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  • 93
    Thermo Fisher anti gaba
    GABAergic population in cortical cultures at DIV15 . Confocal microscopical analysis of double immunofluorescence staining for <t>MAP2</t> (neuronal marker, red signal) and <t>GABA</t> (green signal). In (A,D) MAP2 labelling shows the distribution of neuronal cells in clusters (arrows) in two sampled fields, where GABA immunocytochemistry (B,E) selects inhibitory neurons (yellow signal in merge, C and F ). Large GABAergic cells (green arrows) are preferentially localized among clusters, whereas small GABAergic cells (green arrowheads) lie also inside these neuronal groups. Scale bar: 67 μm.
    Anti Gaba, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 93/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore anti gaba stainings
    Depletion of dMB and vlMB GABAn in the Mgn −/− Mash −/− mice occurred through GABAergic identity failure. (A) Immunohistochemical staining of BrdU on coronal sections showing the distribution of BrdU + cells in the developing dMB and vMB of wild-type (WT) and double mutant mice ( −−/−− ). (B) Neuronal cell density and cytoarchitectural analysis on the coronal sections of E12.5 embryos using NeuN and the Ca 2+ -binding proteins <t>Calretinin</t> and Calbindin, respectively. There were no significant difference between mean WT and double mutant (NeuN: dorsal WT = 64.22±2.08; dorsal −−/−− = 61.33±2.69; n = 18; p = 0.40. Medial WT = 52.28±3.60; medial −−/−− = 56.72±1.97; n = 18; p = 0.29. Ventrolateral WT = 46.44±2.36; ventrolateral −−/−− = 43.67±2.52; n = 18; p = 0.43); (Calbindin: dorsal WT = 43.28±6.20; dorsal −−/−− = 37.50±5.54; n = 18; p = 0.49. Medial WT = 52.22±5.32; medial −−/−− = 46.56±2.69; n = 18; p = 0.35. Ventrolateral WT = 47.39±3.19; ventrolateral −−/−− = 46.17±3.92; n = 18; p = 0.81). (C) Lac Z staining of coronal sections from double mutants and controls at E12.5; C2 and C4 show prolonged staining times. Owing to the long half-life of lacZ protein, signal can also be seen in the intermediate and mantle zones. (D) Immunohistochemical staining with anti-LacZ (in green) and anti-BRN3a ( Pou4f1 _MGI) (in red, as a morphological marker) antibodies that shows radial migration of <t>GABA-defective</t> neurons through the intermediate zone (IZ) toward the mantle zone (MZ) in double mutants. Scale bars: 100 μm in A, and 200 μm in B-C.
    Anti Gaba Stainings, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Abcam anti gaba
    Schematics Summarize the Major Findings of the Current Study Accumulation of htau (green) in hippocampus increases miR-92a, which in turn suppresses the translation of <t>vGAT</t> (blue) by binding to its 3′ UTR, reduces vGAT-mediated intracellular <t>GABA</t> (purple) loading into the inhibitory vesicles, decreases GABA release at the axon terminals, and thus inhibits the GABAergic functions by suppressing eIPSP and arresting γ oscillation activity in hippocampal networks, and finally causes anxiety behaviors. Upregulating GABA tones by intraperitoneal injection of midazolam, photostimulating or overexpressing vGAT, and blocking miR92a by antagomir can rescue the htau-induced GABAergic dysfunctions and attenuate the anxiety behaviors.
    Anti Gaba, supplied by Abcam, used in various techniques. Bioz Stars score: 94/100, based on 33 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Abcam rabbit anti gaba
    Direct conversion of MEFs into GABAergic neurons. ( A ) Phase-contrast microscopic images of the induced cells derived from MEFs and immunostaing with <t>Tuj-1</t> and <t>GABA</t> antibodies of the induced cells at 1–3 weeks. Scale bar, 50μm. ( B ) Quantification of Tuj-1 positive cells and GABA positive cells: The percentages of Tuj-1 positive cells over the total cells, and GABA positive cells over Tuj-1 positive cells. Five to 6 representative visual fields for each of the groups were counted. ( C ) Quantitative real-time PCR analysis of the mRNA levels of Tuj-1, NeuN, Neurofilament L (NF-L), GAT1 and GABA receptors from MEF-derived cells derived from MEFs at 1–3 weeks. MEFs in normal cultures were used as control group, Con. The level of mRNA in MEFs was set as 1. Data were collected from at least 3 separate experiments and are shown as means ± standard deviation (SD). * P
    Rabbit Anti Gaba, supplied by Abcam, used in various techniques. Bioz Stars score: 91/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    89
    Abcam guinea pig anti gaba
    C1q immunoreactivity in inhibitory neurons. A , B , In lightly fixed tissue, our new rabbit anti-mouse C1q monoclonal antibody enabled the additional detection of C1q signals in larger cell bodies (neurons, E–G ), in distinct areas of the brain. These C1q-positive neurons were detected from ∼1 month of age on and aging-independent thereafter (6-month-old shown). C1q-positive neurons were detected in the hippocampus, thalamus, striatum, and midbrain. The exact distribution of C1q-positive neurons visible varied slightly dependent on the location of the slices within the brain. A , Detection of C1q-positive neurons in the hippocampus, thalamus, and midbrain (substantia nigra area). B , Detection of C1q-positive neurons in the thalamus and striatum (mainly globus pallidus). C , In the adult murine hippocampus, C1q immunoreactivity was detected in the neuropil and in both neurons (arrowhead) and microglia (arrow). D , Confocal microscopy colocalization with GFP-immunoreactivity ( Cx3CR1-GFP +/− mice) confirmed that C1q was detected in microglia cell bodies (arrowhead) and processes (arrow). E , Confocal microscopy colocalization with <t>NeuN-immunoreactivity</t> confirmed that C1q was also localized to the cytoplasm of some neurons. F , Confocal microscopy colocalization with <t>GABA-immunoreactivity</t> confirmed that C1q was localized to inhibitory neurons (arrow) but that C1q was not detected in all GABA-positive neurons (arrowheads). G , C1q-positive neurons represent a subset of inhibitory neurons. Neuronal C1q signals exclusively colocalize (arrow) with many but not all GABA-positive neurons in the murine hippocampus (arrowheads: GABA+/C1q− neurons). H , Quantification of C1q-GABA-positive neurons in the murine hippocampus confirmed that C1q-positive neurons represent a subset of inhibitory neurons. At both 3 and 24 months of age all C1q-positive neurons were GABAergic ( n = 3 animals/age). I , J , C1q signals, including signals in neurons, are specific in the wild-type adult hippocampus ( I ), no signals were detected in the C1q-deficient littermate control ( J ). Scale bars: A , B , G , I , J , 500 μm; C , 100 μm; D , E , 10 μm; F , 20 μm.
