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nmdar antagonist memantine  (MedChemExpress)


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    Structured Review

    MedChemExpress nmdar antagonist memantine
    <t>NMDAR</t> was involved in TCF7L2-mediated depressive-like behavior. ( A ) Experimental timeline for NMDAR agonist-NMDA administration and behavioral tests. ( B ) Effects of NMDA administration on latency to the first immobility in the TST with LHb neurons special TCF7L2 knockdown, mean of AAV-sh-scrambled + Saline: 106, mean of AAV-sh-scrambled + NMDA: 111.9, mean of AAV-sh-TCF7L2 + Saline: 111.1, mean of AAV-sh-TCF7L2 + NMDA: 108.8. ( C ) Total immobility time in the TST, mean of AAV-sh-scrambled + Saline: 57.75, mean of AAV-sh-scrambled + NMDA: 52.45, mean of AAV-sh-TCF7L2 + Saline: 8.143, mean of AAV-sh-TCF7L2 + NMDA: 62.63. ( D ) Effects of NMDA administration on latency to the first floating in the FST, mean of AAV-sh-scrambled + Saline: 72.36, mean of AAV-sh-scrambled + NMDA: 95.45, mean of AAV-sh-TCF7L2 + Saline: 110.9, mean of AAV-sh-TCF7L2 + NMDA: 102.6. ( E ) Total floating time in the FST, mean of AAV-sh-scrambled + Saline: 106.1, mean of AAV-sh-scrambled + NMDA: 120.7, mean of AAV-sh-TCF7L2 + Saline: 45, mean of AAV-sh-TCF7L2 + NMDA: 134.7. ( F ) Experimental timeline for NMDAR <t>antagonist-memantine</t> administration and behavioral tests. ( G ) Effects of memantine administration on latency to the first immobility in the TST with LHb neurons special TCF7L2 overexpression, mean of AAV-EGFP + Saline: 85.25, mean of AAV-EGFP + Memantine: 88.25, mean of AAV-TCF7L2 + Saline: 50.75, mean of AAV-TCF7L2 + Memantine: 80.05. ( H ) Total immobility time in the TST, mean of AAV-EGFP + Saline: 79.75, mean of AAV-EGFP + Memantine: 75.38, mean of AAV-TCF7L2 + Saline: 131.5, mean of AAV-TCF7L2 + Memantine: 72.38. ( I ) Effects of memantine administration on latency to the first floating in the FST, mean of AAV-EGFP + Saline: 91.5, mean of AAV-EGFP + Memantine: 100.8, mean of AAV-TCF7L2 + Saline: 35, mean of AAV-TCF7L2 + Memantine: 82.5. ( J ) Total floating time in the FST, mean of AAV-EGFP + Saline: 32.25, mean of AAV-EGFP + Memantine: 44.63, mean of AAV-TCF7L2 + Saline: 157.5, mean of AAV-TCF7L2 + Memantine: 77.88. Comparisons between groups were conducted using one-way ANOVA. Data are expressed as means ± SEM. n = 7–11 per group. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Nmdar Antagonist Memantine, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Neuronal TCF7L2 in Lateral Habenula Is Involved in Stress-Induced Depression"

    Article Title: Neuronal TCF7L2 in Lateral Habenula Is Involved in Stress-Induced Depression

