Metabotrophic P2Y ATP receptors are widely distributed throughout the brain (Ralevic & Burnstock, 1998) and P2Y1 receptor protein is found in the striatum of both humans and rats (Franke et al. 2003; Scheibler et al. 2004). Via activation of protein kinase C and increases in intracellular calcium, P2Y1 receptors have the potential to influence a variety of voltage-dependent and neurotransmitter-activated ion channels during development and in the adult brain. Here we investigated the possibility that P2Y receptor activation may modulate NMDA receptor responses in striatal slices from 7 day old rats. Two minute whole-cell responses to 0.01 mM NMDA and 0.01 mM glycine in the presence of TTX (100 nM) were recorded with ATP (2 mM) and GTP (0.5 mM) in the pipette solution in 17 neurones. Steady-state control responses to NMDA (133 ± 27.2 pA) were recorded followed by a 5 min application of the P2Y agonist, 2-methyl-thio-ADP (2-Me-S-ADP, 250 nM). Following this, NMDA was applied again for a further 2 min in the presence of 2-Me-S-ADP and the mean NMDA current recorded (121 ± 24.5 pA). In control experiments, NMDA was applied twice at 5 min intervals in the absence of 2-Me-S-ADP and the second response was 90.1 ± 4.7% of the first response. In the presence of the P2Y agonist, the NMDA response was 89.3 ± 6.1% of the control current and we therefore conclude that there is no significant effect (n = 17 cells, paired t-test, P>0.05) of P2Y receptors on NMDA responses under these conditions.