    Guinea Pig Anti Gaba, supplied by Abcam, used in various techniques. Bioz Stars score: 89/100, based on 37 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore anti gaba polyclonal ab
    Phenotypic characterization of the superficial and deep strata of the MZ. A–F , En face confocal sections taken through superficial(1–7μm; A–C ) and deep (8–15μm; D–F ) levels of the E15 MZ. Cortical flaps were triple-stained for CellTracker Green (green), CR-50 (blue), and <t>GABA,</t> calretinin, calbindin, or <t>Dlx-2</t> (red). Most of the cells in the superficial stratum of the MZ colabel for calretinin and CR-50 ( A ). These CR-50 cells, however, do not colabel with GABA ( B ) or with Dlx-2 ( C ). Rather, long axonal projections labeled with GABA, such as the one shown in B . Clusters of Dlx-2-labeled cells ( C ) did appear in this superficial stratum, but these cells did not colabel with CR-50. Tangentially oriented cells in the deep stratum of the MZ labeled with calbindin ( D ), GABA ( E ), and Dlx-2 ( F ). The deep stratum was relatively devoid of CR-50 labeling ( D–F ). Scale bars ( C, F ), 50 μm.
    Anti Gaba Polyclonal Ab, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Millipore mouse anti gaba
    CRH+ EPL interneurons are predominantly generated postnatally (a) Expression pattern of Crh-Cre; Rosa lsl-tdTomato/+ mice at P7, P14, and P30 co-stained with the interneuron marker <t>Parvalbumin</t> (scale bar 30 µm). (b) Quantification of the expression of Parvalbumin and CRH+ interneurons in the EPL between P0 and P60. Confocal immunohistochemistry image of (c) <t>GABA</t> on Crh-Cre; Rosa lsl-tdTomato/+ EPL tissue at P14 (scale bar 20 µm), and (d) NeuN at P30 (scale bar 30 µm). (e) Quantification of the expression of NeuN and CRH+ interneurons at P14 and P30. (f) Confocal image of Calretinin in CRH+ EPL interneurons at P30 (scale bar 40 µm). (g) Quantification of the expression of Calretinin and CRH+ interneurons at P14 and P30. (h) Example confocal image of EdU expression in CRH+ neurons pulsed at P7 (scale bar 40 m). (i) Quantification of the percentage of CRH+ EPL interneurons born between E16.5 and P30 (* p
    Mouse Anti Gaba, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 159 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ImmunoStar polyclonal anti gaba
    CRH+ EPL interneurons are predominantly generated postnatally (a) Expression pattern of Crh-Cre; Rosa lsl-tdTomato/+ mice at P7, P14, and P30 co-stained with the interneuron marker <t>Parvalbumin</t> (scale bar 30 µm). (b) Quantification of the expression of Parvalbumin and CRH+ interneurons in the EPL between P0 and P60. Confocal immunohistochemistry image of (c) <t>GABA</t> on Crh-Cre; Rosa lsl-tdTomato/+ EPL tissue at P14 (scale bar 20 µm), and (d) NeuN at P30 (scale bar 30 µm). (e) Quantification of the expression of NeuN and CRH+ interneurons at P14 and P30. (f) Confocal image of Calretinin in CRH+ EPL interneurons at P30 (scale bar 40 µm). (g) Quantification of the expression of Calretinin and CRH+ interneurons at P14 and P30. (h) Example confocal image of EdU expression in CRH+ neurons pulsed at P7 (scale bar 40 m). (i) Quantification of the percentage of CRH+ EPL interneurons born between E16.5 and P30 (* p
    Polyclonal Anti Gaba, supplied by ImmunoStar, used in various techniques. Bioz Stars score: 86/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Abcam gamma aminobutyric acid
    CRH+ EPL interneurons are predominantly generated postnatally (a) Expression pattern of Crh-Cre; Rosa lsl-tdTomato/+ mice at P7, P14, and P30 co-stained with the interneuron marker <t>Parvalbumin</t> (scale bar 30 µm). (b) Quantification of the expression of Parvalbumin and CRH+ interneurons in the EPL between P0 and P60. Confocal immunohistochemistry image of (c) <t>GABA</t> on Crh-Cre; Rosa lsl-tdTomato/+ EPL tissue at P14 (scale bar 20 µm), and (d) NeuN at P30 (scale bar 30 µm). (e) Quantification of the expression of NeuN and CRH+ interneurons at P14 and P30. (f) Confocal image of Calretinin in CRH+ EPL interneurons at P30 (scale bar 40 µm). (g) Quantification of the expression of Calretinin and CRH+ interneurons at P14 and P30. (h) Example confocal image of EdU expression in CRH+ neurons pulsed at P7 (scale bar 40 m). (i) Quantification of the percentage of CRH+ EPL interneurons born between E16.5 and P30 (* p
    Gamma Aminobutyric Acid, supplied by Abcam, used in various techniques. Bioz Stars score: 93/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    GABAergic population in cortical cultures at DIV15 . Confocal microscopical analysis of double immunofluorescence staining for MAP2 (neuronal marker, red signal) and GABA (green signal). In (A,D) MAP2 labelling shows the distribution of neuronal cells in clusters (arrows) in two sampled fields, where GABA immunocytochemistry (B,E) selects inhibitory neurons (yellow signal in merge, C and F ). Large GABAergic cells (green arrows) are preferentially localized among clusters, whereas small GABAergic cells (green arrowheads) lie also inside these neuronal groups. Scale bar: 67 μm.

