The dopaminergic neurons of the substantia nigra pars compacta (SNc) are important in the circuitry of the basal ganglia, and their degeneration underlies the development of motor symptoms in Parkinson’s disease. Several mechanisms may contribute to this degeneration, one of which could be excessive activation of N-methyl-D-aspartate (NMDA) receptors. NMDA receptors are tetrameric assemblies of GluN1 and at least one type of GluN2 (A,B,C and D) subunit which confer distinct and unique characteristics to these receptors. Dopaminergic neurones of the substantia nigra pars compacta (SNc) express a combination of GluN2B and also GluN2D subunits and here we investigated the hypothesis that these receptors are expressed as ‘triheteromeric’ GluN1/GluN2B/GluN2D receptors. Using patch-clamp whole-cell recordings from SNc neurones in coronal brain slices from 3 week old rats (humanely killed by decapitation under deep isofluorane anaesthesia), we investigated how these unusual NMDA receptors are regulated by the subunit selective allosteric inhibitors, ifenprodil (GluN2B) and DQP-1105 (GluN2C/D) during repeated activation (15s durations at 100s intervals, of 100µM NMDA over a 10 minute time scale). NMDA-evoked currents displayed a maximal inhibition of 58 ± 11% by ifenprodil (10μM, n = 10) with an estimated IC50 = 0.21 μM while DQP-1105 (10μM, n = 9) inhibited currents by 64 ± 7.9%. These results suggest that a proportion of NMDA receptors on dopaminergic neurons of the substantia nigra are triheteromeric GluN1/GluN2B/GluN2D receptors.