The hippocampus is an important brain region that is involved in neurological disorders such as Alzheimer disease, schizophrenia, and epilepsy. Ionotropic glutamate receptors—namely, N-methyl-D-aspartate (NMDA) receptors (NMDARs), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors (AMPARs), and kainic acid (KA) receptors (KARs)—are well known to be involved in these diseases by mediating long-term potentiation, excitotoxicity, or both. NBQX is an antagonist of AMPARs and KARs. NBQX for AMPA and KA stimulation (IC50 = 0.7 ± 0.1 and 0.7 ± 0.03 μM, respectively; n = 3). The effects of NBQX on the AMPA- or KA-evoked calcium rise in differentiated HIP-009 cells were assessed. NBQX inhibited both AMPA- and KA-induced signals in a concentration-dependent fashion (IC50 = 0.7 ± 0.1 and 0.7 ± 0.03 μM for AMPA and KA stimulation, respectively, n = 3). The AMPA-evoked calcium rise was completely inhibited by NBQX, whereas 68.6% ± 1.3% inhibition of the KA-induced signal was observed with 30 μM of NBQX treatment. The effect of co-treatment with MK-801 (a NMDAR antagonist) and NBQX on the glutamate-evoked calcium rise was assessed. When 30 μM of MK-801 or NBQX was added alone, 44.5% ± 2.2% or 34.2% ± 5.0%, respectively, of the glutamate-induced calcium rise was inhibited. Co-treatment had an additive inhibitory effect on total calcium rise upon glutamate stimulation (78.6% ± 2.2% inhibition)[1].
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