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non competitive nmdar antagonist  (Tocris)


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    Structured Review

    Tocris non competitive nmdar antagonist
    B-hydroxybutyrate effects on synaptic plasticity. (A) Long-term Potentiation (LTP) at CA1 induced by high frequency stimulation (HFS; 4 × 100 Hz) of Control (blue) and DHB slices (orange) (Control: 10 slices, 9 animals; DHB: 9 slices, 8 animals). DHB slices were 2 h treated with DHB (2 mM) before recordings. Time-course of field excitatory postsynaptic potential (fEPSP; slope), percentual change from baseline, plotted data are average ± SEM (Two-Way repeated measures ANOVA with Bonferroni posttest: DHB p = 0.0411; HFS response p < 0.0001, Interaction p = 0.0005). (B) Examples of Control and DHB fEPSP traces showing the magnitude of change from baseline (gray) and 60 min after HFS (black). (C) Violin plot of percentual field-EPSP (slope) after HFS at 15–20 min (176.5 ± 10.9 vs. 141.2 ± 9.4; unpaired t-test, p = 0.0262), 35–40 min (157.7 ± 12.2 vs. 132.0 ± 7.7; unpaired t-test, p = 0.0924) and 55–60 min (153.2 ± 13.7 vs. 120.3 ± 5.4; unpaired t-test, p = 0.0397) after HFS. (D) Magnitude of AMPAr excitatory postsynaptic current (EPSC) recorded from Control and slices exposed to 2 h DHB (2 mM). Plotted data are average from percentual change from minimal stimulation intensity (Control: 6 cells, 2 animals; DHB: 5 cells, 3 animals). The stimulation intensities are normalized with respect to the intensity value evocating the minimal response. Analysis showed no difference between Control and DHB group (Two-Way repeated measures ANOVA with Bonferroni posttest: DHB p = 0.6287; Stimulus intensity p < 0.0001, Interaction p = 0.8706). (E) Examples of AMPAr-EPSCs traces of Control and DHB group showing the amplitude with higher intensities of stimulation 100% (gray), 150% (dark gray) and 225% (black). (F) Magnitude of <t>NMDAr</t> excitatory postsynaptic current (EPSC) recorded from Control and slices exposed to 2 h DHB (2 mM). Plotted data are average from percentual change from minimal stimulation intensity (Control: 10 cells, 6 animals; DHB: 13 cells, 6 animals). The stimulation intensities are normalized with respect to the intensity value evocating the minimal response. Analysis showed no difference between Control and DHB group (Two-Way repeated measures ANOVA with Bonferroni post test: DHB p = 0.5477; Stimulus intensity p < 0.0001, Interaction p = 0.9446). (G) Examples of NMDAr-EPSCs traces of Control and DHB group showing the amplitude with higher intensities of stimulation 100% (gray), 150% (dark gray) and 225% (black).
    Non Competitive Nmdar Antagonist, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 551 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/non competitive nmdar antagonist/product/Tocris
    Average 94 stars, based on 551 article reviews
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    Images

    1) Product Images from "Exposure to β-hydroxybutyrate reduces the operating set point and increases excitability in hippocampal circuitry of healthy mice"

    Article Title: Exposure to β-hydroxybutyrate reduces the operating set point and increases excitability in hippocampal circuitry of healthy mice