    Journal: Frontiers in Neural Circuits

    Article Title: Orchestration of "Presto" and "Largo" Synchrony in Up-Down Activity of Cortical Networks

    doi: 10.3389/fncir.2010.00011

    Figure Lengend Snippet: GABAergic population in cortical cultures at DIV15 . Confocal microscopical analysis of double immunofluorescence staining for MAP2 (neuronal marker, red signal) and GABA (green signal). In (A,D) MAP2 labelling shows the distribution of neuronal cells in clusters (arrows) in two sampled fields, where GABA immunocytochemistry (B,E) selects inhibitory neurons (yellow signal in merge, C and F ). Large GABAergic cells (green arrows) are preferentially localized among clusters, whereas small GABAergic cells (green arrowheads) lie also inside these neuronal groups. Scale bar: 67 μm.

    Article Snippet: Overnight incubation at 4°C in a solution, containing anti-GABA and either anti-MAP2 (see Figure and Figure S1E in Supplementary Material) or anti-GFAP (see Figure S1D in Supplementary Material) antibodies, was followed by incubation in a mixture of appropriate secondary antibodies conjugated to different fluorochromes, such as Alexa-488 conjugated goat anti-rabbit (1:200, Molecular Probes) for GABA immunolabelling (green fluorescence in Figure and Figures S1D,E in Supplementary Material) and indocarbocyanine Cy3-conjugated donkey anti-mouse (1:400, Jackson ImmunoResearch) for MAP2 and GFAP immunolocalizations (red fluorescence in Figure and Figures S1D,E in Supplementary Material).

    Techniques: Double Immunofluorescence Staining, Marker, Immunocytochemistry

    Spike responses of CA1 neuron populations to combinatorial DG inputs: calcium imaging. A , Experimental design to examine the activity flow through hippocampal polysynaptic networks. Two stimulating electrodes were placed on the infrapyramidal (stim A) and suprapyramidal blades (stim B) of the DG granule cell layer. An incision was made along the thick black lines to anatomically isolate the two stimulation sites. Stim A, stim B, and simultaneous stim A B were given 10 times each, and the spikes of CA1 neurons were monitored using fMCI. B , Simultaneous cell-attached recording and calcium imaging revealed that spikes elicited transient calcium elevations in the soma. C , Representative spike responses of 67 CA1 neurons to a single stim A. Calcium traces were superimposed onto an OGB1 fluorescence image (top). Neurons that fired are indicated by red circles in the bottom cell map. D , Slices were post hoc immunolabeled with NeuN and GABA, and only PCs were analyzed. E , Firing patterns of 183 CA1 PCs in a slice in response to stim A (top), stim B (middle), and stim A B (bottom) (10 trials each). The mean firing probability across 10 trials (mean) is shown in the bottom rastergrams and the right cell map in a pseudocolor scale.

    Journal: The Journal of Neuroscience

    Article Title: Hippocampal Polysynaptic Computation

    doi: 10.1523/JNEUROSCI.1920-11.2011

    Figure Lengend Snippet: Spike responses of CA1 neuron populations to combinatorial DG inputs: calcium imaging. A , Experimental design to examine the activity flow through hippocampal polysynaptic networks. Two stimulating electrodes were placed on the infrapyramidal (stim A) and suprapyramidal blades (stim B) of the DG granule cell layer. An incision was made along the thick black lines to anatomically isolate the two stimulation sites. Stim A, stim B, and simultaneous stim A B were given 10 times each, and the spikes of CA1 neurons were monitored using fMCI. B , Simultaneous cell-attached recording and calcium imaging revealed that spikes elicited transient calcium elevations in the soma. C , Representative spike responses of 67 CA1 neurons to a single stim A. Calcium traces were superimposed onto an OGB1 fluorescence image (top). Neurons that fired are indicated by red circles in the bottom cell map. D , Slices were post hoc immunolabeled with NeuN and GABA, and only PCs were analyzed. E , Firing patterns of 183 CA1 PCs in a slice in response to stim A (top), stim B (middle), and stim A B (bottom) (10 trials each). The mean firing probability across 10 trials (mean) is shown in the bottom rastergrams and the right cell map in a pseudocolor scale.

    Article Snippet: The slices were then treated with primary antibodies against NeuN (mouse, 1:400; MAB377, Millipore Bioscience Research Reagents) and GABA (rabbit, 1:1000; A2052, Sigma-Aldrich) overnight at 4°C and with secondary anti-mouse IgG Alexa Fluor 488 (1:400; A11001, Invitrogen) and anti-rabbit IgG Alexa Fluor 594 (1:400; , Invitrogen) antibodies in 2% goat serum for 6 h at room temperature.

    Techniques: Imaging, Activity Assay, Flow Cytometry, Fluorescence, Immunolabeling

    Depletion of dMB and vlMB GABAn in the Mgn −/− Mash −/− mice occurred through GABAergic identity failure. (A) Immunohistochemical staining of BrdU on coronal sections showing the distribution of BrdU + cells in the developing dMB and vMB of wild-type (WT) and double mutant mice ( −−/−− ). (B) Neuronal cell density and cytoarchitectural analysis on the coronal sections of E12.5 embryos using NeuN and the Ca 2+ -binding proteins Calretinin and Calbindin, respectively. There were no significant difference between mean WT and double mutant (NeuN: dorsal WT = 64.22±2.08; dorsal −−/−− = 61.33±2.69; n = 18; p = 0.40. Medial WT = 52.28±3.60; medial −−/−− = 56.72±1.97; n = 18; p = 0.29. Ventrolateral WT = 46.44±2.36; ventrolateral −−/−− = 43.67±2.52; n = 18; p = 0.43); (Calbindin: dorsal WT = 43.28±6.20; dorsal −−/−− = 37.50±5.54; n = 18; p = 0.49. Medial WT = 52.22±5.32; medial −−/−− = 46.56±2.69; n = 18; p = 0.35. Ventrolateral WT = 47.39±3.19; ventrolateral −−/−− = 46.17±3.92; n = 18; p = 0.81). (C) Lac Z staining of coronal sections from double mutants and controls at E12.5; C2 and C4 show prolonged staining times. Owing to the long half-life of lacZ protein, signal can also be seen in the intermediate and mantle zones. (D) Immunohistochemical staining with anti-LacZ (in green) and anti-BRN3a ( Pou4f1 _MGI) (in red, as a morphological marker) antibodies that shows radial migration of GABA-defective neurons through the intermediate zone (IZ) toward the mantle zone (MZ) in double mutants. Scale bars: 100 μm in A, and 200 μm in B-C.

    Journal: PLoS ONE

    Article Title: Hairy/Enhancer-of-Split MEGANE and Proneural MASH1 Factors Cooperate Synergistically in Midbrain GABAergic Neurogenesis

