Review

glun2b antagonist ro 25 6981 (Tocris)

Tocris is a verified supplier

Tocris manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Tocris glun2b antagonist ro 25 6981
Glun2b Antagonist Ro 25 6981, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 198 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/glun2b+antagonist+ro+25+6981/pm41076009-45-2-9?v=Tocris
Average 93 stars, based on 198 article reviews

glun2b antagonist ro 25 6981 - by Bioz Stars, 2026-08

93/100 stars

Images

Image Search Results

Fig. 5. The pro-survival effect of GluN2B and its transcriptional upregulation by THSG following OGD/R. (A) The relative mRNA levels of GluN2A and GluN2B in neurons after OGD/R by real-time PCR (n = 3, from independent experiments). (B) Cell viability in different concentrations of PEAQX and Ro 25–6981 by CCK-8 (n = 3, from independent experiments). (C) Effect of PEAQX (0.27 μM) and Ro 25–6981(0.9 nM) on autophagic flux and the number of autophagosomes (yellow column) and autolysosomes in neurons (red column), Bar: 40 μm (n = 3). (D) The relative mRNA levels of GluN2B after THSG treatment. The cells were treated with 1 μM THSG. Statistical comparisons were performed with one-way ANOVA. ###p < 0.001 vs. control group. *p < 0.05, ***p < 0.001 vs. model group. Data are shown as the mean ± SEM.

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: THSG alleviates cerebral ischemia/reperfusion injury via the GluN2B-CaMKII-ERK1/2 pathway.

doi: 10.1016/j.phymed.2024.155595

Figure Lengend Snippet: Fig. 5. The pro-survival effect of GluN2B and its transcriptional upregulation by THSG following OGD/R. (A) The relative mRNA levels of GluN2A and GluN2B in neurons after OGD/R by real-time PCR (n = 3, from independent experiments). (B) Cell viability in different concentrations of PEAQX and Ro 25–6981 by CCK-8 (n = 3, from independent experiments). (C) Effect of PEAQX (0.27 μM) and Ro 25–6981(0.9 nM) on autophagic flux and the number of autophagosomes (yellow column) and autolysosomes in neurons (red column), Bar: 40 μm (n = 3). (D) The relative mRNA levels of GluN2B after THSG treatment. The cells were treated with 1 μM THSG. Statistical comparisons were performed with one-way ANOVA. ###p < 0.001 vs. control group. *p < 0.05, ***p < 0.001 vs. model group. Data are shown as the mean ± SEM.

Article Snippet: At the onset of reperfusion, the rats were administered THSG (10, 20, and 40 mg/kg; Topscience, T4956; purity: 98 % determined by highperformance liquid chromatography; chemical structure displayed in Fig. 1B) and the GluN2B antagonist Ro 25–6981 (10 mg/kg; Topscience, T12758) via intraperitoneal injection, and salvianic acid A sodium (SAS) (30 mg/kg, Selleck, S2401; purity: 98 % determined by highperformance liquid chromatography) intravenously.

Techniques: Real-time Polymerase Chain Reaction, CCK-8 Assay, Control

Fig. 6. Upregulation of GluN2B protein by THSG and the reversion of Ro 25–6981. (A-B) Expression of GluN2B in penumbra or in primary neurons after CI/R by WB and the Semi-quantitation (n = 3). (C) Representative TTC-stained brain slices and brain infarct volumes of each group shown in bar graph (n = 6). (D) neurological deficit scores of each group shown in bar graph (n = 6). (E) HE and Nissl staining showing neuron injury in rats after CI/R (blue arrows indicate nuclear pyknosis, green arrows indicate neuronal edema and black arrows indicate Nissl bodies). Bar: 2000 μm (upper panels), 80 μm, (lower panels). (F) Expression of Bcl-2, Bax, Caspase-3 in penumbra by WB and the semi-quantitation (n = 3). (G) Cell viability by CCK8 (n = 3). (H) Expression of Bcl-2, Bax, Caspase-3 in neurons after OGD/R by WB and the semi-quantitation (n = 3). The rats were treated with 10 mg/kg Ro 25–6981 in C-F and the cells were administrated with 1 μM THSG and 0.9 nM Ro 25–6981 in B, G-H. Statistical comparisons were performed with one-way ANOVA. ##p < 0.01, ###p < 0.001 vs. control group. *p < 0.05, **p < 0.01, ***p < 0.001 vs. model group. &p < 0.05, &&p < 0.01, &&&p < 0.001 vs. THSG group. Data are shown as the mean ± SEM.

