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antibody anti-glua3  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology antibody anti-glua3

    Antibody Anti Glua3, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibody anti-glua3/product/Santa Cruz Biotechnology
    Average 90 stars, based on 1 article reviews
    antibody anti-glua3 - by Bioz Stars, 2026-03
    90/100 stars

    Images

    1) Product Images from "CaBP1 and 2 enable sustained Ca V 1.3 calcium currents and synaptic transmission in inner hair cells"

    Article Title: CaBP1 and 2 enable sustained Ca V 1.3 calcium currents and synaptic transmission in inner hair cells

    Journal: eLife

    doi: 10.7554/eLife.93646


    Figure Legend Snippet:

    Techniques Used: Plasmid Preparation, Recombinant, Sequencing, Software, Patch Clamp



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    Nutritional state differentially modulates synaptic transmission in WT and OGT-KO neurons. A , representative trace showing suppression of spontaneous excitatory synaptic events following NBQX application in WT PVN αCaMKII neurons. The red arrow represents a typical excitatory spike. B – D , representative Western blots and quantification of total and surface GluA1 expression in primary cortical neurons. WT values were normalized to 1. OGT-KO total GluA1 = 1.282 ± 0.068; surface GluA1 = 1.629 ± 0.064. E–G , representative Western blots and quantification of total and surface GluA2 expression. WT values were normalized to 1. OGT-KO total GluA2 = 0.7101 ± 0.081; surface GluA2 = 0.5138 ± 0.075. H–J , representative Western blots and quantification of total and surface <t>GluA3</t> expression. WT values were normalized to 1. OGT-KO total GluA3 = 0.6691 ± 0.032; surface GluA3 = 0.3935 ± 0.044. Western blot quantitative analyses were performed using the Wilcoxon signed-rank test. All Western blot data expressed as mean ± SEM. K , representative sEPSC traces in WT neurons under hungry ( top ) and fed ( bottom ) conditions. L , sEPSC frequency in WT neurons comparing hungry vs fed states ( p = 0.021). M , sEPSC amplitude in WT neurons comparing hungry vs fed states (NS, p = 0.851). N , sEPSC decay tau in WT neurons comparing hungry vs fed states (NS, p = 0.142). O , Representative sEPSC traces in OGT-KO neurons under hungry ( top ) and fed ( bottom ) conditions. P , sEPSC frequency in OGT-KO neurons comparing hungry vs fed states (NS, p = 0.095). Q , sEPSC amplitude in OGT-KO neurons comparing hungry vs fed states (NS, p = 0.309). R , sEPSC decay tau in OGT-KO neurons comparing hungry vs fed states (NS, p = 0.547). All sEPSC data ( panels K–R ) were obtained from WT (n = 5) and OGT-KO (n = 5) mice under hungry and fed conditions (n = 5 each condition). Statistical comparisons using Mann-Whitney non-parametric test. Data presented as mean ± SEM. Blue bars: WT neurons ( dark blue = hungry, light blue = fed); yellow bars: OGT-KO neurons ( light yellow = hungry, bright yellow = fed). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001, NS, non-significant.
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    Nutritional state differentially modulates synaptic transmission in WT and OGT-KO neurons. A , representative trace showing suppression of spontaneous excitatory synaptic events following NBQX application in WT PVN αCaMKII neurons. The red arrow represents a typical excitatory spike. B – D , representative Western blots and quantification of total and surface GluA1 expression in primary cortical neurons. WT values were normalized to 1. OGT-KO total GluA1 = 1.282 ± 0.068; surface GluA1 = 1.629 ± 0.064. E–G , representative Western blots and quantification of total and surface GluA2 expression. WT values were normalized to 1. OGT-KO total GluA2 = 0.7101 ± 0.081; surface GluA2 = 0.5138 ± 0.075. H–J , representative Western blots and quantification of total and surface <t>GluA3</t> expression. WT values were normalized to 1. OGT-KO total GluA3 = 0.6691 ± 0.032; surface GluA3 = 0.3935 ± 0.044. Western blot quantitative analyses were performed using the Wilcoxon signed-rank test. All Western blot data expressed as mean ± SEM. K , representative sEPSC traces in WT neurons under hungry ( top ) and fed ( bottom ) conditions. L , sEPSC frequency in WT neurons comparing hungry vs fed states ( p = 0.021). M , sEPSC amplitude in WT neurons comparing hungry vs fed states (NS, p = 0.851). N , sEPSC decay tau in WT neurons comparing hungry vs fed states (NS, p = 0.142). O , Representative sEPSC traces in OGT-KO neurons under hungry ( top ) and fed ( bottom ) conditions. P , sEPSC frequency in OGT-KO neurons comparing hungry vs fed states (NS, p = 0.095). Q , sEPSC amplitude in OGT-KO neurons comparing hungry vs fed states (NS, p = 0.309). R , sEPSC decay tau in OGT-KO neurons comparing hungry vs fed states (NS, p = 0.547). All sEPSC data ( panels K–R ) were obtained from WT (n = 5) and OGT-KO (n = 5) mice under hungry and fed conditions (n = 5 each condition). Statistical comparisons using Mann-Whitney non-parametric test. Data presented as mean ± SEM. Blue bars: WT neurons ( dark blue = hungry, light blue = fed); yellow bars: OGT-KO neurons ( light yellow = hungry, bright yellow = fed). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001, NS, non-significant.
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    Alomone Labs rabbit anti ampar
    Rabbit anti-AMPAR GluR3B immunogenicity response. ( A ) ELISA of protein A-purified AMPAR <t>(GluR3)</t> Aabs against the GluR3 immunisation peptide or an irrelevant peptide; n = 3 technical replicates. ( B ) Western blot of mouse whole brain lysate probed with a commercial anti-AMPAR antibody (cAMPAR), anti-AMPAR Aabs, a class-specific negative control rIgG (naïve) or secondary antibody only (negative control). Representative blots from n = 3 technical replicates. ( C ) Immunocytochemical staining of fixed primary cortical neuron on cultures. Cells (DIV8) were stained with anti-AMPAR Aabs (red), anti-βIII tubulin (green), GFAP (white) and nuclei counterstained with DAPI (blue). Examples of labelling of hippocampal neurons with anti-AMPAR Aabs (red) is indicated by the white arrows. Scale bars = 20 μm. Representative images from n = 3 technical replicates.
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    Rabbit <t>anti-AMPAR</t> GluR3B immunogenicity response. ( A ) ELISA of protein A-purified AMPAR <t>(GluR3)</t> <t>Aabs</t> against the GluR3 immunisation peptide or an irrelevant peptide; n = 3 technical replicates. ( B ) Western blot of mouse whole brain lysate probed with a commercial anti-AMPAR antibody (cAMPAR), anti-AMPAR Aabs, a class-specific negative control rIgG (naïve) or secondary antibody only (negative control). Representative blots from n = 3 technical replicates. ( C ) Immunocytochemical staining of fixed primary cortical neuron on cultures. Cells (DIV8) were stained with anti-AMPAR Aabs (red), anti-βIII tubulin (green), GFAP (white) and nuclei counterstained with DAPI (blue). Examples of labelling of hippocampal neurons with anti-AMPAR Aabs (red) is indicated by the white arrows. Scale bars = 20 μm. Representative images from n = 3 technical replicates.
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    Image Search Results