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2025.1557612

    B-hydroxybutyrate effects on synaptic plasticity. (A) Long-term Potentiation (LTP) at CA1 induced by high frequency stimulation (HFS; 4 × 100 Hz) of Control (blue) and DHB slices (orange) (Control: 10 slices, 9 animals; DHB: 9 slices, 8 animals). DHB slices were 2 h treated with DHB (2 mM) before recordings. Time-course of field excitatory postsynaptic potential (fEPSP; slope), percentual change from baseline, plotted data are average ± SEM (Two-Way repeated measures ANOVA with Bonferroni posttest: DHB p = 0.0411; HFS response p < 0.0001, Interaction p = 0.0005). (B) Examples of Control and DHB fEPSP traces showing the magnitude of change from baseline (gray) and 60 min after HFS (black). (C) Violin plot of percentual field-EPSP (slope) after HFS at 15–20 min (176.5 ± 10.9 vs. 141.2 ± 9.4; unpaired t-test, p = 0.0262), 35–40 min (157.7 ± 12.2 vs. 132.0 ± 7.7; unpaired t-test, p = 0.0924) and 55–60 min (153.2 ± 13.7 vs. 120.3 ± 5.4; unpaired t-test, p = 0.0397) after HFS. (D) Magnitude of AMPAr excitatory postsynaptic current (EPSC) recorded from Control and slices exposed to 2 h DHB (2 mM). Plotted data are average from percentual change from minimal stimulation intensity (Control: 6 cells, 2 animals; DHB: 5 cells, 3 animals). The stimulation intensities are normalized with respect to the intensity value evocating the minimal response. Analysis showed no difference between Control and DHB group (Two-Way repeated measures ANOVA with Bonferroni posttest: DHB p = 0.6287; Stimulus intensity p < 0.0001, Interaction p = 0.8706). (E) Examples of AMPAr-EPSCs traces of Control and DHB group showing the amplitude with higher intensities of stimulation 100% (gray), 150% (dark gray) and 225% (black). (F) Magnitude of NMDAr excitatory postsynaptic current (EPSC) recorded from Control and slices exposed to 2 h DHB (2 mM). Plotted data are average from percentual change from minimal stimulation intensity (Control: 10 cells, 6 animals; DHB: 13 cells, 6 animals). The stimulation intensities are normalized with respect to the intensity value evocating the minimal response. Analysis showed no difference between Control and DHB group (Two-Way repeated measures ANOVA with Bonferroni post test: DHB p = 0.5477; Stimulus intensity p < 0.0001, Interaction p = 0.9446). (G) Examples of NMDAr-EPSCs traces of Control and DHB group showing the amplitude with higher intensities of stimulation 100% (gray), 150% (dark gray) and 225% (black).
    Figure Legend Snippet: B-hydroxybutyrate effects on synaptic plasticity. (A) Long-term Potentiation (LTP) at CA1 induced by high frequency stimulation (HFS; 4 × 100 Hz) of Control (blue) and DHB slices (orange) (Control: 10 slices, 9 animals; DHB: 9 slices, 8 animals). DHB slices were 2 h treated with DHB (2 mM) before recordings. Time-course of field excitatory postsynaptic potential (fEPSP; slope), percentual change from baseline, plotted data are average ± SEM (Two-Way repeated measures ANOVA with Bonferroni posttest: DHB p = 0.0411; HFS response p < 0.0001, Interaction p = 0.0005). (B) Examples of Control and DHB fEPSP traces showing the magnitude of change from baseline (gray) and 60 min after HFS (black). (C) Violin plot of percentual field-EPSP (slope) after HFS at 15–20 min (176.5 ± 10.9 vs. 141.2 ± 9.4; unpaired t-test, p = 0.0262), 35–40 min (157.7 ± 12.2 vs. 132.0 ± 7.7; unpaired t-test, p = 0.0924) and 55–60 min (153.2 ± 13.7 vs. 120.3 ± 5.4; unpaired t-test, p = 0.0397) after HFS. (D) Magnitude of AMPAr excitatory postsynaptic current (EPSC) recorded from Control and slices exposed to 2 h DHB (2 mM). Plotted data are average from percentual change from minimal stimulation intensity (Control: 6 cells, 2 animals; DHB: 5 cells, 3 animals). The stimulation intensities are normalized with respect to the intensity value evocating the minimal response. Analysis showed no difference between Control and DHB group (Two-Way repeated measures ANOVA with Bonferroni posttest: DHB p = 0.6287; Stimulus intensity p < 0.0001, Interaction p = 0.8706). (E) Examples of AMPAr-EPSCs traces of Control and DHB group showing the amplitude with higher intensities of stimulation 100% (gray), 150% (dark gray) and 225% (black). (F) Magnitude of NMDAr excitatory postsynaptic current (EPSC) recorded from Control and slices exposed to 2 h DHB (2 mM). Plotted data are average from percentual change from minimal stimulation intensity (Control: 10 cells, 6 animals; DHB: 13 cells, 6 animals). The stimulation intensities are normalized with respect to the intensity value evocating the minimal response. Analysis showed no difference between Control and DHB group (Two-Way repeated measures ANOVA with Bonferroni post test: DHB p = 0.5477; Stimulus intensity p < 0.0001, Interaction p = 0.9446). (G) Examples of NMDAr-EPSCs traces of Control and DHB group showing the amplitude with higher intensities of stimulation 100% (gray), 150% (dark gray) and 225% (black).