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: THSG alleviates cerebral ischemia/reperfusion injury via the GluN2B-CaMKII-ERK1/2 pathway.

doi: 10.1016/j.phymed.2024.155595

Figure Lengend Snippet: Fig. 6. Upregulation of GluN2B protein by THSG and the reversion of Ro 25–6981. (A-B) Expression of GluN2B in penumbra or in primary neurons after CI/R by WB and the Semi-quantitation (n = 3). (C) Representative TTC-stained brain slices and brain infarct volumes of each group shown in bar graph (n = 6). (D) neurological deficit scores of each group shown in bar graph (n = 6). (E) HE and Nissl staining showing neuron injury in rats after CI/R (blue arrows indicate nuclear pyknosis, green arrows indicate neuronal edema and black arrows indicate Nissl bodies). Bar: 2000 μm (upper panels), 80 μm, (lower panels). (F) Expression of Bcl-2, Bax, Caspase-3 in penumbra by WB and the semi-quantitation (n = 3). (G) Cell viability by CCK8 (n = 3). (H) Expression of Bcl-2, Bax, Caspase-3 in neurons after OGD/R by WB and the semi-quantitation (n = 3). The rats were treated with 10 mg/kg Ro 25–6981 in C-F and the cells were administrated with 1 μM THSG and 0.9 nM Ro 25–6981 in B, G-H. Statistical comparisons were performed with one-way ANOVA. ##p < 0.01, ###p < 0.001 vs. control group. *p < 0.05, **p < 0.01, ***p < 0.001 vs. model group. &p < 0.05, &&p < 0.01, &&&p < 0.001 vs. THSG group. Data are shown as the mean ± SEM.

Techniques: Expressing, Quantitation Assay, Staining, Control

Fig. 7. The activation of PINK1/PARK2 pathway by THSG treatment and the reversion of Ro 25–6981. (A) PARK2 level in neurons of penumbra by IF. Bar: 100 μm. (B) Expression of PINK1, PARK2 in penumbra by WB and the semi-quantitation (n = 3). (C) The colocalization of PARK2 with mitochondria in neurons after OGD/R. Bar: 10 μm. (D) Expression of PINK1, PARK2 in neurons after OGD/R by WB and the semi-quantitation (n = 3). The rats were treated with 10 mg/kg Ro 25–6981 in A-B and the cells were administrated with 1 μM THSG and 0.9 nM Ro 25–6981 in C-D. Statistical comparisons were performed with one-way ANOVA. #p < 0.05, ###p < 0.001 vs. control group. *p < 0.05, **p < 0.01, ***p < 0.001 vs. model group. &&p < 0.01, &&&p < 0.001 vs. THSG group. Data are shown as the mean ± SEM.

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: THSG alleviates cerebral ischemia/reperfusion injury via the GluN2B-CaMKII-ERK1/2 pathway.

doi: 10.1016/j.phymed.2024.155595

Figure Lengend Snippet: Fig. 7. The activation of PINK1/PARK2 pathway by THSG treatment and the reversion of Ro 25–6981. (A) PARK2 level in neurons of penumbra by IF. Bar: 100 μm. (B) Expression of PINK1, PARK2 in penumbra by WB and the semi-quantitation (n = 3). (C) The colocalization of PARK2 with mitochondria in neurons after OGD/R. Bar: 10 μm. (D) Expression of PINK1, PARK2 in neurons after OGD/R by WB and the semi-quantitation (n = 3). The rats were treated with 10 mg/kg Ro 25–6981 in A-B and the cells were administrated with 1 μM THSG and 0.9 nM Ro 25–6981 in C-D. Statistical comparisons were performed with one-way ANOVA. #p < 0.05, ###p < 0.001 vs. control group. *p < 0.05, **p < 0.01, ***p < 0.001 vs. model group. &&p < 0.01, &&&p < 0.001 vs. THSG group. Data are shown as the mean ± SEM.

Techniques: Activation Assay, Expressing, Quantitation Assay, Control

Fig. 9. The upregulation of CaMKII and ERK1/2 phosphorylation by THSG and the reversion of Ro 25–6981. (A) Expression of ERK1/2, P-ERK1/2, CaMKII and P- CaMKII in penumbra by WB and the semi-quantitation (n = 3). (B) P-ERK1/2 level in neurons after OGD/R by IF, Bar: 20 μm. (C) Expression of ERK1/2, P-ERK1/2, CaMKII and P-CaMKII in neurons after OGD/R by WB and the semi-quantitation (n = 3). The rats were treated with 10 mg/kg Ro 25–6981 in A, and the cells were administrated with 1 μM THSG and 0.9 nM Ro 25–6981 in B-C. Statistical comparisons were performed with one-way ANOVA. ###p < 0.001 vs. control group. *p < 0.05, ***p < 0.001 vs. model group. &p < 0.05, &&p < 0.01, &&&p < 0.001 vs. THSG group. Data are shown as the mean ± SEM.

