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yellow fluorescent protein eyfp mice  (Jackson Laboratory)

 
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    Jackson Laboratory yellow fluorescent protein eyfp mice
    TPL enhanced GABAergic “braking effect” in KA mouse model of epilepsy. (A) Schematic diagram of optogenetical stimulation and microelectrode recording on KA model; (B) Clusters view and waveform of recorded neurons (left); autocorrelation of recorded neurons (middle); histological image showing the placement of electrode and optic fiber in dorsal hippocampal DG for extracellular recording (right, Blue‐DAPI); (C) Peri‐event raster histograms of the event‐related response of neurons to optogenetical stimulation; (D) The duration of the light‐induced “braking effect” (Normal, n = 11 cells; Control, n = 10 cells; TPL, n = 11 cells). (E) Example images showing co‐localization of <t>VGAT‐EYFP</t> with astrocytes (GFAP) in hippocampus (scale bar = 200 μm), CA1 and DG region (scale bar = 50 μm); (F) The mean fluorescence intensity of GFAP in CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice); (G) The number of GFAP + astrocytes CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice); (H) The mean fluorescence intensity of VGAT in CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice). Normal means sham operated <t>VGAT‐CHR2‐EYFP</t> mice administrated with solvent at 0.1 mL/10 g; Control means VGAT‐CHR2‐EYFP epileptic mice administrated with solvent at 0.1 mL/10 g; TPL means VGAT‐CHR2‐EYFP epileptic mice administrated with TPL at 50 μg/kg. Data are presented as mean ± SEM. Kruskal‐Wallis test was used for D. * p < 0.05, **** p < 0.0001 compared with Normal. # p < 0.05 compared with Control.
    Yellow Fluorescent Protein Eyfp Mice, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    yellow fluorescent protein eyfp mice - by Bioz Stars, 2026-06
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    Images

    1) Product Images from "Triptolide Inhibits Epileptic Seizures by Rescuing the Neuroinflammation‐Related GABAergic Dysfunction in Mice"

    Article Title: Triptolide Inhibits Epileptic Seizures by Rescuing the Neuroinflammation‐Related GABAergic Dysfunction in Mice

    Journal: CNS Neuroscience & Therapeutics

    doi: 10.1111/cns.70586

    TPL enhanced GABAergic “braking effect” in KA mouse model of epilepsy. (A) Schematic diagram of optogenetical stimulation and microelectrode recording on KA model; (B) Clusters view and waveform of recorded neurons (left); autocorrelation of recorded neurons (middle); histological image showing the placement of electrode and optic fiber in dorsal hippocampal DG for extracellular recording (right, Blue‐DAPI); (C) Peri‐event raster histograms of the event‐related response of neurons to optogenetical stimulation; (D) The duration of the light‐induced “braking effect” (Normal, n = 11 cells; Control, n = 10 cells; TPL, n = 11 cells). (E) Example images showing co‐localization of VGAT‐EYFP with astrocytes (GFAP) in hippocampus (scale bar = 200 μm), CA1 and DG region (scale bar = 50 μm); (F) The mean fluorescence intensity of GFAP in CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice); (G) The number of GFAP + astrocytes CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice); (H) The mean fluorescence intensity of VGAT in CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice). Normal means sham operated VGAT‐CHR2‐EYFP mice administrated with solvent at 0.1 mL/10 g; Control means VGAT‐CHR2‐EYFP epileptic mice administrated with solvent at 0.1 mL/10 g; TPL means VGAT‐CHR2‐EYFP epileptic mice administrated with TPL at 50 μg/kg. Data are presented as mean ± SEM. Kruskal‐Wallis test was used for D. * p < 0.05, **** p < 0.0001 compared with Normal. # p < 0.05 compared with Control.
    Figure Legend Snippet: TPL enhanced GABAergic “braking effect” in KA mouse model of epilepsy. (A) Schematic diagram of optogenetical stimulation and microelectrode recording on KA model; (B) Clusters view and waveform of recorded neurons (left); autocorrelation of recorded neurons (middle); histological image showing the placement of electrode and optic fiber in dorsal hippocampal DG for extracellular recording (right, Blue‐DAPI); (C) Peri‐event raster histograms of the event‐related response of neurons to optogenetical stimulation; (D) The duration of the light‐induced “braking effect” (Normal, n = 11 cells; Control, n = 10 cells; TPL, n = 11 cells). (E) Example images showing co‐localization of VGAT‐EYFP with astrocytes (GFAP) in hippocampus (scale bar = 200 μm), CA1 and DG region (scale bar = 50 μm); (F) The mean fluorescence intensity of GFAP in CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice); (G) The number of GFAP + astrocytes CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice); (H) The mean fluorescence intensity of VGAT in CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice). Normal means sham operated VGAT‐CHR2‐EYFP mice administrated with solvent at 0.1 mL/10 g; Control means VGAT‐CHR2‐EYFP epileptic mice administrated with solvent at 0.1 mL/10 g; TPL means VGAT‐CHR2‐EYFP epileptic mice administrated with TPL at 50 μg/kg. Data are presented as mean ± SEM. Kruskal‐Wallis test was used for D. * p < 0.05, **** p < 0.0001 compared with Normal. # p < 0.05 compared with Control.