    Techniques Used: Control



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    B-hydroxybutyrate effects on synaptic plasticity. (A) Long-term Potentiation (LTP) at CA1 induced by high frequency stimulation (HFS; 4 × 100 Hz) of Control (blue) and DHB slices (orange) (Control: 10 slices, 9 animals; DHB: 9 slices, 8 animals). DHB slices were 2 h treated with DHB (2 mM) before recordings. Time-course of field excitatory postsynaptic potential (fEPSP; slope), percentual change from baseline, plotted data are average ± SEM (Two-Way repeated measures ANOVA with Bonferroni posttest: DHB p = 0.0411; HFS response p < 0.0001, Interaction p = 0.0005). (B) Examples of Control and DHB fEPSP traces showing the magnitude of change from baseline (gray) and 60 min after HFS (black). (C) Violin plot of percentual field-EPSP (slope) after HFS at 15–20 min (176.5 ± 10.9 vs. 141.2 ± 9.4; unpaired t-test, p = 0.0262), 35–40 min (157.7 ± 12.2 vs. 132.0 ± 7.7; unpaired t-test, p = 0.0924) and 55–60 min (153.2 ± 13.7 vs. 120.3 ± 5.4; unpaired t-test, p = 0.0397) after HFS. (D) Magnitude of AMPAr excitatory postsynaptic current (EPSC) recorded from Control and slices exposed to 2 h DHB (2 mM). Plotted data are average from percentual change from minimal stimulation intensity (Control: 6 cells, 2 animals; DHB: 5 cells, 3 animals). The stimulation intensities are normalized with respect to the intensity value evocating the minimal response. Analysis showed no difference between Control and DHB group (Two-Way repeated measures ANOVA with Bonferroni posttest: DHB p = 0.6287; Stimulus intensity p < 0.0001, Interaction p = 0.8706). (E) Examples of AMPAr-EPSCs traces of Control and DHB group showing the amplitude with higher intensities of stimulation 100% (gray), 150% (dark gray) and 225% (black). (F) Magnitude of <t>NMDAr</t> excitatory postsynaptic current (EPSC) recorded from Control and slices exposed to 2 h DHB (2 mM). Plotted data are average from percentual change from minimal stimulation intensity (Control: 10 cells, 6 animals; DHB: 13 cells, 6 animals). The stimulation intensities are normalized with respect to the intensity value evocating the minimal response. Analysis showed no difference between Control and DHB group (Two-Way repeated measures ANOVA with Bonferroni post test: DHB p = 0.5477; Stimulus intensity p < 0.0001, Interaction p = 0.9446). (G) Examples of NMDAr-EPSCs traces of Control and DHB group showing the amplitude with higher intensities of stimulation 100% (gray), 150% (dark gray) and 225% (black).
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    Image Search Results