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: THSG alleviates cerebral ischemia/reperfusion injury via the GluN2B-CaMKII-ERK1/2 pathway.

doi: 10.1016/j.phymed.2024.155595

Figure Lengend Snippet: Fig. 9. The upregulation of CaMKII and ERK1/2 phosphorylation by THSG and the reversion of Ro 25–6981. (A) Expression of ERK1/2, P-ERK1/2, CaMKII and P- CaMKII in penumbra by WB and the semi-quantitation (n = 3). (B) P-ERK1/2 level in neurons after OGD/R by IF, Bar: 20 μm. (C) Expression of ERK1/2, P-ERK1/2, CaMKII and P-CaMKII in neurons after OGD/R by WB and the semi-quantitation (n = 3). The rats were treated with 10 mg/kg Ro 25–6981 in A, and the cells were administrated with 1 μM THSG and 0.9 nM Ro 25–6981 in B-C. Statistical comparisons were performed with one-way ANOVA. ###p < 0.001 vs. control group. *p < 0.05, ***p < 0.001 vs. model group. &p < 0.05, &&p < 0.01, &&&p < 0.001 vs. THSG group. Data are shown as the mean ± SEM.

Techniques: Phospho-proteomics, Expressing, Quantitation Assay, Control

Fig. 11. The neuroprotective effect of THSG against CI/R injury and the underlying mechanisms. THSG promotes the expression of GluN2B, induces the phos phorylation of CaMKII and ERK1/2, enhances the PINK1/PARK2-mediated mitophagy and suppresses the apoptosis of neurons in CI/R injury.

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: THSG alleviates cerebral ischemia/reperfusion injury via the GluN2B-CaMKII-ERK1/2 pathway.

doi: 10.1016/j.phymed.2024.155595

Figure Lengend Snippet: Fig. 11. The neuroprotective effect of THSG against CI/R injury and the underlying mechanisms. THSG promotes the expression of GluN2B, induces the phos phorylation of CaMKII and ERK1/2, enhances the PINK1/PARK2-mediated mitophagy and suppresses the apoptosis of neurons in CI/R injury.

Techniques: Expressing

Fig. 10. Molecular docking analysis of the interaction between THSG and GluN2B. (A) Structure of GluN2B protein from PDB(ID-4PE5). (B) Predicted binding energy and binding values. (C) Docking complex of GluN2B protein with THSG.

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: THSG alleviates cerebral ischemia/reperfusion injury via the GluN2B-CaMKII-ERK1/2 pathway.

doi: 10.1016/j.phymed.2024.155595

Figure Lengend Snippet: Fig. 10. Molecular docking analysis of the interaction between THSG and GluN2B. (A) Structure of GluN2B protein from PDB(ID-4PE5). (B) Predicted binding energy and binding values. (C) Docking complex of GluN2B protein with THSG.

Techniques: Binding Assay

Repeated ethanol (EtOH) selectively enhanced GluN2B-NMDAR phosphorylation in the DMS in WT, but not AC1KO (KO) mice or mice pretreated with NB001 ( n = 3–5/group). Averaged data (left) and representative immunoblots compiled from groups of images from different parts of the same gel (right) are depicted for DMS (A), DLS (B), or NAc (C) lysates prepared following repeated saline (sal) or EtOH treatment and probed for total and pTyr-1472-GluN2B. (A) A significant increase in pGluN2B levels in the DMS of WT mice was observed following repeated EtOH treatment relative to saline-treated controls, which was absent in AC1KO and NB001 pretreated mice. (B) Repeated ethanol treatment decreased levels of pGluN2B in the DLS equivalently across WT, AC1KO, and NB001-treated mice. (C) No changes in pGluN2B levels in the NAc were observed in response to ethanol or absence of AC1 signaling. Total GluN2B levels were unaffected by AC1 status or ethanol treatment in all three regions. Significance determined by two-way ANOVA and Sidak’s post hoc test, * P < 0.05, compared with saline-treated controls; # P < 0.05, compared with WT EtOH.