    doi: 10.1371/journal.pone.0127681

    Figure Lengend Snippet: Depletion of dMB and vlMB GABAn in the Mgn −/− Mash −/− mice occurred through GABAergic identity failure. (A) Immunohistochemical staining of BrdU on coronal sections showing the distribution of BrdU + cells in the developing dMB and vMB of wild-type (WT) and double mutant mice ( −−/−− ). (B) Neuronal cell density and cytoarchitectural analysis on the coronal sections of E12.5 embryos using NeuN and the Ca 2+ -binding proteins Calretinin and Calbindin, respectively. There were no significant difference between mean WT and double mutant (NeuN: dorsal WT = 64.22±2.08; dorsal −−/−− = 61.33±2.69; n = 18; p = 0.40. Medial WT = 52.28±3.60; medial −−/−− = 56.72±1.97; n = 18; p = 0.29. Ventrolateral WT = 46.44±2.36; ventrolateral −−/−− = 43.67±2.52; n = 18; p = 0.43); (Calbindin: dorsal WT = 43.28±6.20; dorsal −−/−− = 37.50±5.54; n = 18; p = 0.49. Medial WT = 52.22±5.32; medial −−/−− = 46.56±2.69; n = 18; p = 0.35. Ventrolateral WT = 47.39±3.19; ventrolateral −−/−− = 46.17±3.92; n = 18; p = 0.81). (C) Lac Z staining of coronal sections from double mutants and controls at E12.5; C2 and C4 show prolonged staining times. Owing to the long half-life of lacZ protein, signal can also be seen in the intermediate and mantle zones. (D) Immunohistochemical staining with anti-LacZ (in green) and anti-BRN3a ( Pou4f1 _MGI) (in red, as a morphological marker) antibodies that shows radial migration of GABA-defective neurons through the intermediate zone (IZ) toward the mantle zone (MZ) in double mutants. Scale bars: 100 μm in A, and 200 μm in B-C.

    Article Snippet: The primary antibodies were as follows: rabbit anti-β-galactosidase (AbD Serotec #AHP1292; 1:100); mouse anti-BRN3a (Santa Cruz #sc-8429; 1:200); mouse anti-calbindin (Swant #300; 1:500); rabbit anti-calretinin (Swant #7699/4; 1:2000); rabbit anti-cleaved caspase-3 (cCASP3; Cell Signalling #9661; 1:1200); rabbit anti-GABA (Sigma #A2052; 1:300); mouse anti-NeuN (Chemicon #MAB377; 1:1000); mouse anti-NKX2-2 (DSHB #74.5A5-c; 1:250); rabbit anti-phospho-histone H3 (pHH3; Upstate #06–570; 1:500); and rabbit anti-tyrosine hydroxylase (TH; Merck Millipore #AB152; 1:150).

    Techniques: Mouse Assay, Immunohistochemistry, Staining, Mutagenesis, Binding Assay, Marker, Migration

    Expression of GAD67 mRNA and GABA in GAD67 −/− and +/+ brain and head region. ( A – C ) In situ hybridization of frontal sections of E14.5 mouse heads using a GAD67 probe. ( A and C ) GAD67 +/+. o, olfactory bulb; n, nasal septa; p, palate; t, tongue. C shows the olfactory bulb at higher magnification. ( B ) GAD67 −/−; counterstained with methyl green. GAD67 signals are found only in neural tissue (olfactory bulb) of GAD67 +/+ or +/− mice. ( D – F ) Hematoxylin-eosin staining of P0.5 GAD67 −/− brain. ( D ) Hippocampus. ( E ) Cerebral cortex. ( F ) Cerebellum. ( G – J ) Immunohistochemistry with anti-GABA antibody (Sigma). ( G and H ) Cerebral cortex. ( I and J ) Cerebellum. ( G and I ) P0.5 wild-type mice. ( H and J ) P0.5 null mutant mice. Arrows in J indicate GABA-positive neurons in the deep part of GAD67 −/− cerebellum. (Bar in J = 500 μm for A , B , and D – F ; 200 μm for G – J ; and 100 μm for C .)

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Cleft palate and decreased brain ?-aminobutyric acid in mice lacking the 67-kDa isoform of glutamic acid decarboxylase

    doi:

    Figure Lengend Snippet: Expression of GAD67 mRNA and GABA in GAD67 −/− and +/+ brain and head region. ( A – C ) In situ hybridization of frontal sections of E14.5 mouse heads using a GAD67 probe. ( A and C ) GAD67 +/+. o, olfactory bulb; n, nasal septa; p, palate; t, tongue. C shows the olfactory bulb at higher magnification. ( B ) GAD67 −/−; counterstained with methyl green. GAD67 signals are found only in neural tissue (olfactory bulb) of GAD67 +/+ or +/− mice. ( D – F ) Hematoxylin-eosin staining of P0.5 GAD67 −/− brain. ( D ) Hippocampus. ( E ) Cerebral cortex. ( F ) Cerebellum. ( G – J ) Immunohistochemistry with anti-GABA antibody (Sigma). ( G and H ) Cerebral cortex. ( I and J ) Cerebellum. ( G and I ) P0.5 wild-type mice. ( H and J ) P0.5 null mutant mice. Arrows in J indicate GABA-positive neurons in the deep part of GAD67 −/− cerebellum. (Bar in J = 500 μm for A , B , and D – F ; 200 μm for G – J ; and 100 μm for C .)

    Article Snippet: Immunohistochemistry with anti-GABA antiserum (A-2052, Sigma) was performed using Vectastain ABC kit (Vector Laboratories).

    Techniques: Expressing, In Situ Hybridization, Mouse Assay, Staining, Immunohistochemistry, Mutagenesis

    Lamination defects and loss of mitral cells in the OB in Rb−/− mice during late development . Immunostaining against PSA-NCAM performed on sagittal sections (A–B′) at E17.5 and showing aberrant lamination inside the OB, primarily affecting the IPL, ML, and EPL in the absence of Rb. (C–E′) Double staining against PSA-NCAM and GABA (gamma-amino-butyric acid) showing scattered GABAergic interneurons inside the IPL and ML with loss of clear boundaries between these layers in Rb−/− vs. Rb+/− mice (arrowheads in C′–F ′). * in B ′ depicts the presence of axonal guidance defects inside the ONL. (F,F′) are higher magnification images of regions shown in (E,E') , respectively. (G–H′) Staining with Reelin, marker of the proximal dendrites of mitral cells, performed on sagittal sections at E15.5 (G,G′) and P0 (H,H′) and showing gradual degeneration of the ML in Rb−/− mice compared with Rb+/− mice at birth. (I) Graph depicting the numbers of GABAergic neurons mislocalized in the IPL and of Reelin-positive cells in the ML in both genotypes t -tests, * p

    Journal: Frontiers in Molecular Neuroscience

    Article Title: Role of Rb during Neurogenesis and Axonal Guidance in the Developing Olfactory System

    doi: 10.3389/fnmol.2016.00081

    Figure Lengend Snippet: Lamination defects and loss of mitral cells in the OB in Rb−/− mice during late development . Immunostaining against PSA-NCAM performed on sagittal sections (A–B′) at E17.5 and showing aberrant lamination inside the OB, primarily affecting the IPL, ML, and EPL in the absence of Rb. (C–E′) Double staining against PSA-NCAM and GABA (gamma-amino-butyric acid) showing scattered GABAergic interneurons inside the IPL and ML with loss of clear boundaries between these layers in Rb−/− vs. Rb+/− mice (arrowheads in C′–F ′). * in B ′ depicts the presence of axonal guidance defects inside the ONL. (F,F′) are higher magnification images of regions shown in (E,E') , respectively. (G–H′) Staining with Reelin, marker of the proximal dendrites of mitral cells, performed on sagittal sections at E15.5 (G,G′) and P0 (H,H′) and showing gradual degeneration of the ML in Rb−/− mice compared with Rb+/− mice at birth. (I) Graph depicting the numbers of GABAergic neurons mislocalized in the IPL and of Reelin-positive cells in the ML in both genotypes t -tests, * p

