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anti glun2b  (Alomone Labs)


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    Structured Review

    Alomone Labs anti glun2b
    Anti Glun2b, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 126 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/glun2b/Anti-NMDAR2B+(GluN2B)+(extracellular)+Antibody/pmc13670132-86-14-15
    Average 96 stars, based on 126 article reviews
    anti glun2b - by Bioz Stars, 2026-10
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    Related Articles

    Immunocytochemistry:

    Article Title: GluN3A subunit tunes NMDA receptor synaptic trafficking and content during postnatal brain development
    Article Snippet: .. QD-based trajectories were considered synaptic if they colocalized with Homer 1-DsRed dendritic clusters for at least five frames. . Immunocytochemistry Neurons were fixed in 2% paraformaldehyde, 2% sucrose and stained in non-permeabilized conditions with primary antibodies against extracellular GluN2A or GluN2B (ACG-002 and ACG-003, Alomone). .. Cells were permeabilized with cold methanol and, after 30 min in blocking solution, incubated with Homer1 antibody (sc-8923, Santa Cruz Biotechnology) for 1h.

    Staining:

    Article Title: GluN3A subunit tunes NMDA receptor synaptic trafficking and content during postnatal brain development
    Article Snippet: .. QD-based trajectories were considered synaptic if they colocalized with Homer 1-DsRed dendritic clusters for at least five frames. . Immunocytochemistry Neurons were fixed in 2% paraformaldehyde, 2% sucrose and stained in non-permeabilized conditions with primary antibodies against extracellular GluN2A or GluN2B (ACG-002 and ACG-003, Alomone). .. Cells were permeabilized with cold methanol and, after 30 min in blocking solution, incubated with Homer1 antibody (sc-8923, Santa Cruz Biotechnology) for 1h.

    Article Title: GluN3A subunit tunes NMDA receptor synaptic trafficking and content during postnatal brain development
    Article Snippet: .. Neurons were fixed in 2% paraformaldehyde, 2% sucrose and stained in non-permeabilized conditions with primary antibodies against extracellular GluN2A or GluN2B (ACG-002 and ACG-003, Alomone). .. Cells were permeabilized with cold methanol and, after 30 min in blocking solution, incubated with Homer1 antibody (sc-8923, Santa Cruz Biotechnology) for 1h.

    Incubation:

    Article Title: Key Roles of CACNA1C /Cav1.2 and CALB1/Calbindin in Prefrontal Neurons Altered in Cognitive Disorders
    Article Snippet: If streptavidin-amplified, sections were then blocked with Component A and Component B for 20 min each using Invitrogen’s Endogenous Biotin Blocking kit, and then blocked for 1 h at RT in 1X TBS containing 5% bovine serum albumin, 2% Triton X-100, and 10% species-specific normal serum. .. Sections were incubated for 48 h at 4°C with specific primary antibodies: Cav1.2 (rabbit anti-Cav1.2 (CACNA1C) at 1:100 [cat# ACC-003, RRID:AB_2039771, Alomone]), 1-AR (goat anti-beta 1 adrenergic receptor at 1:100 [cat# ab77189, RRID:AB_1523202, Abcam]), Calbindin (mouse anti-calbindin D-28k at 1:100 [cat# 300, RRID:AB_10000347, Swant Antibodies]), SK3 (rabbit anti-KCNN3, KCa2.3 at 1:100 [cat# APC-025, RRID:AB_2040130, Alomone]), or GluN2B at 1:100 (rabbit anti-NMDAR2B [cat# AGC-003, RID:AB_2040028, Alomone] in dilution buffer (2% bovine serum albumin, 2% Triton X-100, and 1% species-specific normal serum). .. Sections with GluN2B or SK3 labeling underwent antigen retrieval in sodium citrate (10mM, JT Baker cat # 3646-01) using a water bath at 70- 80°C (30min), followed by washes and incubation for 1h in 50mM glycine (Sigma, cat # G-7126, in 0.1M PB).