Journal: The Journal of Pharmacology and Experimental Therapeutics

Article Title: Adenylyl Cyclase 1 Is Required for Ethanol-Induced Locomotor Sensitization and Associated Increases in NMDA Receptor Phosphorylation and Function in the Dorsal Medial Striatum

doi: 10.1124/jpet.117.242321

Figure Lengend Snippet: Repeated ethanol (EtOH) selectively enhanced GluN2B-NMDAR phosphorylation in the DMS in WT, but not AC1KO (KO) mice or mice pretreated with NB001 ( n = 3–5/group). Averaged data (left) and representative immunoblots compiled from groups of images from different parts of the same gel (right) are depicted for DMS (A), DLS (B), or NAc (C) lysates prepared following repeated saline (sal) or EtOH treatment and probed for total and pTyr-1472-GluN2B. (A) A significant increase in pGluN2B levels in the DMS of WT mice was observed following repeated EtOH treatment relative to saline-treated controls, which was absent in AC1KO and NB001 pretreated mice. (B) Repeated ethanol treatment decreased levels of pGluN2B in the DLS equivalently across WT, AC1KO, and NB001-treated mice. (C) No changes in pGluN2B levels in the NAc were observed in response to ethanol or absence of AC1 signaling. Total GluN2B levels were unaffected by AC1 status or ethanol treatment in all three regions. Significance determined by two-way ANOVA and Sidak’s post hoc test, * P < 0.05, compared with saline-treated controls; # P < 0.05, compared with WT EtOH.

Article Snippet: The contribution of GluN2B-containing NMDARs to the total NMDAR-mediated eEPSC in WT mice was determined using the GluN2B antagonist Ro 25-6981 (0.5 μ M, 1594; Tocris, Bristol, United Kingdom).

Techniques: Phospho-proteomics, Western Blot, Saline

Ethanol (EtOH) upregulation of NMDAR-mediated transmission is absent in AC1KO (KO) mice. (A) Representative traces of NMDAR-mediated eEPSCs and (B) average NMDAR-mediated eEPSC amplitude (± S.E.M.) in WT and AC1KO mice repeatedly treated with saline (sal) or EtOH. EtOH produced an increase in NMDAR-mediated eEPSC amplitude only in WT mice (two-way ANOVA and Sidak’s post hoc test, ** P < 0.01). (C) Average NMDAR-mediated eEPSC amplitude before (BL) and after (+Ro) bath application of the GluN2B selective antagonist Ro 25-6981 (0.5 µ M) in WT mice. EtOH-induced upregulation of NMDAR-mediated transmission involved an increased contribution of GluN2B-containing NMDARs (two-way RM ANOVA and Sidak’s post hoc test, * P < 0.05). (D) Average central location of medium spiny neuron recordings was 1.10 mm from bregma (± 0.5 mm).

Journal: The Journal of Pharmacology and Experimental Therapeutics

Article Title: Adenylyl Cyclase 1 Is Required for Ethanol-Induced Locomotor Sensitization and Associated Increases in NMDA Receptor Phosphorylation and Function in the Dorsal Medial Striatum

doi: 10.1124/jpet.117.242321

Figure Lengend Snippet: Ethanol (EtOH) upregulation of NMDAR-mediated transmission is absent in AC1KO (KO) mice. (A) Representative traces of NMDAR-mediated eEPSCs and (B) average NMDAR-mediated eEPSC amplitude (± S.E.M.) in WT and AC1KO mice repeatedly treated with saline (sal) or EtOH. EtOH produced an increase in NMDAR-mediated eEPSC amplitude only in WT mice (two-way ANOVA and Sidak’s post hoc test, ** P < 0.01). (C) Average NMDAR-mediated eEPSC amplitude before (BL) and after (+Ro) bath application of the GluN2B selective antagonist Ro 25-6981 (0.5 µ M) in WT mice. EtOH-induced upregulation of NMDAR-mediated transmission involved an increased contribution of GluN2B-containing NMDARs (two-way RM ANOVA and Sidak’s post hoc test, * P < 0.05). (D) Average central location of medium spiny neuron recordings was 1.10 mm from bregma (± 0.5 mm).

Techniques: Transmission Assay, Saline, Produced

The effects of enhanced GluN2B expression in the frontal lobe on the performance of aged mice in memory tasks in the Morris water maze. Graphs A–F show the effects of the GluN2B vector or 2 control (control vector or vehicle) treatments on learning performance. In graphs A–D and F, lower proximity scores represent better performance. In graph E, greater differences between naïve and delayed trials represent better performance. The performance of young vehicle-treated mice is included for comparison. (A) Performance across blocks of four place trials for the two-day long-term spatial memory task. (B) Performance averaged across place trials for each individual day of the two-day long-term spatial memory task. (C) Performance within probe trials of the two-day long-term spatial memory task. (D) Performance across blocks of two reversal trials for the flexibility task. (E) Differences in performance between Tnaïve and Tdelay trials, averaged over delayed short-term spatial memory sessions, over eight days. (F) Performance in 6 cued trials for the associative memory task. * p≤0.05 for differences from aged GluN2B vector-treated mice and # p≤0.05 for differences from young vehicle-treated mice as determined by repeated measures and two-way ANOVA, followed by Fisher’s protected least significant difference post-hoc analysis. N=12–14. Bl = block of 4 place trials, Pr = probe trials, Pr0= naïve probe trials, R= reversal trials, C= cued trials. Error bars = standard error of the mean (SEM).