    Techniques Used: Control, Fluorescence, Solvent

    TPL reverses astrocytic and GABAergic neuronal dysregulation in the KA model. (A) Representative WB results of GFAP expression and related quantitative statistical plots. (B) Representative WB results of GAD65/67 expression and related quantitative statistical plots. (C) 3D reconstructions of GFAP + astrocytes and VGAT + GABAergic neurons (scale bar = 10 μm); (D) The total volume of GFAP + astrocytes (Normal, n = 6 fields; Control, n = 5 fields; TPL, n = 5 fields). (E) The volume of single GFAP + astrocytes (Normal, n = 6 cells; Control, n = 5 cells; TPL, n = 5 cells). (F) The total volume of VGAT + GABAergic neurons (Normal, n = 6 fields; Control, n = 6 fields; TPL, n = 6 fields). Normal means sham‐operated VGAT‐CHR2‐EYFP mice administrated with solvent at 0.1 mL/10 g; Control means VGAT‐CHR2‐EYFP epileptic mice administrated with solvent at 0.1 mL/10 g; TPL means VGAT‐CHR2‐EYFP epileptic mice administrated with TPL at 50 μg/kg. Data are presented as mean ± SEM. One‐way ANOVA (with Tukey test for post hoc comparison) was used for A‐B and D‐F. * p < 0.05, *** p < 0.001 compared with Normal. # p < 0.05, ## p < 0.01, #### p < 0.0001 compared with Control.
    Figure Legend Snippet: TPL reverses astrocytic and GABAergic neuronal dysregulation in the KA model. (A) Representative WB results of GFAP expression and related quantitative statistical plots. (B) Representative WB results of GAD65/67 expression and related quantitative statistical plots. (C) 3D reconstructions of GFAP + astrocytes and VGAT + GABAergic neurons (scale bar = 10 μm); (D) The total volume of GFAP + astrocytes (Normal, n = 6 fields; Control, n = 5 fields; TPL, n = 5 fields). (E) The volume of single GFAP + astrocytes (Normal, n = 6 cells; Control, n = 5 cells; TPL, n = 5 cells). (F) The total volume of VGAT + GABAergic neurons (Normal, n = 6 fields; Control, n = 6 fields; TPL, n = 6 fields). Normal means sham‐operated VGAT‐CHR2‐EYFP mice administrated with solvent at 0.1 mL/10 g; Control means VGAT‐CHR2‐EYFP epileptic mice administrated with solvent at 0.1 mL/10 g; TPL means VGAT‐CHR2‐EYFP epileptic mice administrated with TPL at 50 μg/kg. Data are presented as mean ± SEM. One‐way ANOVA (with Tukey test for post hoc comparison) was used for A‐B and D‐F. * p < 0.05, *** p < 0.001 compared with Normal. # p < 0.05, ## p < 0.01, #### p < 0.0001 compared with Control.