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms252212404

    NMDAR was involved in TCF7L2-mediated depressive-like behavior. ( A ) Experimental timeline for NMDAR agonist-NMDA administration and behavioral tests. ( B ) Effects of NMDA administration on latency to the first immobility in the TST with LHb neurons special TCF7L2 knockdown, mean of AAV-sh-scrambled + Saline: 106, mean of AAV-sh-scrambled + NMDA: 111.9, mean of AAV-sh-TCF7L2 + Saline: 111.1, mean of AAV-sh-TCF7L2 + NMDA: 108.8. ( C ) Total immobility time in the TST, mean of AAV-sh-scrambled + Saline: 57.75, mean of AAV-sh-scrambled + NMDA: 52.45, mean of AAV-sh-TCF7L2 + Saline: 8.143, mean of AAV-sh-TCF7L2 + NMDA: 62.63. ( D ) Effects of NMDA administration on latency to the first floating in the FST, mean of AAV-sh-scrambled + Saline: 72.36, mean of AAV-sh-scrambled + NMDA: 95.45, mean of AAV-sh-TCF7L2 + Saline: 110.9, mean of AAV-sh-TCF7L2 + NMDA: 102.6. ( E ) Total floating time in the FST, mean of AAV-sh-scrambled + Saline: 106.1, mean of AAV-sh-scrambled + NMDA: 120.7, mean of AAV-sh-TCF7L2 + Saline: 45, mean of AAV-sh-TCF7L2 + NMDA: 134.7. ( F ) Experimental timeline for NMDAR antagonist-memantine administration and behavioral tests. ( G ) Effects of memantine administration on latency to the first immobility in the TST with LHb neurons special TCF7L2 overexpression, mean of AAV-EGFP + Saline: 85.25, mean of AAV-EGFP + Memantine: 88.25, mean of AAV-TCF7L2 + Saline: 50.75, mean of AAV-TCF7L2 + Memantine: 80.05. ( H ) Total immobility time in the TST, mean of AAV-EGFP + Saline: 79.75, mean of AAV-EGFP + Memantine: 75.38, mean of AAV-TCF7L2 + Saline: 131.5, mean of AAV-TCF7L2 + Memantine: 72.38. ( I ) Effects of memantine administration on latency to the first floating in the FST, mean of AAV-EGFP + Saline: 91.5, mean of AAV-EGFP + Memantine: 100.8, mean of AAV-TCF7L2 + Saline: 35, mean of AAV-TCF7L2 + Memantine: 82.5. ( J ) Total floating time in the FST, mean of AAV-EGFP + Saline: 32.25, mean of AAV-EGFP + Memantine: 44.63, mean of AAV-TCF7L2 + Saline: 157.5, mean of AAV-TCF7L2 + Memantine: 77.88. Comparisons between groups were conducted using one-way ANOVA. Data are expressed as means ± SEM. n = 7–11 per group. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: NMDAR was involved in TCF7L2-mediated depressive-like behavior. ( A ) Experimental timeline for NMDAR agonist-NMDA administration and behavioral tests. ( B ) Effects of NMDA administration on latency to the first immobility in the TST with LHb neurons special TCF7L2 knockdown, mean of AAV-sh-scrambled + Saline: 106, mean of AAV-sh-scrambled + NMDA: 111.9, mean of AAV-sh-TCF7L2 + Saline: 111.1, mean of AAV-sh-TCF7L2 + NMDA: 108.8. ( C ) Total immobility time in the TST, mean of AAV-sh-scrambled + Saline: 57.75, mean of AAV-sh-scrambled + NMDA: 52.45, mean of AAV-sh-TCF7L2 + Saline: 8.143, mean of AAV-sh-TCF7L2 + NMDA: 62.63. ( D ) Effects of NMDA administration on latency to the first floating in the FST, mean of AAV-sh-scrambled + Saline: 72.36, mean of AAV-sh-scrambled + NMDA: 95.45, mean of AAV-sh-TCF7L2 + Saline: 110.9, mean of AAV-sh-TCF7L2 + NMDA: 102.6. ( E ) Total floating time in the FST, mean of AAV-sh-scrambled + Saline: 106.1, mean of AAV-sh-scrambled + NMDA: 120.7, mean of AAV-sh-TCF7L2 + Saline: 45, mean of AAV-sh-TCF7L2 + NMDA: 134.7. ( F ) Experimental timeline for NMDAR antagonist-memantine administration and behavioral tests. ( G ) Effects of memantine administration on latency to the first immobility in the TST with LHb neurons special TCF7L2 overexpression, mean of AAV-EGFP + Saline: 85.25, mean of AAV-EGFP + Memantine: 88.25, mean of AAV-TCF7L2 + Saline: 50.75, mean of AAV-TCF7L2 + Memantine: 80.05. ( H ) Total immobility time in the TST, mean of AAV-EGFP + Saline: 79.75, mean of AAV-EGFP + Memantine: 75.38, mean of AAV-TCF7L2 + Saline: 131.5, mean of AAV-TCF7L2 + Memantine: 72.38. ( I ) Effects of memantine administration on latency to the first floating in the FST, mean of AAV-EGFP + Saline: 91.5, mean of AAV-EGFP + Memantine: 100.8, mean of AAV-TCF7L2 + Saline: 35, mean of AAV-TCF7L2 + Memantine: 82.5. ( J ) Total floating time in the FST, mean of AAV-EGFP + Saline: 32.25, mean of AAV-EGFP + Memantine: 44.63, mean of AAV-TCF7L2 + Saline: 157.5, mean of AAV-TCF7L2 + Memantine: 77.88. Comparisons between groups were conducted using one-way ANOVA. Data are expressed as means ± SEM. n = 7–11 per group. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Knockdown, Saline, Over Expression