    Article Snippet: The following primary antibodies were used: mouse anti-BrdU (1:50; BD Pharmingen), rat anti-BrdU (1:150; Accurate), mouse anti-PSA-NCAM (1:1000; Chemicon), rabbit anti-OMP (1:300; Abcam), rabbit anti-Tuj1 (1:5000; Covance), mouse anti-Bax (6A7) (1:300; Abcam), mouse anti-AC3 (1:500; Cell Signaling), goat anti-Sox2 (1:150, Santa Cruz), rabbit anti-Ki67 (1:500, Cell Marque), goat anti-NeuroD1 (1:100, Santa Cruz), Rabbit anti-PH3 (1:250, Millipore), mouse anti-Reelin (1:750, Calbiochem) and rabbit anti-GABA (1:2000, Sigma).

    Techniques: Mouse Assay, Immunostaining, Double Staining, Staining, Marker

    Schematics Summarize the Major Findings of the Current Study Accumulation of htau (green) in hippocampus increases miR-92a, which in turn suppresses the translation of vGAT (blue) by binding to its 3′ UTR, reduces vGAT-mediated intracellular GABA (purple) loading into the inhibitory vesicles, decreases GABA release at the axon terminals, and thus inhibits the GABAergic functions by suppressing eIPSP and arresting γ oscillation activity in hippocampal networks, and finally causes anxiety behaviors. Upregulating GABA tones by intraperitoneal injection of midazolam, photostimulating or overexpressing vGAT, and blocking miR92a by antagomir can rescue the htau-induced GABAergic dysfunctions and attenuate the anxiety behaviors.

    Journal: Molecular Therapy

    Article Title: Correcting miR92a-vGAT-Mediated GABAergic Dysfunctions Rescues Human Tau-Induced Anxiety in Mice

    doi: 10.1016/j.ymthe.2016.10.010

    Figure Lengend Snippet: Schematics Summarize the Major Findings of the Current Study Accumulation of htau (green) in hippocampus increases miR-92a, which in turn suppresses the translation of vGAT (blue) by binding to its 3′ UTR, reduces vGAT-mediated intracellular GABA (purple) loading into the inhibitory vesicles, decreases GABA release at the axon terminals, and thus inhibits the GABAergic functions by suppressing eIPSP and arresting γ oscillation activity in hippocampal networks, and finally causes anxiety behaviors. Upregulating GABA tones by intraperitoneal injection of midazolam, photostimulating or overexpressing vGAT, and blocking miR92a by antagomir can rescue the htau-induced GABAergic dysfunctions and attenuate the anxiety behaviors.

    Article Snippet: The antibodies used for free-floating brain sections are as follows: PT181, PS214, and PS396 (SAB; 1:250); SMI-32 (Biolegend; 1:500); PHF6 and PHF13 (Santa Cruz Biotechnology; 1:80); HT7 (Thermo Scientific; 1:200); CaMKII (Cell Signaling Technology; 1:200); anti-vGAT (Santa Cruz; 1:150); and anti-GABA (Abcam; 1:1,000).

    Techniques: Binding Assay, Activity Assay, Injection, Blocking Assay

    Tau Accumulation Reduces vGAT Protein, Leading to an Impaired Vesicular GABA Loading (A) Reduction of vGAT protein with unchanged vGAT mRNA, truncated vGAT, GAT1, SYN1, SYT1, VAMP2, GAD65, and GAD67 were detected in the extracts of the htau-expressing CA3 subset by western blotting or RT-PCR. Bar graphs show mean ± SEM (*p

    Journal: Molecular Therapy

    Article Title: Correcting miR92a-vGAT-Mediated GABAergic Dysfunctions Rescues Human Tau-Induced Anxiety in Mice

    doi: 10.1016/j.ymthe.2016.10.010

    Figure Lengend Snippet: Tau Accumulation Reduces vGAT Protein, Leading to an Impaired Vesicular GABA Loading (A) Reduction of vGAT protein with unchanged vGAT mRNA, truncated vGAT, GAT1, SYN1, SYT1, VAMP2, GAD65, and GAD67 were detected in the extracts of the htau-expressing CA3 subset by western blotting or RT-PCR. Bar graphs show mean ± SEM (*p

    Article Snippet: The antibodies used for free-floating brain sections are as follows: PT181, PS214, and PS396 (SAB; 1:250); SMI-32 (Biolegend; 1:500); PHF6 and PHF13 (Santa Cruz Biotechnology; 1:80); HT7 (Thermo Scientific; 1:200); CaMKII (Cell Signaling Technology; 1:200); anti-vGAT (Santa Cruz; 1:150); and anti-GABA (Abcam; 1:1,000).

    Techniques: Expressing, Western Blot, Reverse Transcription Polymerase Chain Reaction

    Taltirelin elevated the level of TH in enkephalin-positive neurons in vitro . Double immunolabeling images showed co-localization of tyrosine hydroxylase (TH) with GABA (A) , enkephalin (B) , dynorphin (C) or dopamine transporter (DAT) (D) in control or Taltirelin treated rat primary striatal neurons. N = 3.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: TRH Analog, Taltirelin Improves Motor Function of Hemi-PD Rats Without Inducing Dyskinesia via Sustained Dopamine Stimulating Effect

    doi: 10.3389/fncel.2018.00417

    Figure Lengend Snippet: Taltirelin elevated the level of TH in enkephalin-positive neurons in vitro . Double immunolabeling images showed co-localization of tyrosine hydroxylase (TH) with GABA (A) , enkephalin (B) , dynorphin (C) or dopamine transporter (DAT) (D) in control or Taltirelin treated rat primary striatal neurons. N = 3.

    Article Snippet: Incubate brain slices or cell slides with following primary antibodies overnight at 4°C: anti-DOPA decarboxylase (AADC) antibody (1:250, Abcam, ab3905), anti-dopamine transporter (DAT) antibody (1:50, Santa Cruz, sc-32258), anti-TH antibody (1:750, Abcam, ab129991), anti-MAP2 antibody (1:500, Servicebio, Wuhan), anti-GABA antibody (1:200, Abcam, ab8891), anti-dynorphin antibody (1:50, Santa Cruz, sc-46313), anti-enkephalin (1:100, Abcam, ab150346).

