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d 2 amino 5 phosphonovaleric acid  (Tocris)
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d ap5 2r amino 5 phosphonovaleric acid  (Tocris)
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Influence of ionotropic receptor antagonists <t>D-AP5</t> (NMDAR antagonist) and NBQX (AMPAR/KAR antagonist) on dopamine and glutamate. (A) Comparison of stimulated ΔF/F 0 for glutamate recorded under control, D-AP5 (50 μM, n=19) and NBQX (5 μM, n=23) (Two-way ANOVA, Time Factor: p=0.0007, F(3.120, 174.7)=5.857; Drug Factor: p=0.0024, F(3.120, 174.7)=5.857. The starred points represent significance between control and D-AP5 at time 30 (p<0.0001), 40 (p<0.0001), 50 (p=0.0005), and 60 (p<0.0001); no points were significantly different for NBQX. (B) Comparison of stimulated dopamine currents recorded under control, D-AP5 (50 μM, n=6) and NBQX (5 μM, n=7) conditions (Two-way ANOVA, Time Factor: p=0.0562, F(2.704, 43.26)=2.804; Drug Factor: p=0.0015, F(2, 16)=10.01). The starred points represent significance between control and NBQX at time 30 (p=0.0227), 40 (p=0.0331), and 50 (p=0.0397); no points were significantly different for D-AP5. (C-D) Paired-comparison graphs depicting the change between the averages of glutamate ΔF/F0 at different experimental conditions for (C) D-AP5 (Wilcoxon Test, n=19, p<0.0001) and (D) NBQX (Wilcoxon Test, n=23, p=0.0172). (E-F) Paired-comparison graphs depicting the change between the averages of dopamine current at different experimental time points for (E) D-AP5 (Wilcoxon Test, n=6, p=0.5625) and (F) NBQX (Wilcoxon Test, n=7, p=0.0156). (G) Cartoon image of presynaptic NMDAR blockage via the introduction of D-AP5. (H) Cartoon image of presynaptic AMPAR blockage via the introduction of NBQX.
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2 amino 5 phosphopentanoic acid  (Alomone Labs)
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Influence of ionotropic receptor antagonists <t>D-AP5</t> (NMDAR antagonist) and NBQX (AMPAR/KAR antagonist) on dopamine and glutamate. (A) Comparison of stimulated ΔF/F 0 for glutamate recorded under control, D-AP5 (50 μM, n=19) and NBQX (5 μM, n=23) (Two-way ANOVA, Time Factor: p=0.0007, F(3.120, 174.7)=5.857; Drug Factor: p=0.0024, F(3.120, 174.7)=5.857. The starred points represent significance between control and D-AP5 at time 30 (p<0.0001), 40 (p<0.0001), 50 (p=0.0005), and 60 (p<0.0001); no points were significantly different for NBQX. (B) Comparison of stimulated dopamine currents recorded under control, D-AP5 (50 μM, n=6) and NBQX (5 μM, n=7) conditions (Two-way ANOVA, Time Factor: p=0.0562, F(2.704, 43.26)=2.804; Drug Factor: p=0.0015, F(2, 16)=10.01). The starred points represent significance between control and NBQX at time 30 (p=0.0227), 40 (p=0.0331), and 50 (p=0.0397); no points were significantly different for D-AP5. (C-D) Paired-comparison graphs depicting the change between the averages of glutamate ΔF/F0 at different experimental conditions for (C) D-AP5 (Wilcoxon Test, n=19, p<0.0001) and (D) NBQX (Wilcoxon Test, n=23, p=0.0172). (E-F) Paired-comparison graphs depicting the change between the averages of dopamine current at different experimental time points for (E) D-AP5 (Wilcoxon Test, n=6, p=0.5625) and (F) NBQX (Wilcoxon Test, n=7, p=0.0156). (G) Cartoon image of presynaptic NMDAR blockage via the introduction of D-AP5. (H) Cartoon image of presynaptic AMPAR blockage via the introduction of NBQX.
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Influence of ionotropic receptor antagonists <t>D-AP5</t> (NMDAR antagonist) and NBQX (AMPAR/KAR antagonist) on dopamine and glutamate. (A) Comparison of stimulated ΔF/F 0 for glutamate recorded under control, D-AP5 (50 μM, n=19) and NBQX (5 μM, n=23) (Two-way ANOVA, Time Factor: p=0.0007, F(3.120, 174.7)=5.857; Drug Factor: p=0.0024, F(3.120, 174.7)=5.857. The starred points represent significance between control and D-AP5 at time 30 (p<0.0001), 40 (p<0.0001), 50 (p=0.0005), and 60 (p<0.0001); no points were significantly different for NBQX. (B) Comparison of stimulated dopamine currents recorded under control, D-AP5 (50 μM, n=6) and NBQX (5 μM, n=7) conditions (Two-way ANOVA, Time Factor: p=0.0562, F(2.704, 43.26)=2.804; Drug Factor: p=0.0015, F(2, 16)=10.01). The starred points represent significance between control and NBQX at time 30 (p=0.0227), 40 (p=0.0331), and 50 (p=0.0397); no points were significantly different for D-AP5. (C-D) Paired-comparison graphs depicting the change between the averages of glutamate ΔF/F0 at different experimental conditions for (C) D-AP5 (Wilcoxon Test, n=19, p<0.0001) and (D) NBQX (Wilcoxon Test, n=23, p=0.0172). (E-F) Paired-comparison graphs depicting the change between the averages of dopamine current at different experimental time points for (E) D-AP5 (Wilcoxon Test, n=6, p=0.5625) and (F) NBQX (Wilcoxon Test, n=7, p=0.0156). (G) Cartoon image of presynaptic NMDAR blockage via the introduction of D-AP5. (H) Cartoon image of presynaptic AMPAR blockage via the introduction of NBQX.
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d amino acid solution without glutamine  (Fresenius Kabi)
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Influence of ionotropic receptor antagonists <t>D-AP5</t> (NMDAR antagonist) and NBQX (AMPAR/KAR antagonist) on dopamine and glutamate. (A) Comparison of stimulated ΔF/F 0 for glutamate recorded under control, D-AP5 (50 μM, n=19) and NBQX (5 μM, n=23) (Two-way ANOVA, Time Factor: p=0.0007, F(3.120, 174.7)=5.857; Drug Factor: p=0.0024, F(3.120, 174.7)=5.857. The starred points represent significance between control and D-AP5 at time 30 (p<0.0001), 40 (p<0.0001), 50 (p=0.0005), and 60 (p<0.0001); no points were significantly different for NBQX. (B) Comparison of stimulated dopamine currents recorded under control, D-AP5 (50 μM, n=6) and NBQX (5 μM, n=7) conditions (Two-way ANOVA, Time Factor: p=0.0562, F(2.704, 43.26)=2.804; Drug Factor: p=0.0015, F(2, 16)=10.01). The starred points represent significance between control and NBQX at time 30 (p=0.0227), 40 (p=0.0331), and 50 (p=0.0397); no points were significantly different for D-AP5. (C-D) Paired-comparison graphs depicting the change between the averages of glutamate ΔF/F0 at different experimental conditions for (C) D-AP5 (Wilcoxon Test, n=19, p<0.0001) and (D) NBQX (Wilcoxon Test, n=23, p=0.0172). (E-F) Paired-comparison graphs depicting the change between the averages of dopamine current at different experimental time points for (E) D-AP5 (Wilcoxon Test, n=6, p=0.5625) and (F) NBQX (Wilcoxon Test, n=7, p=0.0156). (G) Cartoon image of presynaptic NMDAR blockage via the introduction of D-AP5. (H) Cartoon image of presynaptic AMPAR blockage via the introduction of NBQX.
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Influence of ionotropic receptor antagonists D-AP5 (NMDAR antagonist) and NBQX (AMPAR/KAR antagonist) on dopamine and glutamate. (A) Comparison of stimulated ΔF/F 0 for glutamate recorded under control, D-AP5 (50 μM, n=19) and NBQX (5 μM, n=23) (Two-way ANOVA, Time Factor: p=0.0007, F(3.120, 174.7)=5.857; Drug Factor: p=0.0024, F(3.120, 174.7)=5.857. The starred points represent significance between control and D-AP5 at time 30 (p<0.0001), 40 (p<0.0001), 50 (p=0.0005), and 60 (p<0.0001); no points were significantly different for NBQX. (B) Comparison of stimulated dopamine currents recorded under control, D-AP5 (50 μM, n=6) and NBQX (5 μM, n=7) conditions (Two-way ANOVA, Time Factor: p=0.0562, F(2.704, 43.26)=2.804; Drug Factor: p=0.0015, F(2, 16)=10.01). The starred points represent significance between control and NBQX at time 30 (p=0.0227), 40 (p=0.0331), and 50 (p=0.0397); no points were significantly different for D-AP5. (C-D) Paired-comparison graphs depicting the change between the averages of glutamate ΔF/F0 at different experimental conditions for (C) D-AP5 (Wilcoxon Test, n=19, p<0.0001) and (D) NBQX (Wilcoxon Test, n=23, p=0.0172). (E-F) Paired-comparison graphs depicting the change between the averages of dopamine current at different experimental time points for (E) D-AP5 (Wilcoxon Test, n=6, p=0.5625) and (F) NBQX (Wilcoxon Test, n=7, p=0.0156). (G) Cartoon image of presynaptic NMDAR blockage via the introduction of D-AP5. (H) Cartoon image of presynaptic AMPAR blockage via the introduction of NBQX.