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    MedChemExpress nmdar antagonist memantine
    <t>NMDAR</t> was involved in TCF7L2-mediated depressive-like behavior. ( A ) Experimental timeline for NMDAR agonist-NMDA administration and behavioral tests. ( B ) Effects of NMDA administration on latency to the first immobility in the TST with LHb neurons special TCF7L2 knockdown, mean of AAV-sh-scrambled + Saline: 106, mean of AAV-sh-scrambled + NMDA: 111.9, mean of AAV-sh-TCF7L2 + Saline: 111.1, mean of AAV-sh-TCF7L2 + NMDA: 108.8. ( C ) Total immobility time in the TST, mean of AAV-sh-scrambled + Saline: 57.75, mean of AAV-sh-scrambled + NMDA: 52.45, mean of AAV-sh-TCF7L2 + Saline: 8.143, mean of AAV-sh-TCF7L2 + NMDA: 62.63. ( D ) Effects of NMDA administration on latency to the first floating in the FST, mean of AAV-sh-scrambled + Saline: 72.36, mean of AAV-sh-scrambled + NMDA: 95.45, mean of AAV-sh-TCF7L2 + Saline: 110.9, mean of AAV-sh-TCF7L2 + NMDA: 102.6. ( E ) Total floating time in the FST, mean of AAV-sh-scrambled + Saline: 106.1, mean of AAV-sh-scrambled + NMDA: 120.7, mean of AAV-sh-TCF7L2 + Saline: 45, mean of AAV-sh-TCF7L2 + NMDA: 134.7. ( F ) Experimental timeline for NMDAR <t>antagonist-memantine</t> administration and behavioral tests. ( G ) Effects of memantine administration on latency to the first immobility in the TST with LHb neurons special TCF7L2 overexpression, mean of AAV-EGFP + Saline: 85.25, mean of AAV-EGFP + Memantine: 88.25, mean of AAV-TCF7L2 + Saline: 50.75, mean of AAV-TCF7L2 + Memantine: 80.05. ( H ) Total immobility time in the TST, mean of AAV-EGFP + Saline: 79.75, mean of AAV-EGFP + Memantine: 75.38, mean of AAV-TCF7L2 + Saline: 131.5, mean of AAV-TCF7L2 + Memantine: 72.38. ( I ) Effects of memantine administration on latency to the first floating in the FST, mean of AAV-EGFP + Saline: 91.5, mean of AAV-EGFP + Memantine: 100.8, mean of AAV-TCF7L2 + Saline: 35, mean of AAV-TCF7L2 + Memantine: 82.5. ( J ) Total floating time in the FST, mean of AAV-EGFP + Saline: 32.25, mean of AAV-EGFP + Memantine: 44.63, mean of AAV-TCF7L2 + Saline: 157.5, mean of AAV-TCF7L2 + Memantine: 77.88. Comparisons between groups were conducted using one-way ANOVA. Data are expressed as means ± SEM. n = 7–11 per group. * p < 0.05, ** p < 0.01, *** p < 0.001.
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    NMDAR was involved in TCF7L2-mediated depressive-like behavior. ( A ) Experimental timeline for NMDAR agonist-NMDA administration and behavioral tests. ( B ) Effects of NMDA administration on latency to the first immobility in the TST with LHb neurons special TCF7L2 knockdown, mean of AAV-sh-scrambled + Saline: 106, mean of AAV-sh-scrambled + NMDA: 111.9, mean of AAV-sh-TCF7L2 + Saline: 111.1, mean of AAV-sh-TCF7L2 + NMDA: 108.8. ( C ) Total immobility time in the TST, mean of AAV-sh-scrambled + Saline: 57.75, mean of AAV-sh-scrambled + NMDA: 52.45, mean of AAV-sh-TCF7L2 + Saline: 8.143, mean of AAV-sh-TCF7L2 + NMDA: 62.63. ( D ) Effects of NMDA administration on latency to the first floating in the FST, mean of AAV-sh-scrambled + Saline: 72.36, mean of AAV-sh-scrambled + NMDA: 95.45, mean of AAV-sh-TCF7L2 + Saline: 110.9, mean of AAV-sh-TCF7L2 + NMDA: 102.6. ( E ) Total floating time in the FST, mean of AAV-sh-scrambled + Saline: 106.1, mean of AAV-sh-scrambled + NMDA: 120.7, mean of AAV-sh-TCF7L2 + Saline: 45, mean of AAV-sh-TCF7L2 + NMDA: 134.7. ( F ) Experimental timeline for NMDAR antagonist-memantine administration and behavioral tests. ( G ) Effects of memantine administration on latency to the first immobility in the TST with LHb neurons special TCF7L2 overexpression, mean of AAV-EGFP + Saline: 85.25, mean of AAV-EGFP + Memantine: 88.25, mean of AAV-TCF7L2 + Saline: 50.75, mean of AAV-TCF7L2 + Memantine: 80.05. ( H ) Total immobility time in the TST, mean of AAV-EGFP + Saline: 79.75, mean of AAV-EGFP + Memantine: 75.38, mean of AAV-TCF7L2 + Saline: 131.5, mean of AAV-TCF7L2 + Memantine: 72.38. ( I ) Effects of memantine administration on latency to the first floating in the FST, mean of AAV-EGFP + Saline: 91.5, mean of AAV-EGFP + Memantine: 100.8, mean of AAV-TCF7L2 + Saline: 35, mean of AAV-TCF7L2 + Memantine: 82.5. ( J ) Total floating time in the FST, mean of AAV-EGFP + Saline: 32.25, mean of AAV-EGFP + Memantine: 44.63, mean of AAV-TCF7L2 + Saline: 157.5, mean of AAV-TCF7L2 + Memantine: 77.88. Comparisons between groups were conducted using one-way ANOVA. Data are expressed as means ± SEM. n = 7–11 per group. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: International Journal of Molecular Sciences