    Techniques Used: Expressing, Control, Solvent, Comparison



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    Jackson Laboratory rosa26-enhanced yellow fluorescent protein (eyfp) cre-reporter mice
    TPL enhanced GABAergic “braking effect” in KA mouse model of epilepsy. (A) Schematic diagram of optogenetical stimulation and microelectrode recording on KA model; (B) Clusters view and waveform of recorded neurons (left); autocorrelation of recorded neurons (middle); histological image showing the placement of electrode and optic fiber in dorsal hippocampal DG for extracellular recording (right, Blue‐DAPI); (C) Peri‐event raster histograms of the event‐related response of neurons to optogenetical stimulation; (D) The duration of the light‐induced “braking effect” (Normal, n = 11 cells; Control, n = 10 cells; TPL, n = 11 cells). (E) Example images showing co‐localization of <t>VGAT‐EYFP</t> with astrocytes (GFAP) in hippocampus (scale bar = 200 μm), CA1 and DG region (scale bar = 50 μm); (F) The mean fluorescence intensity of GFAP in CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice); (G) The number of GFAP + astrocytes CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice); (H) The mean fluorescence intensity of VGAT in CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice). Normal means sham operated <t>VGAT‐CHR2‐EYFP</t> mice administrated with solvent at 0.1 mL/10 g; Control means VGAT‐CHR2‐EYFP epileptic mice administrated with solvent at 0.1 mL/10 g; TPL means VGAT‐CHR2‐EYFP epileptic mice administrated with TPL at 50 μg/kg. Data are presented as mean ± SEM. Kruskal‐Wallis test was used for D. * p < 0.05, **** p < 0.0001 compared with Normal. # p < 0.05 compared with Control.
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    TPL enhanced GABAergic “braking effect” in KA mouse model of epilepsy. (A) Schematic diagram of optogenetical stimulation and microelectrode recording on KA model; (B) Clusters view and waveform of recorded neurons (left); autocorrelation of recorded neurons (middle); histological image showing the placement of electrode and optic fiber in dorsal hippocampal DG for extracellular recording (right, Blue‐DAPI); (C) Peri‐event raster histograms of the event‐related response of neurons to optogenetical stimulation; (D) The duration of the light‐induced “braking effect” (Normal, n = 11 cells; Control, n = 10 cells; TPL, n = 11 cells). (E) Example images showing co‐localization of VGAT‐EYFP with astrocytes (GFAP) in hippocampus (scale bar = 200 μm), CA1 and DG region (scale bar = 50 μm); (F) The mean fluorescence intensity of GFAP in CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice); (G) The number of GFAP + astrocytes CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice); (H) The mean fluorescence intensity of VGAT in CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice). Normal means sham operated VGAT‐CHR2‐EYFP mice administrated with solvent at 0.1 mL/10 g; Control means VGAT‐CHR2‐EYFP epileptic mice administrated with solvent at 0.1 mL/10 g; TPL means VGAT‐CHR2‐EYFP epileptic mice administrated with TPL at 50 μg/kg. Data are presented as mean ± SEM. Kruskal‐Wallis test was used for D. * p < 0.05, **** p < 0.0001 compared with Normal. # p < 0.05 compared with Control.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: Triptolide Inhibits Epileptic Seizures by Rescuing the Neuroinflammation‐Related GABAergic Dysfunction in Mice

    doi: 10.1111/cns.70586

    Figure Lengend Snippet: TPL enhanced GABAergic “braking effect” in KA mouse model of epilepsy. (A) Schematic diagram of optogenetical stimulation and microelectrode recording on KA model; (B) Clusters view and waveform of recorded neurons (left); autocorrelation of recorded neurons (middle); histological image showing the placement of electrode and optic fiber in dorsal hippocampal DG for extracellular recording (right, Blue‐DAPI); (C) Peri‐event raster histograms of the event‐related response of neurons to optogenetical stimulation; (D) The duration of the light‐induced “braking effect” (Normal, n = 11 cells; Control, n = 10 cells; TPL, n = 11 cells). (E) Example images showing co‐localization of VGAT‐EYFP with astrocytes (GFAP) in hippocampus (scale bar = 200 μm), CA1 and DG region (scale bar = 50 μm); (F) The mean fluorescence intensity of GFAP in CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice); (G) The number of GFAP + astrocytes CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice); (H) The mean fluorescence intensity of VGAT in CA1 and DG region (Normal, n = 3 mice; Control, n = 3 mice; TPL, n = 3 mice). Normal means sham operated VGAT‐CHR2‐EYFP mice administrated with solvent at 0.1 mL/10 g; Control means VGAT‐CHR2‐EYFP epileptic mice administrated with solvent at 0.1 mL/10 g; TPL means VGAT‐CHR2‐EYFP epileptic mice administrated with TPL at 50 μg/kg. Data are presented as mean ± SEM. Kruskal‐Wallis test was used for D. * p < 0.05, **** p < 0.0001 compared with Normal. # p < 0.05 compared with Control.