    Article Title: STIM2 regulates NMDA receptor endocytosis that is induced by short-term NMDA receptor overactivation in cortical neurons.
    Article Snippet: .. Subsequently, cells were incubated with primary antibodies for the extracellular epitope of GluN1 (guinea pig, Alomone, Catalog No. AGP-046, 1:100), GluN2A (mouse, Abcam, Catalog No. ab240884, 1:100), or GluN2B (rabbit, Alomone, Catalog No. AGC-003, 1:100) in blocking solution for 2 h. Cells were then incubated with horseradish peroxidase-conjugated anti-guinea pig, anti-mouse, or anti-rabbit secondary antibody (Sigma-Aldrich, 1:2000) for 1 h. Afterward, 1-Step Turbo TMB-ELISA Substrate Solution (Thermo Fisher, Catalog No. 34022) was added, incubated for 30 min in the dark, and terminated by 1 M H2SO4. .. Absorption was measured at 450 nm using a Tecan INFINITE M1000 PRO plate reader with dedicated software (Tecan Group, Mannedorf, Switzerland).

    Blocking Assay:

    Article Title: STIM2 regulates NMDA receptor endocytosis that is induced by short-term NMDA receptor overactivation in cortical neurons.
    Article Snippet: .. Subsequently, cells were incubated with primary antibodies for the extracellular epitope of GluN1 (guinea pig, Alomone, Catalog No. AGP-046, 1:100), GluN2A (mouse, Abcam, Catalog No. ab240884, 1:100), or GluN2B (rabbit, Alomone, Catalog No. AGC-003, 1:100) in blocking solution for 2 h. Cells were then incubated with horseradish peroxidase-conjugated anti-guinea pig, anti-mouse, or anti-rabbit secondary antibody (Sigma-Aldrich, 1:2000) for 1 h. Afterward, 1-Step Turbo TMB-ELISA Substrate Solution (Thermo Fisher, Catalog No. 34022) was added, incubated for 30 min in the dark, and terminated by 1 M H2SO4. .. Absorption was measured at 450 nm using a Tecan INFINITE M1000 PRO plate reader with dedicated software (Tecan Group, Mannedorf, Switzerland).

    Labeling:

    Article Title: RIN1 regulates developmental and pain-related plasticity in spinal synapses via NMDA receptor subunit trafficking.
    Article Snippet: After cryoprotection for 12 h in 30% sucrose at 4°C, the transverse sections (40-μm thickness) of L4-L5 lumbar segments were cut on a vibratome (VT1200S, Leica). .. The surface proteins were labeled by a rabbit antibody against the N-terminal region of GluN2B (1:200, #AGC-003, Alomone Labs, Jerusalem, Israel) or GluN2A (1:200, #480031, Invitrogen) for 24–36 h at 4°C. ..

    Article Title: RIN1 regulates developmental and pain-related plasticity in spinal synapses via NMDA receptor subunit trafficking
    Article Snippet: .. The surface proteins were labeled by a rabbit antibody against the N-terminal region of GluN2B (1:200, #AGC-003, Alomone Labs, Jerusalem, Israel) or GluN2A (1:200, #480031, Invitrogen) for 24–36 h at 4°C. ..