    Nutritional state differentially modulates synaptic transmission in WT and OGT-KO neurons. A , representative trace showing suppression of spontaneous excitatory synaptic events following NBQX application in WT PVN αCaMKII neurons. The red arrow represents a typical excitatory spike. B – D , representative Western blots and quantification of total and surface GluA1 expression in primary cortical neurons. WT values were normalized to 1. OGT-KO total GluA1 = 1.282 ± 0.068; surface GluA1 = 1.629 ± 0.064. E–G , representative Western blots and quantification of total and surface GluA2 expression. WT values were normalized to 1. OGT-KO total GluA2 = 0.7101 ± 0.081; surface GluA2 = 0.5138 ± 0.075. H–J , representative Western blots and quantification of total and surface GluA3 expression. WT values were normalized to 1. OGT-KO total GluA3 = 0.6691 ± 0.032; surface GluA3 = 0.3935 ± 0.044. Western blot quantitative analyses were performed using the Wilcoxon signed-rank test. All Western blot data expressed as mean ± SEM. K , representative sEPSC traces in WT neurons under hungry ( top ) and fed ( bottom ) conditions. L , sEPSC frequency in WT neurons comparing hungry vs fed states ( p = 0.021). M , sEPSC amplitude in WT neurons comparing hungry vs fed states (NS, p = 0.851). N , sEPSC decay tau in WT neurons comparing hungry vs fed states (NS, p = 0.142). O , Representative sEPSC traces in OGT-KO neurons under hungry ( top ) and fed ( bottom ) conditions. P , sEPSC frequency in OGT-KO neurons comparing hungry vs fed states (NS, p = 0.095). Q , sEPSC amplitude in OGT-KO neurons comparing hungry vs fed states (NS, p = 0.309). R , sEPSC decay tau in OGT-KO neurons comparing hungry vs fed states (NS, p = 0.547). All sEPSC data ( panels K–R ) were obtained from WT (n = 5) and OGT-KO (n = 5) mice under hungry and fed conditions (n = 5 each condition). Statistical comparisons using Mann-Whitney non-parametric test. Data presented as mean ± SEM. Blue bars: WT neurons ( dark blue = hungry, light blue = fed); yellow bars: OGT-KO neurons ( light yellow = hungry, bright yellow = fed). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001, NS, non-significant.