Journal: Behavioural brain research

Article Title: Memory in aged mice is rescued by enhanced expression of the GluN2B subunit of the NMDA receptor

doi: 10.1016/j.bbr.2012.10.026

Figure Lengend Snippet: The effects of enhanced GluN2B expression in the frontal lobe on the performance of aged mice in memory tasks in the Morris water maze. Graphs A–F show the effects of the GluN2B vector or 2 control (control vector or vehicle) treatments on learning performance. In graphs A–D and F, lower proximity scores represent better performance. In graph E, greater differences between naïve and delayed trials represent better performance. The performance of young vehicle-treated mice is included for comparison. (A) Performance across blocks of four place trials for the two-day long-term spatial memory task. (B) Performance averaged across place trials for each individual day of the two-day long-term spatial memory task. (C) Performance within probe trials of the two-day long-term spatial memory task. (D) Performance across blocks of two reversal trials for the flexibility task. (E) Differences in performance between Tnaïve and Tdelay trials, averaged over delayed short-term spatial memory sessions, over eight days. (F) Performance in 6 cued trials for the associative memory task. * p≤0.05 for differences from aged GluN2B vector-treated mice and # p≤0.05 for differences from young vehicle-treated mice as determined by repeated measures and two-way ANOVA, followed by Fisher’s protected least significant difference post-hoc analysis. N=12–14. Bl = block of 4 place trials, Pr = probe trials, Pr0= naïve probe trials, R= reversal trials, C= cued trials. Error bars = standard error of the mean (SEM).

Article Snippet: 2.1.2 GluN2B Antagonist The GluN2B antagonist, Ro 25-6981 (Sigma Aldrich, St. Louis, MO, USA), was diluted in 100% Dimethyl sulfoxide (DMSO) (Sigma Aldrich, St. Louis, MO, USA) to a final concentration of 5 or 10 mg/mL, as previously published [ 58 ].

Techniques: Expressing, Plasmid Preparation, Blocking Assay

The effects of the GluN2B antagonist, Ro 25-6981, on the performance of aged mice with enhanced GluN2B expression in two memory tasks in the Morris water maze. Graphs A–C show the effects of Ro 25-6981 antagonism on the performance of aged mice receiving frontal lobe injections of GluN2B vector or vehicle, with lower proximity scores representing better performance. (A) Learning performance of aged mice across blocks of place trials for the two-day long-term spatial memory task. (B) Learning performance of aged mice averaged across place trials for day 2 of the two-day long-term spatial memory task. (C) Performance of aged mice in 6 cued trials for the associative memory task. * p≤0.05 for differences in performance between treatment groups indicated as determined by repeated measures and two-way ANOVA, followed by Fisher’s protected least significant difference post-hoc analysis. N=4–16. Bl = blocks of 4 place trials, C= cued trials. Error bars = standard error of the mean (SEM).

Journal: Behavioural brain research

Article Title: Memory in aged mice is rescued by enhanced expression of the GluN2B subunit of the NMDA receptor

doi: 10.1016/j.bbr.2012.10.026

Figure Lengend Snippet: The effects of the GluN2B antagonist, Ro 25-6981, on the performance of aged mice with enhanced GluN2B expression in two memory tasks in the Morris water maze. Graphs A–C show the effects of Ro 25-6981 antagonism on the performance of aged mice receiving frontal lobe injections of GluN2B vector or vehicle, with lower proximity scores representing better performance. (A) Learning performance of aged mice across blocks of place trials for the two-day long-term spatial memory task. (B) Learning performance of aged mice averaged across place trials for day 2 of the two-day long-term spatial memory task. (C) Performance of aged mice in 6 cued trials for the associative memory task. * p≤0.05 for differences in performance between treatment groups indicated as determined by repeated measures and two-way ANOVA, followed by Fisher’s protected least significant difference post-hoc analysis. N=4–16. Bl = blocks of 4 place trials, C= cued trials. Error bars = standard error of the mean (SEM).