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    Expression of GluN2A (A) and <t>GluN2B</t> (B) and basal extracellular levels of L‐glutamate (C) and D‐serine (D) in 4‐weeks and 8‐weeks of age S286L‐TG and wild‐type littermate. Ordinates indicate mean ± SD ( n = 6) of (A) expression levels of GluN2A relative to GAPDH in the plasma membrane fraction (B) expression levels of GluN2B relative to GAPDH in the plasma membrane fraction, (C) basal extracellular L‐glutamate level (μM) and (D) basal extracellular D‐serine level (μM) in the frontal cortex of wild‐type (gray column) and S286L‐TG (blue column). The lower‐side panels in A and B indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to 4‐weeks of age (4 W) and # p < 0.05 relative to wild‐type using two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (A) expression of GluN2A ( F age [1, 20] = 46.7 [ p < 0.05], F genotype [1, 20] = 5.34 [ p < 0.05], F age*genotype [1, 20] = 1.1 [ p > 0.05]), (B) expression of GluN2B ( F age [1, 20] = 22.4 [ p < 0.05], F genotype [1, 20] = 8.3 [ p < 0.05], F age*genotype [1, 20] = 2.0 [ p > 0.05]), (C) L‐glutamate level ( F age [1, 20] = 3.2 [ p > 0.05], F genotype [1, 20] = 21.2 [ p < 0.05], F age*genotype [1, 20] = 1.9 [ p > 0.05]) and (D) D‐serine level ( F age [1, 20] = 8.4 [ p < 0.05], F genotype [1, 20] = 21.6 [ p < 0.05], F age*genotype [1, 20] = 2.8 [ p > 0.05]).
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    Expression of GluN2A (A) and <t>GluN2B</t> (B) and basal extracellular levels of L‐glutamate (C) and D‐serine (D) in 4‐weeks and 8‐weeks of age S286L‐TG and wild‐type littermate. Ordinates indicate mean ± SD ( n = 6) of (A) expression levels of GluN2A relative to GAPDH in the plasma membrane fraction (B) expression levels of GluN2B relative to GAPDH in the plasma membrane fraction, (C) basal extracellular L‐glutamate level (μM) and (D) basal extracellular D‐serine level (μM) in the frontal cortex of wild‐type (gray column) and S286L‐TG (blue column). The lower‐side panels in A and B indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to 4‐weeks of age (4 W) and # p < 0.05 relative to wild‐type using two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (A) expression of GluN2A ( F age [1, 20] = 46.7 [ p < 0.05], F genotype [1, 20] = 5.34 [ p < 0.05], F age*genotype [1, 20] = 1.1 [ p > 0.05]), (B) expression of GluN2B ( F age [1, 20] = 22.4 [ p < 0.05], F genotype [1, 20] = 8.3 [ p < 0.05], F age*genotype [1, 20] = 2.0 [ p > 0.05]), (C) L‐glutamate level ( F age [1, 20] = 3.2 [ p > 0.05], F genotype [1, 20] = 21.2 [ p < 0.05], F age*genotype [1, 20] = 1.9 [ p > 0.05]) and (D) D‐serine level ( F age [1, 20] = 8.4 [ p < 0.05], F genotype [1, 20] = 21.6 [ p < 0.05], F age*genotype [1, 20] = 2.8 [ p > 0.05]).
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    Expression of GluN2A (A) and <t>GluN2B</t> (B) and basal extracellular levels of L‐glutamate (C) and D‐serine (D) in 4‐weeks and 8‐weeks of age S286L‐TG and wild‐type littermate. Ordinates indicate mean ± SD ( n = 6) of (A) expression levels of GluN2A relative to GAPDH in the plasma membrane fraction (B) expression levels of GluN2B relative to GAPDH in the plasma membrane fraction, (C) basal extracellular L‐glutamate level (μM) and (D) basal extracellular D‐serine level (μM) in the frontal cortex of wild‐type (gray column) and S286L‐TG (blue column). The lower‐side panels in A and B indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to 4‐weeks of age (4 W) and # p < 0.05 relative to wild‐type using two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (A) expression of GluN2A ( F age [1, 20] = 46.7 [ p < 0.05], F genotype [1, 20] = 5.34 [ p < 0.05], F age*genotype [1, 20] = 1.1 [ p > 0.05]), (B) expression of GluN2B ( F age [1, 20] = 22.4 [ p < 0.05], F genotype [1, 20] = 8.3 [ p < 0.05], F age*genotype [1, 20] = 2.0 [ p > 0.05]), (C) L‐glutamate level ( F age [1, 20] = 3.2 [ p > 0.05], F genotype [1, 20] = 21.2 [ p < 0.05], F age*genotype [1, 20] = 1.9 [ p > 0.05]) and (D) D‐serine level ( F age [1, 20] = 8.4 [ p < 0.05], F genotype [1, 20] = 21.6 [ p < 0.05], F age*genotype [1, 20] = 2.8 [ p > 0.05]).
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    Image Search Results


