosci

Publication Date





1706 - 1710


Animals, Animals, Newborn, Apoptosis, Behavior, Animal, Cell Count, Dizocilpine Maleate, Excitatory Amino Acid Antagonists, Female, Gene Expression Regulation, Developmental, Hippocampus, Immunohistochemistry, In Situ Hybridization, In Situ Nick-End Labeling, Inhibition (Psychology), Male, Motor Activity, Neurons, Rats, Rats, Sprague-Dawley, Receptors, N-Methyl-D-Aspartate, Sex Factors, Synaptophysin, Thalamus, Time