    Journal: The Journal of Biological Chemistry

    Article Title: O-GlcNAc transferase couples nutrient availability to synaptic plasticity in paraventricular neurons to regulate satiety

    doi: 10.1016/j.jbc.2025.111124

    Figure Lengend Snippet: Nutritional state differentially modulates synaptic transmission in WT and OGT-KO neurons. A , representative trace showing suppression of spontaneous excitatory synaptic events following NBQX application in WT PVN αCaMKII neurons. The red arrow represents a typical excitatory spike. B – D , representative Western blots and quantification of total and surface GluA1 expression in primary cortical neurons. WT values were normalized to 1. OGT-KO total GluA1 = 1.282 ± 0.068; surface GluA1 = 1.629 ± 0.064. E–G , representative Western blots and quantification of total and surface GluA2 expression. WT values were normalized to 1. OGT-KO total GluA2 = 0.7101 ± 0.081; surface GluA2 = 0.5138 ± 0.075. H–J , representative Western blots and quantification of total and surface GluA3 expression. WT values were normalized to 1. OGT-KO total GluA3 = 0.6691 ± 0.032; surface GluA3 = 0.3935 ± 0.044. Western blot quantitative analyses were performed using the Wilcoxon signed-rank test. All Western blot data expressed as mean ± SEM. K , representative sEPSC traces in WT neurons under hungry ( top ) and fed ( bottom ) conditions. L , sEPSC frequency in WT neurons comparing hungry vs fed states ( p = 0.021). M , sEPSC amplitude in WT neurons comparing hungry vs fed states (NS, p = 0.851). N , sEPSC decay tau in WT neurons comparing hungry vs fed states (NS, p = 0.142). O , Representative sEPSC traces in OGT-KO neurons under hungry ( top ) and fed ( bottom ) conditions. P , sEPSC frequency in OGT-KO neurons comparing hungry vs fed states (NS, p = 0.095). Q , sEPSC amplitude in OGT-KO neurons comparing hungry vs fed states (NS, p = 0.309). R , sEPSC decay tau in OGT-KO neurons comparing hungry vs fed states (NS, p = 0.547). All sEPSC data ( panels K–R ) were obtained from WT (n = 5) and OGT-KO (n = 5) mice under hungry and fed conditions (n = 5 each condition). Statistical comparisons using Mann-Whitney non-parametric test. Data presented as mean ± SEM. Blue bars: WT neurons ( dark blue = hungry, light blue = fed); yellow bars: OGT-KO neurons ( light yellow = hungry, bright yellow = fed). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001, NS, non-significant.