    Schematic overview of the isolation, culture, and analysis of hippocampal and cortical neurons from postnatal day 1 control (HbAA) and sickle cell (HbSS) mice. The workflow includes brain dissection, enzymatic dissociation, neuronal plating and maintenance, and downstream morphological and immunocytochemical analyses.

    Journal: Cells

    Article Title: Simplified Procedure for Isolation and Culture of Neuronal Cells from Brains of Sickle Cell Mice

    doi: 10.3390/cells15110976

    Figure Lengend Snippet: Schematic overview of the isolation, culture, and analysis of hippocampal and cortical neurons from postnatal day 1 control (HbAA) and sickle cell (HbSS) mice. The workflow includes brain dissection, enzymatic dissociation, neuronal plating and maintenance, and downstream morphological and immunocytochemical analyses.

    Article Snippet: Cells were fixed as described above at 3, 7, and 14 days in vitro (DIVs) with 2% paraformaldehyde in phosphate-buffered saline(Sigma-Aldrich, #158127) for 10 min at room RT and permeabilized with ice-cold 0.1% Triton X-100 (Sigma-Aldrich, #T8787) for 2 min; they were then blocked for 30 min with 3% donkey serum in PBS and incubated overnight at 4 °C with combinations of primary antibodies ( ): goat anti-RBFOX3/NeuN (1:200, Novus Biological, Centennial, CO, USA, #NBP3-05554), chicken anti-NF200 (1:3000, Neuromics, Edina, MN, USA, #CH22104), guinea pig anti-postsynaptic density (PSD) 95 (1:500, Alomone Labs, Jerusalem, Israel, #APZ-009-GP), rabbit anti-GluN2B (1:500, Alomone Labs, #AGC-003), chicken anti-MAP2 (1:2000, Thermo Fisher, #PA1-1005), and rabbit anti-VGLUT1 (1:300, Cell Signaling Technology, Danvers, MA, USA, #47181).

    Techniques: Isolation, Analysis, Control, Dissection, Cell Culture, Phase Contrast, Immunofluorescence, Confocal Microscopy

    Expression of GluN2A (A) and GluN2B (B) and basal extracellular levels of L‐glutamate (C) and D‐serine (D) in 4‐weeks and 8‐weeks of age S286L‐TG and wild‐type littermate. Ordinates indicate mean ± SD ( n = 6) of (A) expression levels of GluN2A relative to GAPDH in the plasma membrane fraction (B) expression levels of GluN2B relative to GAPDH in the plasma membrane fraction, (C) basal extracellular L‐glutamate level (μM) and (D) basal extracellular D‐serine level (μM) in the frontal cortex of wild‐type (gray column) and S286L‐TG (blue column). The lower‐side panels in A and B indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to 4‐weeks of age (4 W) and # p < 0.05 relative to wild‐type using two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (A) expression of GluN2A ( F age [1, 20] = 46.7 [ p < 0.05], F genotype [1, 20] = 5.34 [ p < 0.05], F age*genotype [1, 20] = 1.1 [ p > 0.05]), (B) expression of GluN2B ( F age [1, 20] = 22.4 [ p < 0.05], F genotype [1, 20] = 8.3 [ p < 0.05], F age*genotype [1, 20] = 2.0 [ p > 0.05]), (C) L‐glutamate level ( F age [1, 20] = 3.2 [ p > 0.05], F genotype [1, 20] = 21.2 [ p < 0.05], F age*genotype [1, 20] = 1.9 [ p > 0.05]) and (D) D‐serine level ( F age [1, 20] = 8.4 [ p < 0.05], F genotype [1, 20] = 21.6 [ p < 0.05], F age*genotype [1, 20] = 2.8 [ p > 0.05]).