Techniques: Expressing, Plasmid Preparation

The effects of enhanced GluN2B expression in the hippocampus on the performance of aged mice in memory tasks in the Morris water maze. Graphs A–E show the effects of the GluN2B vector or 2 control (control vector or vehicle) treatments on learning performance. In graphs A–E, lower proximity scores represent better performance. (A) Performance within blocks of four place trials for the three-day long-term spatial memory task. (B) Performance averaged across place trials for individual days for the three-day long-term spatial memory task. (C) Performance within probe trials of the three-day long-term spatial memory task. (D) Performance across blocks of two reversal trials for the flexibility task. (E) Performance in 6 cued trials for the associative memory task. * p≤0.05 for differences from aged GluN2B vector-treated mice and # p≤0.05 for differences from young vehicle-treated mice as determined by repeated measures and two-way ANOVA followed by Fisher’s protected least significant difference post-hoc analysis. N=7–15. Bl = blocks of 4 place trials or 2 reversal trials, Pr = probe trials, Pr0= naïve probe trials, C= cued trials. Error bars = standard error of the mean (SEM).

Journal: Behavioural brain research

Article Title: Memory in aged mice is rescued by enhanced expression of the GluN2B subunit of the NMDA receptor

doi: 10.1016/j.bbr.2012.10.026

Figure Lengend Snippet: The effects of enhanced GluN2B expression in the hippocampus on the performance of aged mice in memory tasks in the Morris water maze. Graphs A–E show the effects of the GluN2B vector or 2 control (control vector or vehicle) treatments on learning performance. In graphs A–E, lower proximity scores represent better performance. (A) Performance within blocks of four place trials for the three-day long-term spatial memory task. (B) Performance averaged across place trials for individual days for the three-day long-term spatial memory task. (C) Performance within probe trials of the three-day long-term spatial memory task. (D) Performance across blocks of two reversal trials for the flexibility task. (E) Performance in 6 cued trials for the associative memory task. * p≤0.05 for differences from aged GluN2B vector-treated mice and # p≤0.05 for differences from young vehicle-treated mice as determined by repeated measures and two-way ANOVA followed by Fisher’s protected least significant difference post-hoc analysis. N=7–15. Bl = blocks of 4 place trials or 2 reversal trials, Pr = probe trials, Pr0= naïve probe trials, C= cued trials. Error bars = standard error of the mean (SEM).

Techniques: Expressing, Plasmid Preparation

The effects of enhanced GluN2B subunit expression in the hippocampus of aged mice on the NMDA receptor-mediated EPSP responses in hippocampal slices. (A) Input-output curves for the mean NMDA receptor-mediated EPSP amplitude versus stimulus intensity. GluN2B vector treated slices exhibited significant increase in NMDA receptor-mediated EPSP for higher stimulus intensities compared to 2 control (control vector or vehicle) treatments. (B) Percent change in NMDA receptor-mediated EPSP compared to baseline (dotted line) for the last 5 min following 60 min bath application of Ro 25-6981. *p≤0.05 for differences in responses from control vector and vehicle treatment groups determined by (A) Fisher’s protected least significant difference between GluN2B and controls for each intensity or §p≤0.05 for differences in response from baseline (B) one sample t-test. N=3–14. Error bars =standard error of the mean (SEM).

Journal: Behavioural brain research

Article Title: Memory in aged mice is rescued by enhanced expression of the GluN2B subunit of the NMDA receptor

doi: 10.1016/j.bbr.2012.10.026

Figure Lengend Snippet: The effects of enhanced GluN2B subunit expression in the hippocampus of aged mice on the NMDA receptor-mediated EPSP responses in hippocampal slices. (A) Input-output curves for the mean NMDA receptor-mediated EPSP amplitude versus stimulus intensity. GluN2B vector treated slices exhibited significant increase in NMDA receptor-mediated EPSP for higher stimulus intensities compared to 2 control (control vector or vehicle) treatments. (B) Percent change in NMDA receptor-mediated EPSP compared to baseline (dotted line) for the last 5 min following 60 min bath application of Ro 25-6981. *p≤0.05 for differences in responses from control vector and vehicle treatment groups determined by (A) Fisher’s protected least significant difference between GluN2B and controls for each intensity or §p≤0.05 for differences in response from baseline (B) one sample t-test. N=3–14. Error bars =standard error of the mean (SEM).