    Techniques: In Vitro, Immunolabeling

    Treatment with VGB inhibited GABA-T expression and reversing the abnormal behaviors caused by Fmr1 KO astrocytes. ( A ) Band image and intensity analysis of GABA-T from cultured astrocytes showed that VGB inhibited GABA-T expression in KO astrocytes. n = 6 wells from three independent experiments. ** p

    Journal: Genes

    Article Title: Imbalance between Glutamate and GABA in Fmr1 Knockout Astrocytes Influences Neuronal Development

    doi: 10.3390/genes7080045

    Figure Lengend Snippet: Treatment with VGB inhibited GABA-T expression and reversing the abnormal behaviors caused by Fmr1 KO astrocytes. ( A ) Band image and intensity analysis of GABA-T from cultured astrocytes showed that VGB inhibited GABA-T expression in KO astrocytes. n = 6 wells from three independent experiments. ** p

    Article Snippet: The following primary antibodies were used: anti-MAP2 (1:1000; Millipore Bioscience Research Reagents, Billerica, MA, USA), anti-PSD95 (postsynaptic density protein 95) (1:2000; Abcam, Cambridge, UK), anti-GluR1 (Glutamate Receptor 1) (1:300; Abcam), anti-MAOB (1:1000; Abcam), anti-GFAP (1:1000; Abcam), anti-GABA-T (1:1000; Abcam), anti-glutaminase (1:1000, Abcam), anti-β-actin (1:10000, Sigma).

    Techniques: Expressing, Cell Culture

    Increased GABA-T and glutaminase, and reduced MAOB expression in Fmr1 KO astrocytes. ( A ) Western blot analysis of GABA-T, glutaminase, and MAOB from cultured astrocytes of WT and KO mice; ( B ) Band intensities were quantified as a percentage of values from WT astrocytes. n = 6 wells from three independent experiments. * p

    Journal: Genes

    Article Title: Imbalance between Glutamate and GABA in Fmr1 Knockout Astrocytes Influences Neuronal Development

    doi: 10.3390/genes7080045

    Figure Lengend Snippet: Increased GABA-T and glutaminase, and reduced MAOB expression in Fmr1 KO astrocytes. ( A ) Western blot analysis of GABA-T, glutaminase, and MAOB from cultured astrocytes of WT and KO mice; ( B ) Band intensities were quantified as a percentage of values from WT astrocytes. n = 6 wells from three independent experiments. * p

    Article Snippet: The following primary antibodies were used: anti-MAP2 (1:1000; Millipore Bioscience Research Reagents, Billerica, MA, USA), anti-PSD95 (postsynaptic density protein 95) (1:2000; Abcam, Cambridge, UK), anti-GluR1 (Glutamate Receptor 1) (1:300; Abcam), anti-MAOB (1:1000; Abcam), anti-GFAP (1:1000; Abcam), anti-GABA-T (1:1000; Abcam), anti-glutaminase (1:1000, Abcam), anti-β-actin (1:10000, Sigma).

    Techniques: Expressing, Western Blot, Cell Culture, Mouse Assay

    Effects of gender, genotype, and drug on γ -aminobutyric acid (GABA) pathway proteins in the cerebral cortex. The levels of GAD65 (a), GABA A α 2 (b), and gephyrin (c) levels normalized to actin levels in the cytoplasmic fractions of female and male cerebral cortices. Female, GAD65: effect of genotype F=6.1, p

    Journal: Neuropsychopharmacology

    Article Title: Gender-Specific Effect of Mthfr Genotype and Neonatal Vigabatrin Interaction on Synaptic Proteins in Mouse Cortex

    doi: 10.1038/npp.2011.52

    Figure Lengend Snippet: Effects of gender, genotype, and drug on γ -aminobutyric acid (GABA) pathway proteins in the cerebral cortex. The levels of GAD65 (a), GABA A α 2 (b), and gephyrin (c) levels normalized to actin levels in the cytoplasmic fractions of female and male cerebral cortices. Female, GAD65: effect of genotype F=6.1, p

    Article Snippet: Membranes were probed with the following primary antibodies: rabbit-anti-GAD65/67 (1 : 5000), rabbit anti-GluR1 (1 : 1000), mouse anti-FMRP (1 : 2500; Chemicon International, Temecula, CA), mouse anti-GABA A, α2 subunit (1 : 1000), mouse anti-reelin (1 : 1000), rabbit anti-Dab1 (1 : 2000; Abcam, Austin, TX), mouse anti-gephyrin (1 : 10 000; Synaptic System, Goettingen, Germany), and mouse anti- β -actin (1 : 10 000; Sigma-Aldrich).

    Techniques:

    Direct conversion of MEFs into GABAergic neurons. ( A ) Phase-contrast microscopic images of the induced cells derived from MEFs and immunostaing with Tuj-1 and GABA antibodies of the induced cells at 1–3 weeks. Scale bar, 50μm. ( B ) Quantification of Tuj-1 positive cells and GABA positive cells: The percentages of Tuj-1 positive cells over the total cells, and GABA positive cells over Tuj-1 positive cells. Five to 6 representative visual fields for each of the groups were counted. ( C ) Quantitative real-time PCR analysis of the mRNA levels of Tuj-1, NeuN, Neurofilament L (NF-L), GAT1 and GABA receptors from MEF-derived cells derived from MEFs at 1–3 weeks. MEFs in normal cultures were used as control group, Con. The level of mRNA in MEFs was set as 1. Data were collected from at least 3 separate experiments and are shown as means ± standard deviation (SD). * P

    Journal: Cell Cycle

    Article Title: Direct conversion of mouse fibroblasts to GABAergic neurons with combined medium without the introduction of transcription factors or miRNAs

    doi: 10.1080/15384101.2015.1060382

    Figure Lengend Snippet: Direct conversion of MEFs into GABAergic neurons. ( A ) Phase-contrast microscopic images of the induced cells derived from MEFs and immunostaing with Tuj-1 and GABA antibodies of the induced cells at 1–3 weeks. Scale bar, 50μm. ( B ) Quantification of Tuj-1 positive cells and GABA positive cells: The percentages of Tuj-1 positive cells over the total cells, and GABA positive cells over Tuj-1 positive cells. Five to 6 representative visual fields for each of the groups were counted. ( C ) Quantitative real-time PCR analysis of the mRNA levels of Tuj-1, NeuN, Neurofilament L (NF-L), GAT1 and GABA receptors from MEF-derived cells derived from MEFs at 1–3 weeks. MEFs in normal cultures were used as control group, Con. The level of mRNA in MEFs was set as 1. Data were collected from at least 3 separate experiments and are shown as means ± standard deviation (SD). * P

    Article Snippet: The following antibodies were used to detect specific proteins: mouse anti-Tuj-1 (Sigma), rabbit anti-GABA (Abcam), rabbit anti-NeuN (Cell Signaling Technology), mouse anti-Neurofilament-L (Cell Signaling Technology), guinea pig anti-GAT1 (Synaptic System) and mouse anti-β-Actin (Sigma).