    Journal: Pharmacology Research & Perspectives

    Article Title: Combined Inhibition of TRPM 4/ NMDA Receptor Complex and Extrasynaptic NMDA Receptors Is Candidate Therapeutic Target for Suppression of Epileptic Seizures and Improvement of Cognitive Impairments

    doi: 10.1002/prp2.70256

    Figure Lengend Snippet: Expression of GluN2A (A) and GluN2B (B) and basal extracellular levels of L‐glutamate (C) and D‐serine (D) in 4‐weeks and 8‐weeks of age S286L‐TG and wild‐type littermate. Ordinates indicate mean ± SD ( n = 6) of (A) expression levels of GluN2A relative to GAPDH in the plasma membrane fraction (B) expression levels of GluN2B relative to GAPDH in the plasma membrane fraction, (C) basal extracellular L‐glutamate level (μM) and (D) basal extracellular D‐serine level (μM) in the frontal cortex of wild‐type (gray column) and S286L‐TG (blue column). The lower‐side panels in A and B indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to 4‐weeks of age (4 W) and # p < 0.05 relative to wild‐type using two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (A) expression of GluN2A ( F age [1, 20] = 46.7 [ p < 0.05], F genotype [1, 20] = 5.34 [ p < 0.05], F age*genotype [1, 20] = 1.1 [ p > 0.05]), (B) expression of GluN2B ( F age [1, 20] = 22.4 [ p < 0.05], F genotype [1, 20] = 8.3 [ p < 0.05], F age*genotype [1, 20] = 2.0 [ p > 0.05]), (C) L‐glutamate level ( F age [1, 20] = 3.2 [ p > 0.05], F genotype [1, 20] = 21.2 [ p < 0.05], F age*genotype [1, 20] = 1.9 [ p > 0.05]) and (D) D‐serine level ( F age [1, 20] = 8.4 [ p < 0.05], F genotype [1, 20] = 21.6 [ p < 0.05], F age*genotype [1, 20] = 2.8 [ p > 0.05]).

    Article Snippet: Primary antibodies against GAPDH (NB300‐327, RRID:AB_10001915, 1:300; Novus Biologicals, Littleton, CO, USA), GluN2A (PPS012, RRID:AB_2112297, 1:100, R&D Systems, Minneapolis, MN, USA), GluN2B (PPS013, RRID:AB_562667, 1:100, R&D Systems), cAMP response element binding protein (CREB) (#4820, 1:50, Cell Signaling Technology, Danvers, MA, USA), and pCREB (#9198, 1:50, Cell Signaling) were used.

    Techniques: Expressing, Clinical Proteomics, Membrane, Western Blot

    Effects of chronic administration of probenecid, MK‐801, memantine, and FP802 on expression of GluN2A and GluN2B in S286L‐TG and wild‐type littermates. All rats were chronically administered by vehicle (control), probenecid (PBN: 100 mg/kg/day), MK‐801 (0.1 mg/kg/day), memantine (MEM: 10 mg/kg/day) and FP802 (40 mg/kg/day) for 2‐weeks (from 6‐weeks to 8‐weeks of age). Ordinates indicate mean ± SD ( n = 6) of expression levels of GluN2A (A1‐A4) and GluN2B (B1‐B4) relative to GAPDH in wild‐type (A1‐A2, B1‐B2) and S286L‐TG (A3‐A4, B3‐B4). The right‐side panels indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to control using one‐way ANOVA with Scheffe's post hoc test. F ‐values regarding effects of probenecid and MK‐801 on GluN2A expression in wild‐type (A1) ( F [2, 15] = 7.8 [ p < 0.05]), GluN2A in S286L (A3) ( F [2, 15] = 19.4 [ p < 0.05]), GluN2B in wild‐type (B1) ( F [2, 15] = 12.1 [ p < 0.05]) and GluN2B in S286L‐TG (B3) ( F [2, 15] = 18.2 [ p < 0.05]). F ‐values regarding effects of memantine and FP802 on GluN2A in wild‐type (A2) ( F [2, 15] = 0.4 [ p > 0.05]), GluN2A in S286L‐TG (A4) ( F [2, 15] = 7.1 [ p < 0.05]), GluN2B in wild‐type (B2) ( F [2, 15] = 0.2 [ p > 0.05]) and GluN2B in S286L‐TG (B4) ( F [2, 15] = 4.8 [ p < 0.05]).

