Uteroplacental insufficiency (UPI), the major cause of intrauterine growth restriction (IUGR) in developed nations, predisposes to learning impairment. The underlying mechanism is unknown. Neuronal N-methyl-d-aspartate receptors (NMDARs) are critical for synaptogenesis and learning throughout life. We hypothesized that UPI-induced IUGR alters rat hippocampal NMDAR NR2A/NR2B subunit ratio and/or NR1 mRNA isoform expression and synaptic density at day 21 (P21). To test this hypothesis, IUGR was induced by bilateral uterine artery ligation of the late-gestation Sprague Dawley dam. At P21, hippocampal NMDAR subunit mRNA and protein was measured, as were levels of synaptophysin. Neuronal, synaptic and glial density in CA1, CA3 and DG was assessed by immunofluorescence. IUGR increased NR1 mRNA isoform NR1-3a and 1-3b expression in both genders. In P21 males, IUGR increased protein levels of NR1 C2 and decreased NR1 C2, NR2A and the NR2A to NR2B ratio, while in females, IUGR increased NR2B protein. In males, IUGR was associated with decreased MBP/NeuN ratio in CA1, CA3 and DG. We conclude that IUGR has gender-specific effects, and that neither neuronal loss nor decreased synaptic density appears to account for the changes in NMDAR subunits. Rather, it is possible that synaptic NMDAR subunit composition is altered. Our results suggest that apparent recovery in the IUGR hippocampus may be associated with synaptic hyperexcitability. We speculate that the NMDAR plays an important role in IUGR-associated cognitive impairment.