    Techniques: Derivative Assay, Real-time Polymerase Chain Reaction, Standard Deviation

    C1q immunoreactivity in inhibitory neurons. A , B , In lightly fixed tissue, our new rabbit anti-mouse C1q monoclonal antibody enabled the additional detection of C1q signals in larger cell bodies (neurons, E–G ), in distinct areas of the brain. These C1q-positive neurons were detected from ∼1 month of age on and aging-independent thereafter (6-month-old shown). C1q-positive neurons were detected in the hippocampus, thalamus, striatum, and midbrain. The exact distribution of C1q-positive neurons visible varied slightly dependent on the location of the slices within the brain. A , Detection of C1q-positive neurons in the hippocampus, thalamus, and midbrain (substantia nigra area). B , Detection of C1q-positive neurons in the thalamus and striatum (mainly globus pallidus). C , In the adult murine hippocampus, C1q immunoreactivity was detected in the neuropil and in both neurons (arrowhead) and microglia (arrow). D , Confocal microscopy colocalization with GFP-immunoreactivity ( Cx3CR1-GFP +/− mice) confirmed that C1q was detected in microglia cell bodies (arrowhead) and processes (arrow). E , Confocal microscopy colocalization with NeuN-immunoreactivity confirmed that C1q was also localized to the cytoplasm of some neurons. F , Confocal microscopy colocalization with GABA-immunoreactivity confirmed that C1q was localized to inhibitory neurons (arrow) but that C1q was not detected in all GABA-positive neurons (arrowheads). G , C1q-positive neurons represent a subset of inhibitory neurons. Neuronal C1q signals exclusively colocalize (arrow) with many but not all GABA-positive neurons in the murine hippocampus (arrowheads: GABA+/C1q− neurons). H , Quantification of C1q-GABA-positive neurons in the murine hippocampus confirmed that C1q-positive neurons represent a subset of inhibitory neurons. At both 3 and 24 months of age all C1q-positive neurons were GABAergic ( n = 3 animals/age). I , J , C1q signals, including signals in neurons, are specific in the wild-type adult hippocampus ( I ), no signals were detected in the C1q-deficient littermate control ( J ). Scale bars: A , B , G , I , J , 500 μm; C , 100 μm; D , E , 10 μm; F , 20 μm.

    Journal: The Journal of Neuroscience

    Article Title: A Dramatic Increase of C1q Protein in the CNS during Normal Aging

    doi: 10.1523/JNEUROSCI.1333-13.2013

    Figure Lengend Snippet: C1q immunoreactivity in inhibitory neurons. A , B , In lightly fixed tissue, our new rabbit anti-mouse C1q monoclonal antibody enabled the additional detection of C1q signals in larger cell bodies (neurons, E–G ), in distinct areas of the brain. These C1q-positive neurons were detected from ∼1 month of age on and aging-independent thereafter (6-month-old shown). C1q-positive neurons were detected in the hippocampus, thalamus, striatum, and midbrain. The exact distribution of C1q-positive neurons visible varied slightly dependent on the location of the slices within the brain. A , Detection of C1q-positive neurons in the hippocampus, thalamus, and midbrain (substantia nigra area). B , Detection of C1q-positive neurons in the thalamus and striatum (mainly globus pallidus). C , In the adult murine hippocampus, C1q immunoreactivity was detected in the neuropil and in both neurons (arrowhead) and microglia (arrow). D , Confocal microscopy colocalization with GFP-immunoreactivity ( Cx3CR1-GFP +/− mice) confirmed that C1q was detected in microglia cell bodies (arrowhead) and processes (arrow). E , Confocal microscopy colocalization with NeuN-immunoreactivity confirmed that C1q was also localized to the cytoplasm of some neurons. F , Confocal microscopy colocalization with GABA-immunoreactivity confirmed that C1q was localized to inhibitory neurons (arrow) but that C1q was not detected in all GABA-positive neurons (arrowheads). G , C1q-positive neurons represent a subset of inhibitory neurons. Neuronal C1q signals exclusively colocalize (arrow) with many but not all GABA-positive neurons in the murine hippocampus (arrowheads: GABA+/C1q− neurons). H , Quantification of C1q-GABA-positive neurons in the murine hippocampus confirmed that C1q-positive neurons represent a subset of inhibitory neurons. At both 3 and 24 months of age all C1q-positive neurons were GABAergic ( n = 3 animals/age). I , J , C1q signals, including signals in neurons, are specific in the wild-type adult hippocampus ( I ), no signals were detected in the C1q-deficient littermate control ( J ). Scale bars: A , B , G , I , J , 500 μm; C , 100 μm; D , E , 10 μm; F , 20 μm.

    Article Snippet: Primary antibodies used: rabbit anti-mouse C1q monoclonal antibody (clones 4.8 and 27.10 at 1.0 μg/ml, Epitomics/Abcam), rabbit anti-human C1q (1:1000, Dako), mouse anti-synaptophysin (1:1000, Millipore), mouse anti-gephyrin (1:500, Synaptic Systems), guinea-pig anti-VGluT1 (1:1000, Millipore), guinea-pig anti-VGAT (1:250, Synaptic Systems), guinea-pig anti-GABA (1:500, abcam), mouse anti-NeuN (1:500, Millipore), chicken anti-GFP (1:1000, Abcam).

    Techniques: Confocal Microscopy, Mouse Assay

    Phenotypic characterization of the superficial and deep strata of the MZ. A–F , En face confocal sections taken through superficial(1–7μm; A–C ) and deep (8–15μm; D–F ) levels of the E15 MZ. Cortical flaps were triple-stained for CellTracker Green (green), CR-50 (blue), and GABA, calretinin, calbindin, or Dlx-2 (red). Most of the cells in the superficial stratum of the MZ colabel for calretinin and CR-50 ( A ). These CR-50 cells, however, do not colabel with GABA ( B ) or with Dlx-2 ( C ). Rather, long axonal projections labeled with GABA, such as the one shown in B . Clusters of Dlx-2-labeled cells ( C ) did appear in this superficial stratum, but these cells did not colabel with CR-50. Tangentially oriented cells in the deep stratum of the MZ labeled with calbindin ( D ), GABA ( E ), and Dlx-2 ( F ). The deep stratum was relatively devoid of CR-50 labeling ( D–F ). Scale bars ( C, F ), 50 μm.