    Journal: Pharmacology Research & Perspectives

    Article Title: Combined Inhibition of TRPM 4/ NMDA Receptor Complex and Extrasynaptic NMDA Receptors Is Candidate Therapeutic Target for Suppression of Epileptic Seizures and Improvement of Cognitive Impairments

    doi: 10.1002/prp2.70256

    Figure Lengend Snippet: Effects of chronic administration of probenecid, MK‐801, memantine, and FP802 on expression of GluN2A and GluN2B in S286L‐TG and wild‐type littermates. All rats were chronically administered by vehicle (control), probenecid (PBN: 100 mg/kg/day), MK‐801 (0.1 mg/kg/day), memantine (MEM: 10 mg/kg/day) and FP802 (40 mg/kg/day) for 2‐weeks (from 6‐weeks to 8‐weeks of age). Ordinates indicate mean ± SD ( n = 6) of expression levels of GluN2A (A1‐A4) and GluN2B (B1‐B4) relative to GAPDH in wild‐type (A1‐A2, B1‐B2) and S286L‐TG (A3‐A4, B3‐B4). The right‐side panels indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to control using one‐way ANOVA with Scheffe's post hoc test. F ‐values regarding effects of probenecid and MK‐801 on GluN2A expression in wild‐type (A1) ( F [2, 15] = 7.8 [ p < 0.05]), GluN2A in S286L (A3) ( F [2, 15] = 19.4 [ p < 0.05]), GluN2B in wild‐type (B1) ( F [2, 15] = 12.1 [ p < 0.05]) and GluN2B in S286L‐TG (B3) ( F [2, 15] = 18.2 [ p < 0.05]). F ‐values regarding effects of memantine and FP802 on GluN2A in wild‐type (A2) ( F [2, 15] = 0.4 [ p > 0.05]), GluN2A in S286L‐TG (A4) ( F [2, 15] = 7.1 [ p < 0.05]), GluN2B in wild‐type (B2) ( F [2, 15] = 0.2 [ p > 0.05]) and GluN2B in S286L‐TG (B4) ( F [2, 15] = 4.8 [ p < 0.05]).

    Article Snippet: Primary antibodies against GAPDH (NB300‐327, RRID:AB_10001915, 1:300; Novus Biologicals, Littleton, CO, USA), GluN2A (PPS012, RRID:AB_2112297, 1:100, R&D Systems, Minneapolis, MN, USA), GluN2B (PPS013, RRID:AB_562667, 1:100, R&D Systems), cAMP response element binding protein (CREB) (#4820, 1:50, Cell Signaling Technology, Danvers, MA, USA), and pCREB (#9198, 1:50, Cell Signaling) were used.