    Article Title: Neuronal TCF7L2 in Lateral Habenula Is Involved in Stress-Induced Depression

    doi: 10.3390/ijms252212404

    Figure Lengend Snippet: NMDAR was involved in TCF7L2-mediated depressive-like behavior. ( A ) Experimental timeline for NMDAR agonist-NMDA administration and behavioral tests. ( B ) Effects of NMDA administration on latency to the first immobility in the TST with LHb neurons special TCF7L2 knockdown, mean of AAV-sh-scrambled + Saline: 106, mean of AAV-sh-scrambled + NMDA: 111.9, mean of AAV-sh-TCF7L2 + Saline: 111.1, mean of AAV-sh-TCF7L2 + NMDA: 108.8. ( C ) Total immobility time in the TST, mean of AAV-sh-scrambled + Saline: 57.75, mean of AAV-sh-scrambled + NMDA: 52.45, mean of AAV-sh-TCF7L2 + Saline: 8.143, mean of AAV-sh-TCF7L2 + NMDA: 62.63. ( D ) Effects of NMDA administration on latency to the first floating in the FST, mean of AAV-sh-scrambled + Saline: 72.36, mean of AAV-sh-scrambled + NMDA: 95.45, mean of AAV-sh-TCF7L2 + Saline: 110.9, mean of AAV-sh-TCF7L2 + NMDA: 102.6. ( E ) Total floating time in the FST, mean of AAV-sh-scrambled + Saline: 106.1, mean of AAV-sh-scrambled + NMDA: 120.7, mean of AAV-sh-TCF7L2 + Saline: 45, mean of AAV-sh-TCF7L2 + NMDA: 134.7. ( F ) Experimental timeline for NMDAR antagonist-memantine administration and behavioral tests. ( G ) Effects of memantine administration on latency to the first immobility in the TST with LHb neurons special TCF7L2 overexpression, mean of AAV-EGFP + Saline: 85.25, mean of AAV-EGFP + Memantine: 88.25, mean of AAV-TCF7L2 + Saline: 50.75, mean of AAV-TCF7L2 + Memantine: 80.05. ( H ) Total immobility time in the TST, mean of AAV-EGFP + Saline: 79.75, mean of AAV-EGFP + Memantine: 75.38, mean of AAV-TCF7L2 + Saline: 131.5, mean of AAV-TCF7L2 + Memantine: 72.38. ( I ) Effects of memantine administration on latency to the first floating in the FST, mean of AAV-EGFP + Saline: 91.5, mean of AAV-EGFP + Memantine: 100.8, mean of AAV-TCF7L2 + Saline: 35, mean of AAV-TCF7L2 + Memantine: 82.5. ( J ) Total floating time in the FST, mean of AAV-EGFP + Saline: 32.25, mean of AAV-EGFP + Memantine: 44.63, mean of AAV-TCF7L2 + Saline: 157.5, mean of AAV-TCF7L2 + Memantine: 77.88. Comparisons between groups were conducted using one-way ANOVA. Data are expressed as means ± SEM. n = 7–11 per group. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: The mice in these groups received intraperitoneal injections of the NMDAR agonist NMDA (75 mg/kg, MCE, HY-17551), or the NMDAR antagonist memantine (15 mg/kg, MCE, HY-B0365A), or saline as a solvent.