    B-hydroxybutyrate effects on synaptic plasticity. (A) Long-term Potentiation (LTP) at CA1 induced by high frequency stimulation (HFS; 4 × 100 Hz) of Control (blue) and DHB slices (orange) (Control: 10 slices, 9 animals; DHB: 9 slices, 8 animals). DHB slices were 2 h treated with DHB (2 mM) before recordings. Time-course of field excitatory postsynaptic potential (fEPSP; slope), percentual change from baseline, plotted data are average ± SEM (Two-Way repeated measures ANOVA with Bonferroni posttest: DHB p = 0.0411; HFS response p < 0.0001, Interaction p = 0.0005). (B) Examples of Control and DHB fEPSP traces showing the magnitude of change from baseline (gray) and 60 min after HFS (black). (C) Violin plot of percentual field-EPSP (slope) after HFS at 15–20 min (176.5 ± 10.9 vs. 141.2 ± 9.4; unpaired t-test, p = 0.0262), 35–40 min (157.7 ± 12.2 vs. 132.0 ± 7.7; unpaired t-test, p = 0.0924) and 55–60 min (153.2 ± 13.7 vs. 120.3 ± 5.4; unpaired t-test, p = 0.0397) after HFS. (D) Magnitude of AMPAr excitatory postsynaptic current (EPSC) recorded from Control and slices exposed to 2 h DHB (2 mM). Plotted data are average from percentual change from minimal stimulation intensity (Control: 6 cells, 2 animals; DHB: 5 cells, 3 animals). The stimulation intensities are normalized with respect to the intensity value evocating the minimal response. Analysis showed no difference between Control and DHB group (Two-Way repeated measures ANOVA with Bonferroni posttest: DHB p = 0.6287; Stimulus intensity p < 0.0001, Interaction p = 0.8706). (E) Examples of AMPAr-EPSCs traces of Control and DHB group showing the amplitude with higher intensities of stimulation 100% (gray), 150% (dark gray) and 225% (black). (F) Magnitude of NMDAr excitatory postsynaptic current (EPSC) recorded from Control and slices exposed to 2 h DHB (2 mM). Plotted data are average from percentual change from minimal stimulation intensity (Control: 10 cells, 6 animals; DHB: 13 cells, 6 animals). The stimulation intensities are normalized with respect to the intensity value evocating the minimal response. Analysis showed no difference between Control and DHB group (Two-Way repeated measures ANOVA with Bonferroni post test: DHB p = 0.5477; Stimulus intensity p < 0.0001, Interaction p = 0.9446). (G) Examples of NMDAr-EPSCs traces of Control and DHB group showing the amplitude with higher intensities of stimulation 100% (gray), 150% (dark gray) and 225% (black).

    Journal: Frontiers in Pharmacology

    Article Title: Exposure to β-hydroxybutyrate reduces the operating set point and increases excitability in hippocampal circuitry of healthy mice

    doi: 10.3389/fphar.2025.1557612

    Figure Lengend Snippet: B-hydroxybutyrate effects on synaptic plasticity. (A) Long-term Potentiation (LTP) at CA1 induced by high frequency stimulation (HFS; 4 × 100 Hz) of Control (blue) and DHB slices (orange) (Control: 10 slices, 9 animals; DHB: 9 slices, 8 animals). DHB slices were 2 h treated with DHB (2 mM) before recordings. Time-course of field excitatory postsynaptic potential (fEPSP; slope), percentual change from baseline, plotted data are average ± SEM (Two-Way repeated measures ANOVA with Bonferroni posttest: DHB p = 0.0411; HFS response p < 0.0001, Interaction p = 0.0005). (B) Examples of Control and DHB fEPSP traces showing the magnitude of change from baseline (gray) and 60 min after HFS (black). (C) Violin plot of percentual field-EPSP (slope) after HFS at 15–20 min (176.5 ± 10.9 vs. 141.2 ± 9.4; unpaired t-test, p = 0.0262), 35–40 min (157.7 ± 12.2 vs. 132.0 ± 7.7; unpaired t-test, p = 0.0924) and 55–60 min (153.2 ± 13.7 vs. 120.3 ± 5.4; unpaired t-test, p = 0.0397) after HFS. (D) Magnitude of AMPAr excitatory postsynaptic current (EPSC) recorded from Control and slices exposed to 2 h DHB (2 mM). Plotted data are average from percentual change from minimal stimulation intensity (Control: 6 cells, 2 animals; DHB: 5 cells, 3 animals). The stimulation intensities are normalized with respect to the intensity value evocating the minimal response. Analysis showed no difference between Control and DHB group (Two-Way repeated measures ANOVA with Bonferroni posttest: DHB p = 0.6287; Stimulus intensity p < 0.0001, Interaction p = 0.8706). (E) Examples of AMPAr-EPSCs traces of Control and DHB group showing the amplitude with higher intensities of stimulation 100% (gray), 150% (dark gray) and 225% (black). (F) Magnitude of NMDAr excitatory postsynaptic current (EPSC) recorded from Control and slices exposed to 2 h DHB (2 mM). Plotted data are average from percentual change from minimal stimulation intensity (Control: 10 cells, 6 animals; DHB: 13 cells, 6 animals). The stimulation intensities are normalized with respect to the intensity value evocating the minimal response. Analysis showed no difference between Control and DHB group (Two-Way repeated measures ANOVA with Bonferroni post test: DHB p = 0.5477; Stimulus intensity p < 0.0001, Interaction p = 0.9446). (G) Examples of NMDAr-EPSCs traces of Control and DHB group showing the amplitude with higher intensities of stimulation 100% (gray), 150% (dark gray) and 225% (black).

