Dopamine receptor signalling is essential for normal basal ganglia function. In Parkinson’s Disease (PD) there is a loss of dopaminergic (DAergic) neurons of the substantia nigra pars compact (SNc) with consequent loss of dopamine signalling. SNc DAergic neurons express D2 autoreceptors and somatodendritically released dopamine mediates a negative feedback via D2 receptors on DAergic neuron activity. D2 receptors mediate inhibition of NMDA responses in both hippocampus (Kotecha et al., 2002) and striatum (Higley & Sabatini, 2010). Here we tested whether D2 receptor activation modulates DAergic neuron NMDA responses in SNc using ropinirole, a D2 receptor agonist currently used in PD therapy. Whole-cell patch clamp recordings were made from DAergic neurons in the SNc of acute midbrain slices from neonatal (P7) rats. Brain slices were made in accordance with the guidelines of the UK Animals (Scientific Procedure) Act 1986 and following local ethical approval. DAergic neurons were identified by the presence of a prominent hyperpolarisation-activated inward current (amplitude, 193.4 ± 17.4 pA; activation time constant, 937 ± 73 ms; mean ± S.E.M) in response to a voltage step from -60 to -120 mV. In each cell two successive responses to 20 µM NMDA with 10 µM glycine were recorded. Control experiments gave responses of 919 ± 89 pA (1st response) and 881 ± 113 pA, n = 11 (2nd response). Following application of 20 µM ropinirole, the NMDA response was not significantly different (control NMDA response, 946 ± 88.8 pA; in presence of ropinirole, 895 ± 75 pA, n = 24, paired t-test, P = 0.514). In order to block G-protein activation, intracellular 0.5 mM GDP-β-S was used (in absence of any added GTP) and allowed to equilibrate for 5 minutes prior to ropinirole application. GDP-β-S did not significantly change the NMDA response (control, 1208 ± 63 pA, n = 6, one-way ANOVA, P > 0.05) and there was no significant effect of ropinirole (NMDA response: 813 ± 163 pA, n = 6, paired t-test, P = 0.05). As dopamine receptor desensitization could obscure an effect of D2 receptor activation, a novel G-protein receptor kinase (GRK2/3) inhibitor, Cmpd101 (Lowe et al., 2015), was applied (10 µM) intracellularly. Surprisingly, compared to experiments in the absence of Cmpd101 the NMDA response was smaller (one-way ANOVA, P = 0.0004) in the presence of Cmpd101 (control, 417 ± 101 pA, n = 10). However, there was no significant effect of ropinirole (570 ± 77 pA, n = 10, paired t-test, P = 0.289). These results suggest that D2-R activation does not modulate NMDA receptor responses in neonatal rat substantia nigra neurones.