    Techniques: Knockdown, Saline, Over Expression

    Neither Aβ nor memantine caused significant changes in different NMDAR subunits expression. (A) Representative western-blots of DIV14 neuronal cultures showing the effect of 24 h of 25 μM Aβ 25–35 and 1 μM memantine on GluN1 and GluN2B. (B) The panels show the average band intensity of GluN1 (left histogram) and GluN2B (right histogram). Results were normalized to the loading control, GAPDH. Values are mean ± SEM.

    Journal: Frontiers in Pharmacology

    Article Title: Inhibition of NMDA Receptors Prevents the Loss of BDNF Function Induced by Amyloid β

    doi: 10.3389/fphar.2018.00237

    Figure Lengend Snippet: Neither Aβ nor memantine caused significant changes in different NMDAR subunits expression. (A) Representative western-blots of DIV14 neuronal cultures showing the effect of 24 h of 25 μM Aβ 25–35 and 1 μM memantine on GluN1 and GluN2B. (B) The panels show the average band intensity of GluN1 (left histogram) and GluN2B (right histogram). Results were normalized to the loading control, GAPDH. Values are mean ± SEM.

    Article Snippet: In these experiments, cells were also co-incubated with Aβ 25–35 and 1 μM memantine, a NMDAR antagonist (Sigma-Aldrich).

    Techniques: Expressing, Western Blot

    Brain-derived neurotrophic factor (BDNF) restores its capacity to increase spine density after inhibition of Aβ-induced NMDAR activation. (A) Representative image of an untreated neuron obtained from primary cultures. DIV14 neurons were incubated with BDNF (20 ng/mL) for 24 h, in the presence or absence of Aβ 25–35 (25 μM) and/or memantine (1 μM) or calpastatin (1 μM). MAP2 (red) specifically detects neurons, while phalloidin (green), recognizes F-actin, thus labeling protrusions (filopodia and spines). The merge of both elements is represented in yellow. Six neurons were analyzed per condition and spine density was considered, in each cell, as the number of protrusions per 10 μm of the parent dendrite with a distance of 25 μm from the cell body. Protrusions were counted in each neuron in three different dendrites. (B) Treatments effects on synaptic growth. Aβ significantly reduces the number of protrusions, whereas BDNF increases the number of protrusions when incubated alone. In the presence of Aβ, BDNF loses its ability to increase the number of protrusions, which is rescued when cells are incubated with memantine. (C) The panels show the average number of protrusions in different conditions when neurons were treated with memantine and (D) calpastatin ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, n = 6–14, three-way ANOVA with Tukey post hoc test). Values are mean ± SEM.