    Article Snippet: To evaluate intrinsic excitability, extra synaptic blockers were added to aCSF before current steps: selective and non-competitive NMDAr antagonist (50 μm, MK-801; Tocris, Cat. No. 0924); AMPA/Kainate Glutamate receptor antagonist (10 μm, DNQX; Tocris: Cat. No. 0189); GABA A receptor antagonist (50 μM, PTX; Tocris: Cat. No. 1128).

    Techniques: Control

    Immunohistochemical staining for Nestin in the subventricular zone at different time points (2, 6, 24 and 48 h) after hypoxic-ischemic injury in the control, sham and hypoxic-ischemia groups. MK, MK-801; Ro, Ro25-6981; NVP, NVP-AAM077.

    Journal: Molecular Medicine Reports

    Article Title: NMDA receptors promote neurogenesis in the neonatal rat subventricular zone following hypoxic-ischemic injury

    doi: 10.3892/mmr.2015.4501

    Figure Lengend Snippet: Immunohistochemical staining for Nestin in the subventricular zone at different time points (2, 6, 24 and 48 h) after hypoxic-ischemic injury in the control, sham and hypoxic-ischemia groups. MK, MK-801; Ro, Ro25-6981; NVP, NVP-AAM077.

    Article Snippet: Selective non-competitive NMDAR antagonist MK-801 (M107), NR2A antagonist NVP-AAM077 (P1999), and NR2B antagonist Ro25-6981 (R7150) were purchased from Sigma-Aldrich (St. Louis, MO, USA).

    Techniques: Immunohistochemical staining, Staining

    Comparison of the number of integrated optical density (IOD) value of Nestin-positive cells in the subventricular zone (SVZ) at different time points (2, 6, 24 and 48 h) after hypoxic-ischemic injury in the sham group, hypoxic-ischemia (labeled 'model') group, hypoxic-ischemia+treatment with MK-801 group, hypoxic-ischemia+treatment with Ro25-6981 group, and hypoxic-ischemia+treatment with NVP-AAM077 group. Data are presented as mean ± standard deviation. Positive cell counts in five 100×100 μ m 2 areas in the SVZ of three serially sectioned brains at each tested time point. * P<0.05 and ** P<0.01 vs. hypoxic-ischemia group. # P<0.05 and ## P<0.01 vs. hypoxic-ischemia+treatment with MK group.

    Journal: Molecular Medicine Reports

    Article Title: NMDA receptors promote neurogenesis in the neonatal rat subventricular zone following hypoxic-ischemic injury

    doi: 10.3892/mmr.2015.4501

    Figure Lengend Snippet: Comparison of the number of integrated optical density (IOD) value of Nestin-positive cells in the subventricular zone (SVZ) at different time points (2, 6, 24 and 48 h) after hypoxic-ischemic injury in the sham group, hypoxic-ischemia (labeled 'model') group, hypoxic-ischemia+treatment with MK-801 group, hypoxic-ischemia+treatment with Ro25-6981 group, and hypoxic-ischemia+treatment with NVP-AAM077 group. Data are presented as mean ± standard deviation. Positive cell counts in five 100×100 μ m 2 areas in the SVZ of three serially sectioned brains at each tested time point. * P<0.05 and ** P<0.01 vs. hypoxic-ischemia group. # P<0.05 and ## P<0.01 vs. hypoxic-ischemia+treatment with MK group.