    Article Snippet: C57BL/6 mice and vesicular GABA transporter (VGAT)‐Channelrhodopsin 2 (ChR2)‐enhanced Yellow Fluorescent Protein (eYFP) mice (VGAT‐ChR2‐eYFP mice; No. 014548) were reared as previously described and were genotyped according to the protocols promulgated by the Jackson Laboratory.

    Techniques: Control, Fluorescence, Solvent

    TPL reverses astrocytic and GABAergic neuronal dysregulation in the KA model. (A) Representative WB results of GFAP expression and related quantitative statistical plots. (B) Representative WB results of GAD65/67 expression and related quantitative statistical plots. (C) 3D reconstructions of GFAP + astrocytes and VGAT + GABAergic neurons (scale bar = 10 μm); (D) The total volume of GFAP + astrocytes (Normal, n = 6 fields; Control, n = 5 fields; TPL, n = 5 fields). (E) The volume of single GFAP + astrocytes (Normal, n = 6 cells; Control, n = 5 cells; TPL, n = 5 cells). (F) The total volume of VGAT + GABAergic neurons (Normal, n = 6 fields; Control, n = 6 fields; TPL, n = 6 fields). Normal means sham‐operated VGAT‐CHR2‐EYFP mice administrated with solvent at 0.1 mL/10 g; Control means VGAT‐CHR2‐EYFP epileptic mice administrated with solvent at 0.1 mL/10 g; TPL means VGAT‐CHR2‐EYFP epileptic mice administrated with TPL at 50 μg/kg. Data are presented as mean ± SEM. One‐way ANOVA (with Tukey test for post hoc comparison) was used for A‐B and D‐F. * p < 0.05, *** p < 0.001 compared with Normal. # p < 0.05, ## p < 0.01, #### p < 0.0001 compared with Control.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: Triptolide Inhibits Epileptic Seizures by Rescuing the Neuroinflammation‐Related GABAergic Dysfunction in Mice

    doi: 10.1111/cns.70586

    Figure Lengend Snippet: TPL reverses astrocytic and GABAergic neuronal dysregulation in the KA model. (A) Representative WB results of GFAP expression and related quantitative statistical plots. (B) Representative WB results of GAD65/67 expression and related quantitative statistical plots. (C) 3D reconstructions of GFAP + astrocytes and VGAT + GABAergic neurons (scale bar = 10 μm); (D) The total volume of GFAP + astrocytes (Normal, n = 6 fields; Control, n = 5 fields; TPL, n = 5 fields). (E) The volume of single GFAP + astrocytes (Normal, n = 6 cells; Control, n = 5 cells; TPL, n = 5 cells). (F) The total volume of VGAT + GABAergic neurons (Normal, n = 6 fields; Control, n = 6 fields; TPL, n = 6 fields). Normal means sham‐operated VGAT‐CHR2‐EYFP mice administrated with solvent at 0.1 mL/10 g; Control means VGAT‐CHR2‐EYFP epileptic mice administrated with solvent at 0.1 mL/10 g; TPL means VGAT‐CHR2‐EYFP epileptic mice administrated with TPL at 50 μg/kg. Data are presented as mean ± SEM. One‐way ANOVA (with Tukey test for post hoc comparison) was used for A‐B and D‐F. * p < 0.05, *** p < 0.001 compared with Normal. # p < 0.05, ## p < 0.01, #### p < 0.0001 compared with Control.

    Article Snippet: C57BL/6 mice and vesicular GABA transporter (VGAT)‐Channelrhodopsin 2 (ChR2)‐enhanced Yellow Fluorescent Protein (eYFP) mice (VGAT‐ChR2‐eYFP mice; No. 014548) were reared as previously described and were genotyped according to the protocols promulgated by the Jackson Laboratory.

    Techniques: Expressing, Control, Solvent, Comparison