    Journal: Frontiers in Pharmacology

    Article Title: Inhibition of NMDA Receptors Prevents the Loss of BDNF Function Induced by Amyloid β

    doi: 10.3389/fphar.2018.00237

    Figure Lengend Snippet: Brain-derived neurotrophic factor (BDNF) restores its capacity to increase spine density after inhibition of Aβ-induced NMDAR activation. (A) Representative image of an untreated neuron obtained from primary cultures. DIV14 neurons were incubated with BDNF (20 ng/mL) for 24 h, in the presence or absence of Aβ 25–35 (25 μM) and/or memantine (1 μM) or calpastatin (1 μM). MAP2 (red) specifically detects neurons, while phalloidin (green), recognizes F-actin, thus labeling protrusions (filopodia and spines). The merge of both elements is represented in yellow. Six neurons were analyzed per condition and spine density was considered, in each cell, as the number of protrusions per 10 μm of the parent dendrite with a distance of 25 μm from the cell body. Protrusions were counted in each neuron in three different dendrites. (B) Treatments effects on synaptic growth. Aβ significantly reduces the number of protrusions, whereas BDNF increases the number of protrusions when incubated alone. In the presence of Aβ, BDNF loses its ability to increase the number of protrusions, which is rescued when cells are incubated with memantine. (C) The panels show the average number of protrusions in different conditions when neurons were treated with memantine and (D) calpastatin ( ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, n = 6–14, three-way ANOVA with Tukey post hoc test). Values are mean ± SEM.

    Article Snippet: In these experiments, cells were also co-incubated with Aβ 25–35 and 1 μM memantine, a NMDAR antagonist (Sigma-Aldrich).

    Techniques: Derivative Assay, Inhibition, Activation Assay, Incubation, Labeling

    The inhibition of eNMDAR reduces the cleavage of TrkB-FL by modulating calpains activation. (A) TrkB-FL protein levels. Representative western-blots of DIV14 neuronal cultures showing the effect of 24 h of 25 μM Aβ 25–35 and 1 μM memantine on TrkB-FL (∼145 kDa). The panel shows the average band intensity of TrkB-FL ( ∗∗ p < 0.01, n = 9–22, two-way ANOVA with Tukey post hoc test). (B) TrkB-ICD protein levels. Representative western-blots of DIV14 neuronal cultures showing the effect of 24 h of 25 μM Aβ 25–35 and 1 μM memantine on TrkB-ICD (∼32 kDa). The panel shows the average band intensity of TrkB-ICD ( ∗∗ p < 0.01, ∗∗∗ p < 0.001, n = 10–20, two-way ANOVA with Tukey post hoc test) and (C) Calpains activation. Representative western-blots of DIV14 neuronal cultures showing the effect of 24 h of 25 μM Aβ 25–35 and 1 μM memantine on SBDP (150 kDa). The panel shows the average ratio of the SBDP (150) to intact spectrin ( ∗∗ p < 0.01, ∗∗∗ p < 0.001, n = 7–20, two-way ANOVA with Tukey post hoc test). Results were normalized to the loading control, GAPDH. Values are mean ± SEM.

    Journal: Frontiers in Pharmacology

    Article Title: Inhibition of NMDA Receptors Prevents the Loss of BDNF Function Induced by Amyloid β

    doi: 10.3389/fphar.2018.00237

    Figure Lengend Snippet: The inhibition of eNMDAR reduces the cleavage of TrkB-FL by modulating calpains activation. (A) TrkB-FL protein levels. Representative western-blots of DIV14 neuronal cultures showing the effect of 24 h of 25 μM Aβ 25–35 and 1 μM memantine on TrkB-FL (∼145 kDa). The panel shows the average band intensity of TrkB-FL ( ∗∗ p < 0.01, n = 9–22, two-way ANOVA with Tukey post hoc test). (B) TrkB-ICD protein levels. Representative western-blots of DIV14 neuronal cultures showing the effect of 24 h of 25 μM Aβ 25–35 and 1 μM memantine on TrkB-ICD (∼32 kDa). The panel shows the average band intensity of TrkB-ICD ( ∗∗ p < 0.01, ∗∗∗ p < 0.001, n = 10–20, two-way ANOVA with Tukey post hoc test) and (C) Calpains activation. Representative western-blots of DIV14 neuronal cultures showing the effect of 24 h of 25 μM Aβ 25–35 and 1 μM memantine on SBDP (150 kDa). The panel shows the average ratio of the SBDP (150) to intact spectrin ( ∗∗ p < 0.01, ∗∗∗ p < 0.001, n = 7–20, two-way ANOVA with Tukey post hoc test). Results were normalized to the loading control, GAPDH. Values are mean ± SEM.

    Article Snippet: In these experiments, cells were also co-incubated with Aβ 25–35 and 1 μM memantine, a NMDAR antagonist (Sigma-Aldrich).

    Techniques: Inhibition, Activation Assay, Western Blot