Journal: Neurochemistry international

Article Title: Multiplexed Neurochemical Monitoring Reveals Glutamate Modulates Dopamine Neurotransmission in the Nucleus Accumbens

doi: 10.1016/j.neuint.2026.106148

Figure Lengend Snippet: Influence of ionotropic receptor antagonists D-AP5 (NMDAR antagonist) and NBQX (AMPAR/KAR antagonist) on dopamine and glutamate. (A) Comparison of stimulated ΔF/F 0 for glutamate recorded under control, D-AP5 (50 μM, n=19) and NBQX (5 μM, n=23) (Two-way ANOVA, Time Factor: p=0.0007, F(3.120, 174.7)=5.857; Drug Factor: p=0.0024, F(3.120, 174.7)=5.857. The starred points represent significance between control and D-AP5 at time 30 (p<0.0001), 40 (p<0.0001), 50 (p=0.0005), and 60 (p<0.0001); no points were significantly different for NBQX. (B) Comparison of stimulated dopamine currents recorded under control, D-AP5 (50 μM, n=6) and NBQX (5 μM, n=7) conditions (Two-way ANOVA, Time Factor: p=0.0562, F(2.704, 43.26)=2.804; Drug Factor: p=0.0015, F(2, 16)=10.01). The starred points represent significance between control and NBQX at time 30 (p=0.0227), 40 (p=0.0331), and 50 (p=0.0397); no points were significantly different for D-AP5. (C-D) Paired-comparison graphs depicting the change between the averages of glutamate ΔF/F0 at different experimental conditions for (C) D-AP5 (Wilcoxon Test, n=19, p<0.0001) and (D) NBQX (Wilcoxon Test, n=23, p=0.0172). (E-F) Paired-comparison graphs depicting the change between the averages of dopamine current at different experimental time points for (E) D-AP5 (Wilcoxon Test, n=6, p=0.5625) and (F) NBQX (Wilcoxon Test, n=7, p=0.0156). (G) Cartoon image of presynaptic NMDAR blockage via the introduction of D-AP5. (H) Cartoon image of presynaptic AMPAR blockage via the introduction of NBQX.

Article Snippet: D-AP5 ((2R)-amino-5-phosphonovaleric acid), DL-TBOA (DL-threo-β-Benzyloxyaspartate), NBQX (2,3-Dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide) Disodium Salt, LY 379268, and LY 341495 Disodium Salt were purchased from Tocris Bioscience (St. Louis, Missouri).

Techniques: Comparison, Control