    Article Snippet: Membranes were blocked in 5% non-fat milk prepared in TBS-T and incubated overnight at 4 °C with primary antibodies against OGT (Proteintech, 11576-2-AP; 1:2000), HSP70 (Proteintech, 10995-1-AP; 1:10,000), GluA1 (NeuroMab, N355/1; 5μg/blot), GluA2 (NeuroMab, L21/32; 5μg/blot), or GluA3 (Almone labs, AGC-010-GP; 1:1000).

    Techniques: Transmission Assay, Western Blot, Expressing, MANN-WHITNEY

    Journal: eLife

    Article Title: CaBP1 and 2 enable sustained Ca V 1.3 calcium currents and synaptic transmission in inner hair cells

    doi: 10.7554/eLife.93646

    Figure Lengend Snippet:

    Article Snippet: Antibody , anti-GluA3 (Goat polyclonal) , Santa Cruz Biotechnology , Cat#: sc-7612, RRID: AB_2113895 , 1:200.

    Techniques: Plasmid Preparation, Recombinant, Sequencing, Software, Patch Clamp

    Journal: iScience

    Article Title: GluK2 Q/R editing regulates kainate receptor signaling and long-term potentiation of AMPA receptors

    doi: 10.1016/j.isci.2023.107708

    Figure Lengend Snippet:

    Article Snippet: Rabbit Polyclonal Anti-GluA3 , Alomone , RRID: AB_2039883.

    Techniques: Recombinant, Protein Extraction, Software

    Rabbit anti-AMPAR GluR3B immunogenicity response. ( A ) ELISA of protein A-purified AMPAR (GluR3) Aabs against the GluR3 immunisation peptide or an irrelevant peptide; n = 3 technical replicates. ( B ) Western blot of mouse whole brain lysate probed with a commercial anti-AMPAR antibody (cAMPAR), anti-AMPAR Aabs, a class-specific negative control rIgG (naïve) or secondary antibody only (negative control). Representative blots from n = 3 technical replicates. ( C ) Immunocytochemical staining of fixed primary cortical neuron on cultures. Cells (DIV8) were stained with anti-AMPAR Aabs (red), anti-βIII tubulin (green), GFAP (white) and nuclei counterstained with DAPI (blue). Examples of labelling of hippocampal neurons with anti-AMPAR Aabs (red) is indicated by the white arrows. Scale bars = 20 μm. Representative images from n = 3 technical replicates.

    Journal: Pharmaceuticals

    Article Title: Anti-AMPA Receptor Autoantibodies Reduce Excitatory Currents in Rat Hippocampal Neurons

    doi: 10.3390/ph16010077

    Figure Lengend Snippet: Rabbit anti-AMPAR GluR3B immunogenicity response. ( A ) ELISA of protein A-purified AMPAR (GluR3) Aabs against the GluR3 immunisation peptide or an irrelevant peptide; n = 3 technical replicates. ( B ) Western blot of mouse whole brain lysate probed with a commercial anti-AMPAR antibody (cAMPAR), anti-AMPAR Aabs, a class-specific negative control rIgG (naïve) or secondary antibody only (negative control). Representative blots from n = 3 technical replicates. ( C ) Immunocytochemical staining of fixed primary cortical neuron on cultures. Cells (DIV8) were stained with anti-AMPAR Aabs (red), anti-βIII tubulin (green), GFAP (white) and nuclei counterstained with DAPI (blue). Examples of labelling of hippocampal neurons with anti-AMPAR Aabs (red) is indicated by the white arrows. Scale bars = 20 μm. Representative images from n = 3 technical replicates.

    Article Snippet: Primary and secondary antibodies used were as follows: rabbit anti-AMPAR (1:100; raised against residues 60–73 of rat GluR3 ATD, AGC-010, Alomone Labs, Jerusalem, Israel); rabbit anti-IgG 1 (rIgG, 1:100, 011-000-003, Jackson ImmunoResearch, Cambridge, UK); mouse anti-IgG 2b (1:100, 70–4732, BioLegend, London, UK); mouse anti-βIII-tubulin (mIgG2b, 1:500, 801201, BioLegend, London, UK); mouse anti-glial fibrillary acidic protein (GFAP) (1:400, MAB3402, Millipore); goat anti-rabbit or anti-mouse Alexa Fluor 488/594/647 (all at 1:1000, Life Technologies, Loughborough, UK).

