We further examined the role of NMDA receptors in modulating the macrophage TNF response to the CA-MRSA bacteria by studying the effects of a competitive NMDA receptor antagonist, APV, and the effects of the NMDA substrate itself ( Figure 5 ). We found that APV (at either 300 μM or 3 mM) also inhibited macrophage TNF secretion in response to vancomycin-exposed MW2 (p < 0.05, Figure 5 ). The magnitude of the inhibition was comparable to that observed with either ketamine or MK-801 (and, as in the case of MK-801, was not additive or synergistic with ketamine). Furthermore, the addition of the NMDA substrate (30 μM) resulted in a marked augmentation of the macrophage TNF response to the antibiotic-treated CA-MRSA bacteria (p < 0.05), and this effect was blocked by ketamine and by the competitive NMDA receptor antagonist, APV ( Figure 5 ).