Techniques: Expressing, Plasmid Preparation

Enhanced GluN2B subunit expression in vivo in the frontal lobe. Representative images of coronal sections showing GluN2B subunit, GFP (vector reporter) and GFAP (glial marker) protein expression within the frontal lobe in different treatments: (A, D) vehicle, (B, E) control vector and (C, F) GluN2B vector within aged mice. Panels D–F are higher magnification images of areas shown in panels A–C, respectively. Green= GFP (in vivo), Red= GluN2B subunit, Blue= GFAP, Yellow= lipofuscin, co-localized GFP and GluN2B = orange, co-localized GFAP and GluN2B= purple, GluN2B subunit in neuronal-like cells (arrows), GluN2B subunit in astrocytes (arrowheads). Bar= 25 μm.

Journal: Behavioural brain research

Article Title: Memory in aged mice is rescued by enhanced expression of the GluN2B subunit of the NMDA receptor

doi: 10.1016/j.bbr.2012.10.026

Figure Lengend Snippet: Enhanced GluN2B subunit expression in vivo in the frontal lobe. Representative images of coronal sections showing GluN2B subunit, GFP (vector reporter) and GFAP (glial marker) protein expression within the frontal lobe in different treatments: (A, D) vehicle, (B, E) control vector and (C, F) GluN2B vector within aged mice. Panels D–F are higher magnification images of areas shown in panels A–C, respectively. Green= GFP (in vivo), Red= GluN2B subunit, Blue= GFAP, Yellow= lipofuscin, co-localized GFP and GluN2B = orange, co-localized GFAP and GluN2B= purple, GluN2B subunit in neuronal-like cells (arrows), GluN2B subunit in astrocytes (arrowheads). Bar= 25 μm.

Techniques: Expressing, In Vivo, Plasmid Preparation, Marker

Enhanced GluN2B subunit expression in vivo in the hippocampus. Representative images of coronal sections showing GluN2B subunit, GFP (vector reporter) and GFAP (glial marker) protein expression within the hippocampus in different treatments: (A, D, G) vehicle, (B, E, H) control vector and (C, F, I, J, K) GluN2B vector in aged mice. Panels D–K represent higher magnification images of areas shown in panels A–C, respectively. Green= GFP (in vivo), Red= GluN2B subunit, Blue= GFAP, Yellow= lipofuscin, co-localized GFP and GluN2B = orange, co-localized GFAP and GluN2B= purple, GluN2B subunit in neuronal-like cells (arrows), GluN2B subunit in astrocytes (arrowheads). I) CA1 stratum radiatum. J) CA1 stratum pyramidale. K) dentate gyrus molecular layer, upper blade. Bar= 25 μm.

Journal: Behavioural brain research

Article Title: Memory in aged mice is rescued by enhanced expression of the GluN2B subunit of the NMDA receptor

doi: 10.1016/j.bbr.2012.10.026

Figure Lengend Snippet: Enhanced GluN2B subunit expression in vivo in the hippocampus. Representative images of coronal sections showing GluN2B subunit, GFP (vector reporter) and GFAP (glial marker) protein expression within the hippocampus in different treatments: (A, D, G) vehicle, (B, E, H) control vector and (C, F, I, J, K) GluN2B vector in aged mice. Panels D–K represent higher magnification images of areas shown in panels A–C, respectively. Green= GFP (in vivo), Red= GluN2B subunit, Blue= GFAP, Yellow= lipofuscin, co-localized GFP and GluN2B = orange, co-localized GFAP and GluN2B= purple, GluN2B subunit in neuronal-like cells (arrows), GluN2B subunit in astrocytes (arrowheads). I) CA1 stratum radiatum. J) CA1 stratum pyramidale. K) dentate gyrus molecular layer, upper blade. Bar= 25 μm.

Techniques: Expressing, In Vivo, Plasmid Preparation, Marker

Enhanced GluN2B subunit expression in vivo in neurons. Representative image of a coronal section showing GluN2B subunit and neurofilament (neuronal marker) protein expression within the frontal lobe of an aged mouse treated with GluN2B vector. Panel A shows neurofilament only and Panel B shows GluN2B subunit only. Panel C shows GluN2B subunit with neurofilament. Red= GluN2B subunit, Green= neurofilament, co-localized neurofilament and GluN2B= orange, Bar= 5 μm.

Journal: Behavioural brain research

Article Title: Memory in aged mice is rescued by enhanced expression of the GluN2B subunit of the NMDA receptor

doi: 10.1016/j.bbr.2012.10.026

Figure Lengend Snippet: Enhanced GluN2B subunit expression in vivo in neurons. Representative image of a coronal section showing GluN2B subunit and neurofilament (neuronal marker) protein expression within the frontal lobe of an aged mouse treated with GluN2B vector. Panel A shows neurofilament only and Panel B shows GluN2B subunit only. Panel C shows GluN2B subunit with neurofilament. Red= GluN2B subunit, Green= neurofilament, co-localized neurofilament and GluN2B= orange, Bar= 5 μm.

Techniques: Expressing, In Vivo, Marker, Plasmid Preparation

Brain regions with enhanced GluN2B expression in the frontal lobe and caudate nucleus. Representative diagrams of coronal sections (adapted from [130]) show the locations of cells that were intensely labeled for the GluN2B subunit across the frontal lobe and caudate nucleus. cc= corpus callosum; Cg= cingulate cortex; CN= caudate nucleus; fmi= forceps minor of the corpus callosum; I=insular cortex; IL= infralimbic cortex; LO=lateral orbital cortex; LV= lateral ventricle; M1=primary motor cortex M2=secondary motor cortex; MO=medial orbital cortex; PrL= prelimbic cortex; S= somatosensory cortex; VO= ventral orbital cortex.

Journal: Behavioural brain research

Article Title: Memory in aged mice is rescued by enhanced expression of the GluN2B subunit of the NMDA receptor

doi: 10.1016/j.bbr.2012.10.026

Figure Lengend Snippet: Brain regions with enhanced GluN2B expression in the frontal lobe and caudate nucleus. Representative diagrams of coronal sections (adapted from [130]) show the locations of cells that were intensely labeled for the GluN2B subunit across the frontal lobe and caudate nucleus. cc= corpus callosum; Cg= cingulate cortex; CN= caudate nucleus; fmi= forceps minor of the corpus callosum; I=insular cortex; IL= infralimbic cortex; LO=lateral orbital cortex; LV= lateral ventricle; M1=primary motor cortex M2=secondary motor cortex; MO=medial orbital cortex; PrL= prelimbic cortex; S= somatosensory cortex; VO= ventral orbital cortex.

Techniques: Expressing, Labeling

Brain regions with enhanced GluN2B expression in the hippocampus. Representative diagrams of coronal sections (adapted from [130]) show the location of cells intensely labeled for the GluN2B subunit across the hippocampus. CA1= Cornu Ammonis 1; CA2= Cornu Ammonis 2; CA3= Cornu Ammonis 3; cc= corpus callosum; D3V= dorsal 3rd ventricle; LV= lateral ventricle; RSA= retrosplenial agranular cortex, RSG= retrosplenial granular cortex; S= somatosensory cortex; V= visual cortex.

Journal: Behavioural brain research

Article Title: Memory in aged mice is rescued by enhanced expression of the GluN2B subunit of the NMDA receptor

doi: 10.1016/j.bbr.2012.10.026

Figure Lengend Snippet: Brain regions with enhanced GluN2B expression in the hippocampus. Representative diagrams of coronal sections (adapted from [130]) show the location of cells intensely labeled for the GluN2B subunit across the hippocampus. CA1= Cornu Ammonis 1; CA2= Cornu Ammonis 2; CA3= Cornu Ammonis 3; cc= corpus callosum; D3V= dorsal 3rd ventricle; LV= lateral ventricle; RSA= retrosplenial agranular cortex, RSG= retrosplenial granular cortex; S= somatosensory cortex; V= visual cortex.

Techniques: Expressing, Labeling

Inflammation in vector-treated mice was not increased over vehicle-treated mice in the frontal lobe or hippocampus. Panels A–G show isolectin B4 staining of microglia in representative coronal sections taken at the injection site in the frontal lobe or hippocampus. (D) Inflammation was visible in a lipopolysaccharide-treated brain (positive control) and, to a lesser extent, equally across the different treatments, within the injection sites only: (A, E) vehicle, (B, F) control vector and (C, G) GluN2B vector. Bar=50 μm.

Journal: Behavioural brain research

Article Title: Memory in aged mice is rescued by enhanced expression of the GluN2B subunit of the NMDA receptor

doi: 10.1016/j.bbr.2012.10.026

Figure Lengend Snippet: Inflammation in vector-treated mice was not increased over vehicle-treated mice in the frontal lobe or hippocampus. Panels A–G show isolectin B4 staining of microglia in representative coronal sections taken at the injection site in the frontal lobe or hippocampus. (D) Inflammation was visible in a lipopolysaccharide-treated brain (positive control) and, to a lesser extent, equally across the different treatments, within the injection sites only: (A, E) vehicle, (B, F) control vector and (C, G) GluN2B vector. Bar=50 μm.

Techniques: Plasmid Preparation, Staining, Injection, Positive Control

Review

Structured Review

Images

Similar Products

Image Search Results