    Techniques: Enzyme-linked Immunosorbent Assay, Purification, Western Blot, Negative Control, Staining

    Rabbit anti-AMPAR GluR3B immunogenicity response. ( A ) ELISA of protein A-purified AMPAR (GluR3) Aabs against the GluR3 immunisation peptide or an irrelevant peptide; n = 3 technical replicates. ( B ) Western blot of mouse whole brain lysate probed with a commercial anti-AMPAR antibody (cAMPAR), anti-AMPAR Aabs, a class-specific negative control rIgG (naïve) or secondary antibody only (negative control). Representative blots from n = 3 technical replicates. ( C ) Immunocytochemical staining of fixed primary cortical neuron on cultures. Cells (DIV8) were stained with anti-AMPAR Aabs (red), anti-βIII tubulin (green), GFAP (white) and nuclei counterstained with DAPI (blue). Examples of labelling of hippocampal neurons with anti-AMPAR Aabs (red) is indicated by the white arrows. Scale bars = 20 μm. Representative images from n = 3 technical replicates.

    Journal: Pharmaceuticals

    Article Title: Anti-AMPA Receptor Autoantibodies Reduce Excitatory Currents in Rat Hippocampal Neurons

    doi: 10.3390/ph16010077

    Figure Lengend Snippet: Rabbit anti-AMPAR GluR3B immunogenicity response. ( A ) ELISA of protein A-purified AMPAR (GluR3) Aabs against the GluR3 immunisation peptide or an irrelevant peptide; n = 3 technical replicates. ( B ) Western blot of mouse whole brain lysate probed with a commercial anti-AMPAR antibody (cAMPAR), anti-AMPAR Aabs, a class-specific negative control rIgG (naïve) or secondary antibody only (negative control). Representative blots from n = 3 technical replicates. ( C ) Immunocytochemical staining of fixed primary cortical neuron on cultures. Cells (DIV8) were stained with anti-AMPAR Aabs (red), anti-βIII tubulin (green), GFAP (white) and nuclei counterstained with DAPI (blue). Examples of labelling of hippocampal neurons with anti-AMPAR Aabs (red) is indicated by the white arrows. Scale bars = 20 μm. Representative images from n = 3 technical replicates.

    Article Snippet: Blots were probed with anti-AMPAR Aabs, a commercial anti-AMPAR antibody (cAMPAR, Alomone AGC-010), IgG (negative) control or a secondary antibody only (negative) control (each 1:100) ( B).

    Techniques: Enzyme-linked Immunosorbent Assay, Purification, Western Blot, Negative Control, Staining

    Effects of acute (10 min) anti-AMPAR Aabs and rIgG application on sEPSC frequency and amplitude. ( A ) Anti-AMPAR Aabs had a significantly lower mean sEPSC frequency than rIgG treated cells over the 10 min period ( p < 0.05). ( B ) Significant differences in cumulative inter-event interval frequency were also observed for anti-AMPAR Aabs 10 min incubation compared to rIgG incubated cells ( p < 0.0001). ( C ) Selected raw sEPSC traces for rIgG- and AMPAR-treated cells. ( D ) Anti-AMPAR Aabs had no significant effect on mean sEPSC amplitude vs rIgG treated cells over the 10 min period. Data were collected over three separate neuronal cultures, presented as mean ± SD and analysed by unpaired t -tests ( A , D ), or via Kolmogorov–Smirnov test ( C ). * = p < 0.05.

    Journal: Pharmaceuticals

    Article Title: Anti-AMPA Receptor Autoantibodies Reduce Excitatory Currents in Rat Hippocampal Neurons

    doi: 10.3390/ph16010077

    Figure Lengend Snippet: Effects of acute (10 min) anti-AMPAR Aabs and rIgG application on sEPSC frequency and amplitude. ( A ) Anti-AMPAR Aabs had a significantly lower mean sEPSC frequency than rIgG treated cells over the 10 min period ( p < 0.05). ( B ) Significant differences in cumulative inter-event interval frequency were also observed for anti-AMPAR Aabs 10 min incubation compared to rIgG incubated cells ( p < 0.0001). ( C ) Selected raw sEPSC traces for rIgG- and AMPAR-treated cells. ( D ) Anti-AMPAR Aabs had no significant effect on mean sEPSC amplitude vs rIgG treated cells over the 10 min period. Data were collected over three separate neuronal cultures, presented as mean ± SD and analysed by unpaired t -tests ( A , D ), or via Kolmogorov–Smirnov test ( C ). * = p < 0.05.