    Techniques: Expressing, Control, Western Blot

    Effects of chronic combined administration of memantine with FP802 on ADSHE seizure frequency (A), sucrose preference (B), expression of GluN2A (C1) and GluN2B (C2), and basal extracellular levels of L‐glutamate (D) and D‐serine (E) in S286L‐TG and wild‐type littermate. All rats were chronically administered by vehicle (control) and combined of memantine (MEM: 10 mg/kg/day) with FP802 (40 mg/kg/day) for 2‐weeks (from 6‐weeks to 8‐weeks of age). Ordinates indicate mean ± SD ( n = 6) of (A) ADSHE seizure frequency (count h −1 ), (B) consumption of sucrose preference (%), (C1) expression levels of GluN2A relative to GAPDH, (C2) expression levels of GluN2B relative to GAPDH, (D) basal extracellular L‐glutamate level (μM) and (E) basal extracellular D‐serine level (μM). The right‐side panels in C1‐C2 indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to control and # p < 0.05 relative to wild‐type using student T ‐test or one‐way or two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (B) sucrose preference: MEM ( F memantine+FP802 [1, 20] = 21.3 [ p < 0.05], F genotype [1, 20] = 5.1 [ p < 0.05], F rmemantine+FP802*genotype [1, 20] = 5.3 [ p < 0.05]), (D) L‐glutamate level: ( F memantine+FP802 [1, 20] = 5.3 [ p < 0.05], F genotype [1, 20] = 15.9 [ p < 0.05], F rmemantine+FP802*genotype [1, 20] = 4.8 [ p < 0.05]), (E) D‐serine level: ( F memantine+FP802 [1, 20] = 7.6 [ p < 0.05], F genotype [1, 20] = 22.4 [ p < 0.05], F rmemantine+FP802*genotype [1, 20] = 10.4 [ p < 0.05]).

    Journal: Pharmacology Research & Perspectives

    Article Title: Combined Inhibition of TRPM 4/ NMDA Receptor Complex and Extrasynaptic NMDA Receptors Is Candidate Therapeutic Target for Suppression of Epileptic Seizures and Improvement of Cognitive Impairments

    doi: 10.1002/prp2.70256

    Figure Lengend Snippet: Effects of chronic combined administration of memantine with FP802 on ADSHE seizure frequency (A), sucrose preference (B), expression of GluN2A (C1) and GluN2B (C2), and basal extracellular levels of L‐glutamate (D) and D‐serine (E) in S286L‐TG and wild‐type littermate. All rats were chronically administered by vehicle (control) and combined of memantine (MEM: 10 mg/kg/day) with FP802 (40 mg/kg/day) for 2‐weeks (from 6‐weeks to 8‐weeks of age). Ordinates indicate mean ± SD ( n = 6) of (A) ADSHE seizure frequency (count h −1 ), (B) consumption of sucrose preference (%), (C1) expression levels of GluN2A relative to GAPDH, (C2) expression levels of GluN2B relative to GAPDH, (D) basal extracellular L‐glutamate level (μM) and (E) basal extracellular D‐serine level (μM). The right‐side panels in C1‐C2 indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to control and # p < 0.05 relative to wild‐type using student T ‐test or one‐way or two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (B) sucrose preference: MEM ( F memantine+FP802 [1, 20] = 21.3 [ p < 0.05], F genotype [1, 20] = 5.1 [ p < 0.05], F rmemantine+FP802*genotype [1, 20] = 5.3 [ p < 0.05]), (D) L‐glutamate level: ( F memantine+FP802 [1, 20] = 5.3 [ p < 0.05], F genotype [1, 20] = 15.9 [ p < 0.05], F rmemantine+FP802*genotype [1, 20] = 4.8 [ p < 0.05]), (E) D‐serine level: ( F memantine+FP802 [1, 20] = 7.6 [ p < 0.05], F genotype [1, 20] = 22.4 [ p < 0.05], F rmemantine+FP802*genotype [1, 20] = 10.4 [ p < 0.05]).

    Article Snippet: Primary antibodies against GAPDH (NB300‐327, RRID:AB_10001915, 1:300; Novus Biologicals, Littleton, CO, USA), GluN2A (PPS012, RRID:AB_2112297, 1:100, R&D Systems, Minneapolis, MN, USA), GluN2B (PPS013, RRID:AB_562667, 1:100, R&D Systems), cAMP response element binding protein (CREB) (#4820, 1:50, Cell Signaling Technology, Danvers, MA, USA), and pCREB (#9198, 1:50, Cell Signaling) were used.

    Techniques: Expressing, Control, Western Blot