    Journal: The Journal of Neuroscience

    Article Title: Four-Dimensional Migratory Coordinates of GABAergic Interneurons in the Developing Mouse Cortex

    doi: 10.1523/JNEUROSCI.23-13-05805.2003

    Figure Lengend Snippet: Phenotypic characterization of the superficial and deep strata of the MZ. A–F , En face confocal sections taken through superficial(1–7μm; A–C ) and deep (8–15μm; D–F ) levels of the E15 MZ. Cortical flaps were triple-stained for CellTracker Green (green), CR-50 (blue), and GABA, calretinin, calbindin, or Dlx-2 (red). Most of the cells in the superficial stratum of the MZ colabel for calretinin and CR-50 ( A ). These CR-50 cells, however, do not colabel with GABA ( B ) or with Dlx-2 ( C ). Rather, long axonal projections labeled with GABA, such as the one shown in B . Clusters of Dlx-2-labeled cells ( C ) did appear in this superficial stratum, but these cells did not colabel with CR-50. Tangentially oriented cells in the deep stratum of the MZ labeled with calbindin ( D ), GABA ( E ), and Dlx-2 ( F ). The deep stratum was relatively devoid of CR-50 labeling ( D–F ). Scale bars ( C, F ), 50 μm.

    Article Snippet: Primary anti-calbindin (1:1000; Chemicon, Temecula, CA), anti-calretinin (1:1000; Chemicon), anti-reelin (1:100; a gift from Dr. M. Ogawa, Riken Brain Science Institute), anti-GABA (1:1000; Sigma, St. Louis, MO), and Dlx-2 (1:150; a gift from J. Rubenstein, University of California San Francisco, San Francisco, CA) were incubated on whole-mount explant flaps or entire telencephali overnight at 4°C followed by species-specific fluorophore-labeled secondary antibodies (see figure legends for details).

    Techniques: Staining, Labeling

    CRH+ EPL interneurons are predominantly generated postnatally (a) Expression pattern of Crh-Cre; Rosa lsl-tdTomato/+ mice at P7, P14, and P30 co-stained with the interneuron marker Parvalbumin (scale bar 30 µm). (b) Quantification of the expression of Parvalbumin and CRH+ interneurons in the EPL between P0 and P60. Confocal immunohistochemistry image of (c) GABA on Crh-Cre; Rosa lsl-tdTomato/+ EPL tissue at P14 (scale bar 20 µm), and (d) NeuN at P30 (scale bar 30 µm). (e) Quantification of the expression of NeuN and CRH+ interneurons at P14 and P30. (f) Confocal image of Calretinin in CRH+ EPL interneurons at P30 (scale bar 40 µm). (g) Quantification of the expression of Calretinin and CRH+ interneurons at P14 and P30. (h) Example confocal image of EdU expression in CRH+ neurons pulsed at P7 (scale bar 40 m). (i) Quantification of the percentage of CRH+ EPL interneurons born between E16.5 and P30 (* p

    Journal: Brain structure & function

    Article Title: Brain atlas of the Mongolian gerbil (Meriones unguiculatus) in CT/MRI-aided stereotaxic coordinates

    doi: 10.1007/s00429-016-1259-0

    Figure Lengend Snippet: CRH+ EPL interneurons are predominantly generated postnatally (a) Expression pattern of Crh-Cre; Rosa lsl-tdTomato/+ mice at P7, P14, and P30 co-stained with the interneuron marker Parvalbumin (scale bar 30 µm). (b) Quantification of the expression of Parvalbumin and CRH+ interneurons in the EPL between P0 and P60. Confocal immunohistochemistry image of (c) GABA on Crh-Cre; Rosa lsl-tdTomato/+ EPL tissue at P14 (scale bar 20 µm), and (d) NeuN at P30 (scale bar 30 µm). (e) Quantification of the expression of NeuN and CRH+ interneurons at P14 and P30. (f) Confocal image of Calretinin in CRH+ EPL interneurons at P30 (scale bar 40 µm). (g) Quantification of the expression of Calretinin and CRH+ interneurons at P14 and P30. (h) Example confocal image of EdU expression in CRH+ neurons pulsed at P7 (scale bar 40 m). (i) Quantification of the percentage of CRH+ EPL interneurons born between E16.5 and P30 (* p

    Article Snippet: OB tissue sections were stained overnight at 4°C using the following primary antibodies diluted in blocking solution: guinea pig anti-Parvalbumin (1:500, Synaptic Systems 195004, Germany), mouse anti-GABA (1:2000, Millipore MAB316, Billerica MA), rabbit anti-Calretinin (1:1000, Millipore MAB377, Billerica MA), rabbit anti-VGlut1 (1:500, Synaptic Systems 135302, Germany), rabbit anti-TBX21 (1:500, gift from Dr. Sachiko Mitsui, RIKEN Brain Science Institute, Japan), rabbit anti-Tyrosine Hydroxylase (1:2000, Millipore AB152, Billerica MA), and rabbit anti-Calbindin (1:500, Abcam AB9481, Cambridge MA).

    Techniques: Generated, Expressing, Mouse Assay, Staining, Marker, Immunohistochemistry

    Histamine H1 and H2 receptors are expressed on GABAergic VP neurons. A – C Double immunofluorescence staining for H1 ( A ) and H2 ( B ) in rat VP neurons. D – F Double immunofluorescence staining for GABA ( D ) and H1 ( E ) in rat VP neurons. G–I

    Journal: Neuroscience Bulletin

    Article Title: Histamine Excites Rat GABAergic Ventral Pallidum Neurons via Co-activation of H1 and H2 Receptors

    doi: 10.1007/s12264-018-0277-8

    Figure Lengend Snippet: Histamine H1 and H2 receptors are expressed on GABAergic VP neurons. A – C Double immunofluorescence staining for H1 ( A ) and H2 ( B ) in rat VP neurons. D – F Double immunofluorescence staining for GABA ( D ) and H1 ( E ) in rat VP neurons. G–I

    Article Snippet: Sections were incubated overnight at 4°C with the primary antibodies mouse anti-GABA (1:1000; Sigma), goat anti-H1 receptor (1:200; Everest Biotech, Bicester, UK), rabbit anti-H1 receptor (1:200; Alamone Labs, Jerusalem, Israel), and/or goat anti-H2 receptor (1:200; Everest Biotech).

    Techniques: Double Immunofluorescence Staining