    Article Snippet: Blots were probed with anti-AMPAR Aabs, a commercial anti-AMPAR antibody (cAMPAR, Alomone AGC-010), IgG (negative) control or a secondary antibody only (negative) control (each 1:100) ( B).

    Techniques: Incubation

    Effects of acute (30 min) anti-AMPAR Aabs and rIgG application on sEPSC frequency and amplitude. ( A ) Anti-AMPAR Aabs had a significantly lower mean sEPSC frequency than rIgG treated cells over the 30 min period ( p < 0.05). ( B ) Significant differences in cumulative inter-event interval frequency were also observed for anti-AMPAR Aabs 30 min incubation compared to rIgG incubated cells ( p < 0.0001). ( C ) Anti-AMPAR Aabs had no significant effect on mean sEPSC amplitude vs. rIgG treated cells over the 30 min period. Data were collected over three separate neuronal cultures, presented as mean ± SD and analysed by unpaired t -tests ( A , C ), or via Kolmogorov–Smirnov test ( B ). * = p < 0.05.

    Journal: Pharmaceuticals

    Article Title: Anti-AMPA Receptor Autoantibodies Reduce Excitatory Currents in Rat Hippocampal Neurons

    doi: 10.3390/ph16010077

    Figure Lengend Snippet: Effects of acute (30 min) anti-AMPAR Aabs and rIgG application on sEPSC frequency and amplitude. ( A ) Anti-AMPAR Aabs had a significantly lower mean sEPSC frequency than rIgG treated cells over the 30 min period ( p < 0.05). ( B ) Significant differences in cumulative inter-event interval frequency were also observed for anti-AMPAR Aabs 30 min incubation compared to rIgG incubated cells ( p < 0.0001). ( C ) Anti-AMPAR Aabs had no significant effect on mean sEPSC amplitude vs. rIgG treated cells over the 30 min period. Data were collected over three separate neuronal cultures, presented as mean ± SD and analysed by unpaired t -tests ( A , C ), or via Kolmogorov–Smirnov test ( B ). * = p < 0.05.

    Article Snippet: Blots were probed with anti-AMPAR Aabs, a commercial anti-AMPAR antibody (cAMPAR, Alomone AGC-010), IgG (negative) control or a secondary antibody only (negative) control (each 1:100) ( B).

    Techniques: Incubation

    Effects of 24 h anti-AMPAR Aabs and rIgG application on sEPSC frequency and amplitude. ( A ) Anti-AMPAR Aabs had a significantly lower mean sEPSC frequency than rIgG treated cells over the 24 h period ( p < 0.05). ( B ) Significant differences in cumulative inter-event interval frequency were also observed for anti-AMPAR Aabs 24 h incubation compared to rIgG incubated cells ( p < 0.0001). ( C ) Anti-AMPAR Aabs had no significant effect on mean sEPSC amplitude vs. rIgG treated cells following 24 h incubation. Data were collected over three separate neuronal cultures, presented as mean ± SD and analysed by unpaired t -tests ( A , C ), or via Kolmogorov–Smirnov test ( B ). * = p < 0.05.

    Journal: Pharmaceuticals

    Article Title: Anti-AMPA Receptor Autoantibodies Reduce Excitatory Currents in Rat Hippocampal Neurons

    doi: 10.3390/ph16010077

    Figure Lengend Snippet: Effects of 24 h anti-AMPAR Aabs and rIgG application on sEPSC frequency and amplitude. ( A ) Anti-AMPAR Aabs had a significantly lower mean sEPSC frequency than rIgG treated cells over the 24 h period ( p < 0.05). ( B ) Significant differences in cumulative inter-event interval frequency were also observed for anti-AMPAR Aabs 24 h incubation compared to rIgG incubated cells ( p < 0.0001). ( C ) Anti-AMPAR Aabs had no significant effect on mean sEPSC amplitude vs. rIgG treated cells following 24 h incubation. Data were collected over three separate neuronal cultures, presented as mean ± SD and analysed by unpaired t -tests ( A , C ), or via Kolmogorov–Smirnov test ( B ). * = p < 0.05.