    Article Snippet: Selective non-competitive NMDAR antagonist MK-801 (M107), NR2A antagonist NVP-AAM077 (P1999), and NR2B antagonist Ro25-6981 (R7150) were purchased from Sigma-Aldrich (St. Louis, MO, USA).

    Techniques: Labeling, Standard Deviation

    Immunohistochemical staining for DCX in the subventricular zone at different time points (2, 6, 24 and 48 h) after hypoxic-ischemic injury in the control, sham and hypoxic-ischemia groups. DCX, Nestin and doublecortin; MK, MK-801; Ro, Ro25-6981; NVP, NVP-AAM077.

    Journal: Molecular Medicine Reports

    Article Title: NMDA receptors promote neurogenesis in the neonatal rat subventricular zone following hypoxic-ischemic injury

    doi: 10.3892/mmr.2015.4501

    Figure Lengend Snippet: Immunohistochemical staining for DCX in the subventricular zone at different time points (2, 6, 24 and 48 h) after hypoxic-ischemic injury in the control, sham and hypoxic-ischemia groups. DCX, Nestin and doublecortin; MK, MK-801; Ro, Ro25-6981; NVP, NVP-AAM077.

    Article Snippet: Selective non-competitive NMDAR antagonist MK-801 (M107), NR2A antagonist NVP-AAM077 (P1999), and NR2B antagonist Ro25-6981 (R7150) were purchased from Sigma-Aldrich (St. Louis, MO, USA).

    Techniques: Immunohistochemical staining, Staining

    Comparison of the number of DCX-positive cells in the subventricular zone (SVZ) at different time points (2, 6, 24 and 48 h) after hypoxic-ischemic in the sham group, hypoxic-ischemia (labeled 'model') group, hypoxic-ischemia+treatment with MK-801 group, hypoxic-ischemia+treatment with Ro25-6981 group, and hypoxic-ischemia+treatment with NVP-AAM077 group. Data are presented as mean ± standard deviation. Positive cell counts in five 100×100 μ m 2 areas in the SVZ of three serially sectioned brains at each tested time point. * P<0.05, ** P<0.01, and △ P<0.001 vs. hypoxic-ischemia group. #P<0.05, ## P<0.01, and ★ P<0.001 vs. hypoxic-ischemia+treatment with MK group.

    Journal: Molecular Medicine Reports

    Article Title: NMDA receptors promote neurogenesis in the neonatal rat subventricular zone following hypoxic-ischemic injury

    doi: 10.3892/mmr.2015.4501

    Figure Lengend Snippet: Comparison of the number of DCX-positive cells in the subventricular zone (SVZ) at different time points (2, 6, 24 and 48 h) after hypoxic-ischemic in the sham group, hypoxic-ischemia (labeled 'model') group, hypoxic-ischemia+treatment with MK-801 group, hypoxic-ischemia+treatment with Ro25-6981 group, and hypoxic-ischemia+treatment with NVP-AAM077 group. Data are presented as mean ± standard deviation. Positive cell counts in five 100×100 μ m 2 areas in the SVZ of three serially sectioned brains at each tested time point. * P<0.05, ** P<0.01, and △ P<0.001 vs. hypoxic-ischemia group. #P<0.05, ## P<0.01, and ★ P<0.001 vs. hypoxic-ischemia+treatment with MK group.

    Article Snippet: Selective non-competitive NMDAR antagonist MK-801 (M107), NR2A antagonist NVP-AAM077 (P1999), and NR2B antagonist Ro25-6981 (R7150) were purchased from Sigma-Aldrich (St. Louis, MO, USA).

    Techniques: Labeling, Standard Deviation