    Article Snippet: Blots were probed with anti-AMPAR Aabs, a commercial anti-AMPAR antibody (cAMPAR, Alomone AGC-010), IgG (negative) control or a secondary antibody only (negative) control (each 1:100) ( B).

    Techniques: Incubation

    Effects of acute (30 min) and 24 h anti-AMPAR Aabs and rIgG application on mEPSC frequency and amplitude. ( A ) Anti-AMPAR Aabs had a significantly lower mean mEPSC frequency than rIgG treated cells over the 30 min period ( p < 0.05). ( B ) Anti-AMPAR Aabs had a significantly lower mean mEPSC frequency than rIgG treated cells following 24 h incubation ( p < 0.05). Significant differences in cumulative inter-event interval frequency were also observed for anti-AMPAR Aabs compared to rIgG incubated cells for ( C ) 30 min incubation and ( D ) following 24 h incubation (both p < 0.0001). Data were collected over three separate neuronal cultures, presented as mean ± SD and analysed by unpaired t -tests ( A , C ), or via Kolmogorov–Smirnov test ( B , D ). ( E ) Selected raw sEPSC traces for rIgG- and AMPAR-treated cells. * = p < 0.05.

    Journal: Pharmaceuticals

    Article Title: Anti-AMPA Receptor Autoantibodies Reduce Excitatory Currents in Rat Hippocampal Neurons

    doi: 10.3390/ph16010077

    Figure Lengend Snippet: Effects of acute (30 min) and 24 h anti-AMPAR Aabs and rIgG application on mEPSC frequency and amplitude. ( A ) Anti-AMPAR Aabs had a significantly lower mean mEPSC frequency than rIgG treated cells over the 30 min period ( p < 0.05). ( B ) Anti-AMPAR Aabs had a significantly lower mean mEPSC frequency than rIgG treated cells following 24 h incubation ( p < 0.05). Significant differences in cumulative inter-event interval frequency were also observed for anti-AMPAR Aabs compared to rIgG incubated cells for ( C ) 30 min incubation and ( D ) following 24 h incubation (both p < 0.0001). Data were collected over three separate neuronal cultures, presented as mean ± SD and analysed by unpaired t -tests ( A , C ), or via Kolmogorov–Smirnov test ( B , D ). ( E ) Selected raw sEPSC traces for rIgG- and AMPAR-treated cells. * = p < 0.05.

    Article Snippet: Blots were probed with anti-AMPAR Aabs, a commercial anti-AMPAR antibody (cAMPAR, Alomone AGC-010), IgG (negative) control or a secondary antibody only (negative) control (each 1:100) ( B).

    Techniques: Incubation

    Schematic of potential mechanisms of anti-AMPAR Aabs. Anti-AMPAR Aabs may exert their inhibitory effect on glutamate release via presynaptic AMPARs. Additionally, anti-AMPAR Aabs may cause antibody-induced internalisation of AMPARs pre- and/or post-synaptically, resulting in an imbalance of the excitatory/inhibitory network.

    Journal: Pharmaceuticals

    Article Title: Anti-AMPA Receptor Autoantibodies Reduce Excitatory Currents in Rat Hippocampal Neurons

    doi: 10.3390/ph16010077

    Figure Lengend Snippet: Schematic of potential mechanisms of anti-AMPAR Aabs. Anti-AMPAR Aabs may exert their inhibitory effect on glutamate release via presynaptic AMPARs. Additionally, anti-AMPAR Aabs may cause antibody-induced internalisation of AMPARs pre- and/or post-synaptically, resulting in an imbalance of the excitatory/inhibitory network.

    Article Snippet: Blots were probed with anti-AMPAR Aabs, a commercial anti-AMPAR antibody (cAMPAR, Alomone AGC-010), IgG (negative) control or a secondary antibody only (negative) control (each 1:100) ( B).

    Techniques: