antibody against d1r  (Millipore)

 
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    Millipore antibody against d1r
    Antibody Against D1r, supplied by Millipore, 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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    antibodies against d1r  (Proteintech)

     
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    Proteintech antibodies against d1r
    Antibodies Against D1r, supplied by Proteintech, 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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    antibodies against d1r  (Santa Cruz Biotechnology)

     
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    Santa Cruz Biotechnology antibodies against d1r
    Antibodies Against D1r, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against d1r/product/Santa Cruz Biotechnology
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    antibodies against d1r  (Santa Cruz Biotechnology)

     
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    Santa Cruz Biotechnology antibodies against d1r
    a Experimental design of the single Qd tracking. Receptors were labeled with antibodies directed against extracellular tags. Qd-655 and Qd-705 were used to distinguish receptor types. The interaction between receptors occurs intracellularly at the T2 domain (C1 cassette of the GluN1 subunit). b Microscopy setting to perform MS-SMLM using two microscopes and cameras. PFS: perfect focus system. c SM-SMLM principle. d Representative reconstruction of GuN1-NMDAR and <t>D1R</t> surface diffusion, scale bar, 1 µm. e Example trajectories of one GluN1-NMDAR and one D1R laterally diffusing (x, y) onto the neuronal surface over time.
    Antibodies Against D1r, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against d1r/product/Santa Cruz Biotechnology
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies against d1r - by Bioz Stars, 2024-09
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    Images

    1) Product Images from "Non-canonical interplay between glutamatergic NMDA and dopamine receptors shapes synaptogenesis"

    Article Title: Non-canonical interplay between glutamatergic NMDA and dopamine receptors shapes synaptogenesis

    Journal: Nature Communications

    doi: 10.1038/s41467-023-44301-z

    a Experimental design of the single Qd tracking. Receptors were labeled with antibodies directed against extracellular tags. Qd-655 and Qd-705 were used to distinguish receptor types. The interaction between receptors occurs intracellularly at the T2 domain (C1 cassette of the GluN1 subunit). b Microscopy setting to perform MS-SMLM using two microscopes and cameras. PFS: perfect focus system. c SM-SMLM principle. d Representative reconstruction of GuN1-NMDAR and D1R surface diffusion, scale bar, 1 µm. e Example trajectories of one GluN1-NMDAR and one D1R laterally diffusing (x, y) onto the neuronal surface over time.
    Figure Legend Snippet: a Experimental design of the single Qd tracking. Receptors were labeled with antibodies directed against extracellular tags. Qd-655 and Qd-705 were used to distinguish receptor types. The interaction between receptors occurs intracellularly at the T2 domain (C1 cassette of the GluN1 subunit). b Microscopy setting to perform MS-SMLM using two microscopes and cameras. PFS: perfect focus system. c SM-SMLM principle. d Representative reconstruction of GuN1-NMDAR and D1R surface diffusion, scale bar, 1 µm. e Example trajectories of one GluN1-NMDAR and one D1R laterally diffusing (x, y) onto the neuronal surface over time.

    Techniques Used: Labeling, Microscopy, Diffusion-based Assay

    a Experimental design of the surface single Qd tracking of NMDAR and D1R. b Representative images with quantification of the normalized overlap between GluN1-NMDAR-D1R-wt ( n = 50 neuronal fields) and GluN1-NMDAR-D1R-dT2 ( n = 44 neuronal fields; two-tailed unpaired t-test). Data are presented as mean +/- SEM. Scale bar, 5 µm. c Representative normalized timeline of the distances separating one GluN1 from one D1R-wt or one GluN1 from one D1R-dT2. d Comparison of the average observed lifetime of the receptors ( left ) in non-confined space (monomeric state) for GluN1-D1R-wt ( n = 168 events), GluN1-D1R-dT2 ( n = 45), GluN1-GluN1 with D1R-wt ( n = 165) or D1R-dT2 ( n = 65); ( right ) in a co-confined space (dimeric state) between GluN1 and D1R-wt ( n = 138), GluN1 and D1R-dT2 ( n = 40), GluN1 and GluN1 expressed with D1R-wt ( n = 159) or D1R-dT2 ( n = 50; Kruskal-Wallis with Dunn’s multiple comparisons test). Data are presented as mean +/- SEM. e Distribution and one exponential fit of the interaction events. f Comparison of the estimated K off , i.e. dissociation rate (One-way ANOVA with Tukey’s multiple comparisons test). Data are presented as mean +/- SEM. Source data are provided as a Source Data file.
    Figure Legend Snippet: a Experimental design of the surface single Qd tracking of NMDAR and D1R. b Representative images with quantification of the normalized overlap between GluN1-NMDAR-D1R-wt ( n = 50 neuronal fields) and GluN1-NMDAR-D1R-dT2 ( n = 44 neuronal fields; two-tailed unpaired t-test). Data are presented as mean +/- SEM. Scale bar, 5 µm. c Representative normalized timeline of the distances separating one GluN1 from one D1R-wt or one GluN1 from one D1R-dT2. d Comparison of the average observed lifetime of the receptors ( left ) in non-confined space (monomeric state) for GluN1-D1R-wt ( n = 168 events), GluN1-D1R-dT2 ( n = 45), GluN1-GluN1 with D1R-wt ( n = 165) or D1R-dT2 ( n = 65); ( right ) in a co-confined space (dimeric state) between GluN1 and D1R-wt ( n = 138), GluN1 and D1R-dT2 ( n = 40), GluN1 and GluN1 expressed with D1R-wt ( n = 159) or D1R-dT2 ( n = 50; Kruskal-Wallis with Dunn’s multiple comparisons test). Data are presented as mean +/- SEM. e Distribution and one exponential fit of the interaction events. f Comparison of the estimated K off , i.e. dissociation rate (One-way ANOVA with Tukey’s multiple comparisons test). Data are presented as mean +/- SEM. Source data are provided as a Source Data file.

    Techniques Used: Two Tailed Test, Comparison

    a Representative image of hippocampal dendrites over in vitro development. Dendrites were labeled with MAP-2 (magenta), postsynaptic densities with PSD-95 (green), and presynaptic terminals with synapsin (blue). Scale bar, 5 µm. b (left) Quantification of the number of post-synapses (PSD-95) and pre-synapses (synapsin) at 4 DIV ( n = 18 fields for both PSD-95 and synapsin), 9 DIV ( n = 17 fields for both PSD-95 and synapsin), 12 DIV ( n = 30 fields for PSD-95 and 29 for synapsin), 15 DIV ( n = 21 for PSD-95 and 20 for synapsin), 21 DIV ( n = 21 for PSD-95 and 20 for synapsin), 24 DIV ( n = 11 for both PSD-95 and synapsin). Error bars represent the mean values; (right) non-linear fitting of the number of post-synapses over time, inflection point is at ~12 DIV. Data are presented as mean +/- SEM. c (left) Experimental design. (right) Representative normalized timeline of the distance separating one GluN1 from one D1R in immature and mature neurons. d Comparison of the observed mean lifetime of (left) non-interacting GluN1-NMDAR-D1R in immature ( n = 168 events) and mature ( n = 55) neurons, (right) individual interacting events between GluN1 and D1R in immature ( n = 138) and mature neurons ( n = 61; two-tailed Mann-Whitney U test). Data are presented as mean +/- SEM. e Distribution and one exponential fit of the interaction events between GluN1-D1R in immature and mature neurons with estimated K off (two-tailed unpaired t-test). Data are presented as mean +/- SEM. f Representative images of hippocampal dendrites on which surface GluN1-NMDAR (green), D1R (magenta), and Homer 1 C (white) were imaged in immature and mature neurons alongside corresponding intensity plots. Scale bar, 5 and 2 µm. g Quantification of the colocalization between D1R and GluN1-NMDAR in immature ( n = 17 cells) and mature ( n = 10 cells) neurons (two-tailed unpaired t-test). Data are presented as mean +/- SEM. h Experimental set-up and immunoblots. i Densitometric analysis of the levels of GluN2A and GluN2B co-immunoprecipitated by antibody directed towards D1R or D2R, respectively. The levels of D1R-NMDAR interaction were considered as the ratio of NMDAR co-IP with D1R-IP. Results are normalized to P8, 3 animals per condition (One-way ANOVA with Tukey’s post hoc test). Data are presented as mean +/- SEM. Source data are provided as a Source Data file.
    Figure Legend Snippet: a Representative image of hippocampal dendrites over in vitro development. Dendrites were labeled with MAP-2 (magenta), postsynaptic densities with PSD-95 (green), and presynaptic terminals with synapsin (blue). Scale bar, 5 µm. b (left) Quantification of the number of post-synapses (PSD-95) and pre-synapses (synapsin) at 4 DIV ( n = 18 fields for both PSD-95 and synapsin), 9 DIV ( n = 17 fields for both PSD-95 and synapsin), 12 DIV ( n = 30 fields for PSD-95 and 29 for synapsin), 15 DIV ( n = 21 for PSD-95 and 20 for synapsin), 21 DIV ( n = 21 for PSD-95 and 20 for synapsin), 24 DIV ( n = 11 for both PSD-95 and synapsin). Error bars represent the mean values; (right) non-linear fitting of the number of post-synapses over time, inflection point is at ~12 DIV. Data are presented as mean +/- SEM. c (left) Experimental design. (right) Representative normalized timeline of the distance separating one GluN1 from one D1R in immature and mature neurons. d Comparison of the observed mean lifetime of (left) non-interacting GluN1-NMDAR-D1R in immature ( n = 168 events) and mature ( n = 55) neurons, (right) individual interacting events between GluN1 and D1R in immature ( n = 138) and mature neurons ( n = 61; two-tailed Mann-Whitney U test). Data are presented as mean +/- SEM. e Distribution and one exponential fit of the interaction events between GluN1-D1R in immature and mature neurons with estimated K off (two-tailed unpaired t-test). Data are presented as mean +/- SEM. f Representative images of hippocampal dendrites on which surface GluN1-NMDAR (green), D1R (magenta), and Homer 1 C (white) were imaged in immature and mature neurons alongside corresponding intensity plots. Scale bar, 5 and 2 µm. g Quantification of the colocalization between D1R and GluN1-NMDAR in immature ( n = 17 cells) and mature ( n = 10 cells) neurons (two-tailed unpaired t-test). Data are presented as mean +/- SEM. h Experimental set-up and immunoblots. i Densitometric analysis of the levels of GluN2A and GluN2B co-immunoprecipitated by antibody directed towards D1R or D2R, respectively. The levels of D1R-NMDAR interaction were considered as the ratio of NMDAR co-IP with D1R-IP. Results are normalized to P8, 3 animals per condition (One-way ANOVA with Tukey’s post hoc test). Data are presented as mean +/- SEM. Source data are provided as a Source Data file.

    Techniques Used: In Vitro, Labeling, Comparison, Two Tailed Test, MANN-WHITNEY, Western Blot, Immunoprecipitation, Co-Immunoprecipitation Assay

    a – d Representative images of hippocampal dendrites on which surface GluN1-NMDAR (green) and D1R (magenta) were labeled after exposures to various pharmacological treatments with respective quantification of D1R-GluN1-NMDAR mean overlap, ( a ) Buffer (CTL, n = 105 fields), TTX (1 µM, n = 49) and glutamate (50 µM, n = 37); ( b ) KCl 2.5 mM (CTL, n = 55) or KCl 50 mM ( n = 60); ( d ) Buffer (CTL, n = 47) or DHPG (50 µM, n = 51); ( c ) glutamate alone ( n = 47) or together with APV (50 µM, n = 40), LY-341495 (100 µM, n = 52) or NBQX (2 µM, n = 43) ( a , c One-way ANOVA with Dunnett’s post hoc test; b-d, two-tailed unpaired t-test). Scale bar, 5 µm. Results are normalized to CTL ( a , b , d ) or glutamate ( c ). e Cartoon illustrating putative D1R phosphorylation sites. f Representative images of hippocampal dendrites on which surface GluN1-NMDAR (green) and D1R (magenta) were labeled after exposures to various kinase inhibitors with respective quantification of the normalized GluN1-NMDAR-D1R mean overlap in control (CTL) condition ( n = 126 fields) or following acute treatment with CKI-7 (100 µM, n = 57), KT-5720 (25 µM, n = 49), Gö−6976 (1 µM, n = 41), TMCB (5 µM, n = 37), CMPD101 (1 µM, n = 50) and AIP2 (1 µM, n = 40; One-way ANOVA with Dunnett’s post-hoc test). Scale bar, 5 µm. g Representative images of hippocampal dendrites on which surface GluN1-NMDAR (green) and D1R (magenta) were labeled after treatment with buffer (CTL, n = 48 fields), DHPG alone (50 µM, n = 44) or together with CKI-7 (100 µM, n = 45) with respective quantification of D1R-GluN1-NMDAR mean overlap (One-way ANOVA with Dunnett’s post-hoc test). Scale bar, 5 µm. Data are presented as box-and-whisker plots: line at median, IQR in box, whiskers represent 10–90 percentile. Source data are provided as a Source Data file.
    Figure Legend Snippet: a – d Representative images of hippocampal dendrites on which surface GluN1-NMDAR (green) and D1R (magenta) were labeled after exposures to various pharmacological treatments with respective quantification of D1R-GluN1-NMDAR mean overlap, ( a ) Buffer (CTL, n = 105 fields), TTX (1 µM, n = 49) and glutamate (50 µM, n = 37); ( b ) KCl 2.5 mM (CTL, n = 55) or KCl 50 mM ( n = 60); ( d ) Buffer (CTL, n = 47) or DHPG (50 µM, n = 51); ( c ) glutamate alone ( n = 47) or together with APV (50 µM, n = 40), LY-341495 (100 µM, n = 52) or NBQX (2 µM, n = 43) ( a , c One-way ANOVA with Dunnett’s post hoc test; b-d, two-tailed unpaired t-test). Scale bar, 5 µm. Results are normalized to CTL ( a , b , d ) or glutamate ( c ). e Cartoon illustrating putative D1R phosphorylation sites. f Representative images of hippocampal dendrites on which surface GluN1-NMDAR (green) and D1R (magenta) were labeled after exposures to various kinase inhibitors with respective quantification of the normalized GluN1-NMDAR-D1R mean overlap in control (CTL) condition ( n = 126 fields) or following acute treatment with CKI-7 (100 µM, n = 57), KT-5720 (25 µM, n = 49), Gö−6976 (1 µM, n = 41), TMCB (5 µM, n = 37), CMPD101 (1 µM, n = 50) and AIP2 (1 µM, n = 40; One-way ANOVA with Dunnett’s post-hoc test). Scale bar, 5 µm. g Representative images of hippocampal dendrites on which surface GluN1-NMDAR (green) and D1R (magenta) were labeled after treatment with buffer (CTL, n = 48 fields), DHPG alone (50 µM, n = 44) or together with CKI-7 (100 µM, n = 45) with respective quantification of D1R-GluN1-NMDAR mean overlap (One-way ANOVA with Dunnett’s post-hoc test). Scale bar, 5 µm. Data are presented as box-and-whisker plots: line at median, IQR in box, whiskers represent 10–90 percentile. Source data are provided as a Source Data file.

    Techniques Used: Labeling, Two Tailed Test, Whisker Assay

    a Representative image of hippocampal dendrites on which surface GluN1-NMDAR (green) and D1R (magenta) were labeled from D1R-wt, D1R-S397D (grey), or D1R-dT2 (orange) expressing neurons from 3 independent experiments. Scale bar, 2 µm. b Correlation between the size of GluN1-NMDAR cluster and the overlap between GluN1-NMDAR and D1R when co-expressed with D1R-wt, D1R-S397D or D1R-dT2. P-value were calculated using a two-sided t -test. c Example of diffraction-limited and super-resolution images of surface GluN1-NMDAR. Scale bar, 300 nm. d Representative images of super-resolved surface GluN1-NMDAR and diffraction-limited Homer 1 C staining. Scale bar, 1 µm. c , d Representative images from 4 independent experiments. e Representative clustering images obtained with SR-Tesseler software. Scale bar, 100 nm. f Comparison of the density of localizations per nanodomains inside and outside synapses when GluN1 is co-transfected with either D1R-WT ( n = 7 cells), D1R-dT2 ( n = 7) or D1R-S397D ( n = 6; two-tailed Mann-Whitney U test). Data are presented as mean +/- SEM. g Representative immunofluorescence image of surface D1R (magenta) and Homer 1 C (green) from 3 independent experiments. Scale bar, 10 and 5 µm. h Cumulative distribution of the area in nm 2 of extra-synaptic GluN1-NMDAR nanodomains synapses when GluN1 is co-transfected with either D1R-WT ( n = 88 nanodomains), D1R-dT2 ( n = 136 nanodomains) or D1R-S397D ( n = 102 nanodomains; two-tailed Kolmogorov-Smirnov test). Bar graphs represent mean +/- SEM. i Representative GCaMP6f-fluorescence images from 3 independent experiments. Scale bar, 2 µm. j Representative NMDAR-mediated Ca 2+ signals, scale is 0.05 (D1R-WT and -dT2) or 0.2 (D1R-397D) ΔF/F. k Comparison of the NMDAR-mediated Ca 2+ -transient frequency in protrusions and dendrite when GluN1 is expressed together with D1R-wt ( n = 153 spines and 54 shaft), D1R-S397D ( n = 145 spines, 56 shafts) or D1R-dT2 ( n = 105 spines, 45 shafts; two-tailed Mann–Whitney U test). Data are presented as mean +/- SEM. Source data are provided as a Source Data file.
    Figure Legend Snippet: a Representative image of hippocampal dendrites on which surface GluN1-NMDAR (green) and D1R (magenta) were labeled from D1R-wt, D1R-S397D (grey), or D1R-dT2 (orange) expressing neurons from 3 independent experiments. Scale bar, 2 µm. b Correlation between the size of GluN1-NMDAR cluster and the overlap between GluN1-NMDAR and D1R when co-expressed with D1R-wt, D1R-S397D or D1R-dT2. P-value were calculated using a two-sided t -test. c Example of diffraction-limited and super-resolution images of surface GluN1-NMDAR. Scale bar, 300 nm. d Representative images of super-resolved surface GluN1-NMDAR and diffraction-limited Homer 1 C staining. Scale bar, 1 µm. c , d Representative images from 4 independent experiments. e Representative clustering images obtained with SR-Tesseler software. Scale bar, 100 nm. f Comparison of the density of localizations per nanodomains inside and outside synapses when GluN1 is co-transfected with either D1R-WT ( n = 7 cells), D1R-dT2 ( n = 7) or D1R-S397D ( n = 6; two-tailed Mann-Whitney U test). Data are presented as mean +/- SEM. g Representative immunofluorescence image of surface D1R (magenta) and Homer 1 C (green) from 3 independent experiments. Scale bar, 10 and 5 µm. h Cumulative distribution of the area in nm 2 of extra-synaptic GluN1-NMDAR nanodomains synapses when GluN1 is co-transfected with either D1R-WT ( n = 88 nanodomains), D1R-dT2 ( n = 136 nanodomains) or D1R-S397D ( n = 102 nanodomains; two-tailed Kolmogorov-Smirnov test). Bar graphs represent mean +/- SEM. i Representative GCaMP6f-fluorescence images from 3 independent experiments. Scale bar, 2 µm. j Representative NMDAR-mediated Ca 2+ signals, scale is 0.05 (D1R-WT and -dT2) or 0.2 (D1R-397D) ΔF/F. k Comparison of the NMDAR-mediated Ca 2+ -transient frequency in protrusions and dendrite when GluN1 is expressed together with D1R-wt ( n = 153 spines and 54 shaft), D1R-S397D ( n = 145 spines, 56 shafts) or D1R-dT2 ( n = 105 spines, 45 shafts; two-tailed Mann–Whitney U test). Data are presented as mean +/- SEM. Source data are provided as a Source Data file.

    Techniques Used: Labeling, Expressing, Staining, Software, Comparison, Transfection, Two Tailed Test, MANN-WHITNEY, Immunofluorescence, Fluorescence

    a Experimental design of the TAT-competing peptide challenge in developing immature neurons with representative images of hippocampal dendrites on which Homer 1 C cluster (synapses), GluN2A subunit, or GluN2B subunit were labeled in the presence of TAT-NS or TAT-T2 competing peptides. Scale bar, 5 and 1 µm. b Comparison of the number of synapses (e.g. number of Homer 1 C clusters per µm of dendrite) after treatment with TAT-NS ( n = 60 fields) or TAT-T2 ( n = 62) and ( c ) the percentage of synapses that are positive for GluN2B (TAT-NS, n = 23; TAT-T2, n = 34) and/or GluN2A (TAT-NS, n = 25, TAT-T2, n = 33; two-tailed Unpaired t-test). Data are presented as mean +/- SEM. Scale bar, 5 and 1 µm. d Experimental design alongside representative images of hippocampal dendrites on which Homer 1 C cluster (synapses), GluN2A subunit, or GluN2B subunit were labeled in the presence of TAT-NS or TAT-T2 competing peptides. Scale bar, 5 and 1 µm. e Comparison of the number of synapses after treatment with TAT-NS ( n = 59 fields) or TAT-T2 ( n = 55) and ( f ) the percentage of synapses that are positive for GluN2B (TAT-NS, n = 19; TAT-T2, n = 11) and/or GluN2A (TAT-NS, n = 19; TAT-T2, n = 14; two-tailed unpaired t-test). Data are presented as mean +/- SEM. g Experimental set-up with representative images and ( h ) corresponding comparison of the number of synapses following expression of D1R-WT ( n = 44 fields) or D1R-S397D ( n = 41; two-tailed unpaired t-test). Data are presented as mean +/- SEM. Scale bar, 5 µm. i Representative images of TH immunostaining. Scale bar, (i) 500 µm and 100 µm. j Experimental setup with representative fluorescence images from 4 independent experiments. Scale bar, 100 µm and 5 µm. k Representative Homer 1 C images. l comparison of the synaptic density in hippocampal neurons co-cultured with hippocampal (h-h, n = 24 fields) or midbrain neurons (m-h, n = 25; two-tailed unpaired t-test). Data are presented as mean +/- SEM. Scale bar, 5 µm. m Representative images and ( n ) comparison of the synaptic density in hippocampal neurons co-cultured with midbrain neurons and chronically treated with competing peptides, either TAT-NS ( n = 12 fields) or TAT-T2 ( n = 25; two-tailed unpaired t-test). Data are presented as mean +/- SEM. Scale bar, 5 µm. Source data are provided as a Source Data file.
    Figure Legend Snippet: a Experimental design of the TAT-competing peptide challenge in developing immature neurons with representative images of hippocampal dendrites on which Homer 1 C cluster (synapses), GluN2A subunit, or GluN2B subunit were labeled in the presence of TAT-NS or TAT-T2 competing peptides. Scale bar, 5 and 1 µm. b Comparison of the number of synapses (e.g. number of Homer 1 C clusters per µm of dendrite) after treatment with TAT-NS ( n = 60 fields) or TAT-T2 ( n = 62) and ( c ) the percentage of synapses that are positive for GluN2B (TAT-NS, n = 23; TAT-T2, n = 34) and/or GluN2A (TAT-NS, n = 25, TAT-T2, n = 33; two-tailed Unpaired t-test). Data are presented as mean +/- SEM. Scale bar, 5 and 1 µm. d Experimental design alongside representative images of hippocampal dendrites on which Homer 1 C cluster (synapses), GluN2A subunit, or GluN2B subunit were labeled in the presence of TAT-NS or TAT-T2 competing peptides. Scale bar, 5 and 1 µm. e Comparison of the number of synapses after treatment with TAT-NS ( n = 59 fields) or TAT-T2 ( n = 55) and ( f ) the percentage of synapses that are positive for GluN2B (TAT-NS, n = 19; TAT-T2, n = 11) and/or GluN2A (TAT-NS, n = 19; TAT-T2, n = 14; two-tailed unpaired t-test). Data are presented as mean +/- SEM. g Experimental set-up with representative images and ( h ) corresponding comparison of the number of synapses following expression of D1R-WT ( n = 44 fields) or D1R-S397D ( n = 41; two-tailed unpaired t-test). Data are presented as mean +/- SEM. Scale bar, 5 µm. i Representative images of TH immunostaining. Scale bar, (i) 500 µm and 100 µm. j Experimental setup with representative fluorescence images from 4 independent experiments. Scale bar, 100 µm and 5 µm. k Representative Homer 1 C images. l comparison of the synaptic density in hippocampal neurons co-cultured with hippocampal (h-h, n = 24 fields) or midbrain neurons (m-h, n = 25; two-tailed unpaired t-test). Data are presented as mean +/- SEM. Scale bar, 5 µm. m Representative images and ( n ) comparison of the synaptic density in hippocampal neurons co-cultured with midbrain neurons and chronically treated with competing peptides, either TAT-NS ( n = 12 fields) or TAT-T2 ( n = 25; two-tailed unpaired t-test). Data are presented as mean +/- SEM. Scale bar, 5 µm. Source data are provided as a Source Data file.

    Techniques Used: Labeling, Comparison, Two Tailed Test, Expressing, Immunostaining, Fluorescence, Cell Culture


    Figure Legend Snippet:

    Techniques Used:

    antibodies against d1r  (Millipore)

     
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    Millipore antibodies against d1r
    Pain relief increased dopaminergic D2 receptor expression in injured mice. D2 receptor expression in the CeA was significantly decreased in incised mice treated with PNB compared with incised mice treated with saline (n = 6; * p < 0.05 vs the incision+saline group; one-way ANOVA,Interaction::F (3, 20) = 6.274). The expression of <t>D1</t> <t>receptor</t> was not significantly changed. (b) In the CeA, D1 receptor was mainly expressed in glutamatergic excitatory neurons (positive for glutaminase). In the CeA, D2 receptor was predominantly expressed in GABAergic inhibitory neurons (positive for GABA). Scale bar, 50 μm.
    Antibodies Against D1r, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against d1r/product/Millipore
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies against d1r - by Bioz Stars, 2024-09
    86/100 stars

    Images

    1) Product Images from "Dopamine receptor D2, but not D1, mediates the reward circuit from the ventral tegmental area to the central amygdala, which is involved in pain relief"

    Article Title: Dopamine receptor D2, but not D1, mediates the reward circuit from the ventral tegmental area to the central amygdala, which is involved in pain relief

    Journal: Molecular Pain

    doi: 10.1177/17448069221145096

    Pain relief increased dopaminergic D2 receptor expression in injured mice. D2 receptor expression in the CeA was significantly decreased in incised mice treated with PNB compared with incised mice treated with saline (n = 6; * p < 0.05 vs the incision+saline group; one-way ANOVA,Interaction::F (3, 20) = 6.274). The expression of D1 receptor was not significantly changed. (b) In the CeA, D1 receptor was mainly expressed in glutamatergic excitatory neurons (positive for glutaminase). In the CeA, D2 receptor was predominantly expressed in GABAergic inhibitory neurons (positive for GABA). Scale bar, 50 μm.
    Figure Legend Snippet: Pain relief increased dopaminergic D2 receptor expression in injured mice. D2 receptor expression in the CeA was significantly decreased in incised mice treated with PNB compared with incised mice treated with saline (n = 6; * p < 0.05 vs the incision+saline group; one-way ANOVA,Interaction::F (3, 20) = 6.274). The expression of D1 receptor was not significantly changed. (b) In the CeA, D1 receptor was mainly expressed in glutamatergic excitatory neurons (positive for glutaminase). In the CeA, D2 receptor was predominantly expressed in GABAergic inhibitory neurons (positive for GABA). Scale bar, 50 μm.

    Techniques Used: Expressing


    Figure Legend Snippet:

    Techniques Used:

    rabbit antibody against d1r  (Millipore)

     
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    Millipore rabbit antibody against d1r
    Effects of intrastriatal administration of Tat-fusion interfering peptide (Tat-D1Ri) on <t>D1R–GluN1</t> interactions. Notes: Tat-D1Ri, Tat-D1Rc, or saline were locally injected into the striatum of the normal adult rat at a rate of 0.2 µL/min. Rat striatal tissues were then used for coimmunoprecipitation experiments to validate the efficacy and selectivity of interfering peptide. The intrastriatal injection of Tat-D1Ri rather than Tat-D1Rc caused reduction of <t>D1R–GluN1</t> interactions, which demonstrated the effectiveness of Tat-D1Ri. Abbreviations: Tat-D1Rc, Tat-fusion control peptide; Ig, Immunoglobulin; IP, immunoprecipitation; IB, immunoblot.
    Rabbit Antibody Against D1r, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit antibody against d1r/product/Millipore
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    Images

    1) Product Images from "Targeting the D1-N-methyl- d -aspartate receptor complex reduces l -dopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats"

    Article Title: Targeting the D1-N-methyl- d -aspartate receptor complex reduces l -dopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    Journal: Drug Design, Development and Therapy

    doi: 10.2147/DDDT.S93487

    Effects of intrastriatal administration of Tat-fusion interfering peptide (Tat-D1Ri) on D1R–GluN1 interactions. Notes: Tat-D1Ri, Tat-D1Rc, or saline were locally injected into the striatum of the normal adult rat at a rate of 0.2 µL/min. Rat striatal tissues were then used for coimmunoprecipitation experiments to validate the efficacy and selectivity of interfering peptide. The intrastriatal injection of Tat-D1Ri rather than Tat-D1Rc caused reduction of D1R–GluN1 interactions, which demonstrated the effectiveness of Tat-D1Ri. Abbreviations: Tat-D1Rc, Tat-fusion control peptide; Ig, Immunoglobulin; IP, immunoprecipitation; IB, immunoblot.
    Figure Legend Snippet: Effects of intrastriatal administration of Tat-fusion interfering peptide (Tat-D1Ri) on D1R–GluN1 interactions. Notes: Tat-D1Ri, Tat-D1Rc, or saline were locally injected into the striatum of the normal adult rat at a rate of 0.2 µL/min. Rat striatal tissues were then used for coimmunoprecipitation experiments to validate the efficacy and selectivity of interfering peptide. The intrastriatal injection of Tat-D1Ri rather than Tat-D1Rc caused reduction of D1R–GluN1 interactions, which demonstrated the effectiveness of Tat-D1Ri. Abbreviations: Tat-D1Rc, Tat-fusion control peptide; Ig, Immunoglobulin; IP, immunoprecipitation; IB, immunoblot.

    Techniques Used: Injection, Immunoprecipitation, Western Blot

    Effects of intrastriatal administration of Tat-D1Ri on membrane D1R subunit expression. Notes: Protein levels were evaluated by Western blotting of proteins extracted from the lesioned striatum of the rat brains. They were assessed in extracts from 6-OHDA-lesioned rats treated with pulsatile l -dopa plus intrastriatal administration of Tat-D1Rc or Tat-D1Ri. ( A ) Representative Western blot analysis of D1R in the membrane fraction; ( B ) densitometric analysis of two blots with specific protein signals normalized to the corresponding GAPDH levels. Data are expressed as means ± SEM. Statistical analysis was conducted by independent-samples t -test. * P =0.05 versus LID + Tat-D1Rc. Abbreviations: 6-OHDA, 6-hydroxydopamine; l -dopa, L-3,4-dihydroxyphenylalanine; LID, l -dopa-induced dyskinesia; SEM, standard error of mean; Tat-D1Ri, Tat-fusion interfering peptide; Tat-D1Rc, Tat-fusion control peptide; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.
    Figure Legend Snippet: Effects of intrastriatal administration of Tat-D1Ri on membrane D1R subunit expression. Notes: Protein levels were evaluated by Western blotting of proteins extracted from the lesioned striatum of the rat brains. They were assessed in extracts from 6-OHDA-lesioned rats treated with pulsatile l -dopa plus intrastriatal administration of Tat-D1Rc or Tat-D1Ri. ( A ) Representative Western blot analysis of D1R in the membrane fraction; ( B ) densitometric analysis of two blots with specific protein signals normalized to the corresponding GAPDH levels. Data are expressed as means ± SEM. Statistical analysis was conducted by independent-samples t -test. * P =0.05 versus LID + Tat-D1Rc. Abbreviations: 6-OHDA, 6-hydroxydopamine; l -dopa, L-3,4-dihydroxyphenylalanine; LID, l -dopa-induced dyskinesia; SEM, standard error of mean; Tat-D1Ri, Tat-fusion interfering peptide; Tat-D1Rc, Tat-fusion control peptide; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

    Techniques Used: Expressing, Western Blot

    rabbit primary antibody against d1r  (Millipore)

     
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    Millipore rabbit primary antibody against d1r
    Effects of intrastriatal administration of Tat-fusion interfering peptide (Tat-D1Ri) on <t>D1R–GluN1</t> interactions. Notes: Tat-D1Ri, Tat-D1Rc, or saline were locally injected into the striatum of the normal adult rat at a rate of 0.2 µL/min. Rat striatal tissues were then used for coimmunoprecipitation experiments to validate the efficacy and selectivity of interfering peptide. The intrastriatal injection of Tat-D1Ri rather than Tat-D1Rc caused reduction of <t>D1R–GluN1</t> interactions, which demonstrated the effectiveness of Tat-D1Ri. Abbreviations: Tat-D1Rc, Tat-fusion control peptide; Ig, Immunoglobulin; IP, immunoprecipitation; IB, immunoblot.
    Rabbit Primary Antibody Against D1r, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit primary antibody against d1r/product/Millipore
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit primary antibody against d1r - by Bioz Stars, 2024-09
    86/100 stars

    Images

    1) Product Images from "Targeting the D1-N-methyl- d -aspartate receptor complex reduces l -dopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats"

    Article Title: Targeting the D1-N-methyl- d -aspartate receptor complex reduces l -dopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    Journal: Drug Design, Development and Therapy

    doi: 10.2147/DDDT.S93487

    Effects of intrastriatal administration of Tat-fusion interfering peptide (Tat-D1Ri) on D1R–GluN1 interactions. Notes: Tat-D1Ri, Tat-D1Rc, or saline were locally injected into the striatum of the normal adult rat at a rate of 0.2 µL/min. Rat striatal tissues were then used for coimmunoprecipitation experiments to validate the efficacy and selectivity of interfering peptide. The intrastriatal injection of Tat-D1Ri rather than Tat-D1Rc caused reduction of D1R–GluN1 interactions, which demonstrated the effectiveness of Tat-D1Ri. Abbreviations: Tat-D1Rc, Tat-fusion control peptide; Ig, Immunoglobulin; IP, immunoprecipitation; IB, immunoblot.
    Figure Legend Snippet: Effects of intrastriatal administration of Tat-fusion interfering peptide (Tat-D1Ri) on D1R–GluN1 interactions. Notes: Tat-D1Ri, Tat-D1Rc, or saline were locally injected into the striatum of the normal adult rat at a rate of 0.2 µL/min. Rat striatal tissues were then used for coimmunoprecipitation experiments to validate the efficacy and selectivity of interfering peptide. The intrastriatal injection of Tat-D1Ri rather than Tat-D1Rc caused reduction of D1R–GluN1 interactions, which demonstrated the effectiveness of Tat-D1Ri. Abbreviations: Tat-D1Rc, Tat-fusion control peptide; Ig, Immunoglobulin; IP, immunoprecipitation; IB, immunoblot.

    Techniques Used: Injection, Immunoprecipitation, Western Blot

    Effects of intrastriatal administration of Tat-D1Ri on membrane D1R subunit expression. Notes: Protein levels were evaluated by Western blotting of proteins extracted from the lesioned striatum of the rat brains. They were assessed in extracts from 6-OHDA-lesioned rats treated with pulsatile l -dopa plus intrastriatal administration of Tat-D1Rc or Tat-D1Ri. ( A ) Representative Western blot analysis of D1R in the membrane fraction; ( B ) densitometric analysis of two blots with specific protein signals normalized to the corresponding GAPDH levels. Data are expressed as means ± SEM. Statistical analysis was conducted by independent-samples t -test. * P =0.05 versus LID + Tat-D1Rc. Abbreviations: 6-OHDA, 6-hydroxydopamine; l -dopa, L-3,4-dihydroxyphenylalanine; LID, l -dopa-induced dyskinesia; SEM, standard error of mean; Tat-D1Ri, Tat-fusion interfering peptide; Tat-D1Rc, Tat-fusion control peptide; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.
    Figure Legend Snippet: Effects of intrastriatal administration of Tat-D1Ri on membrane D1R subunit expression. Notes: Protein levels were evaluated by Western blotting of proteins extracted from the lesioned striatum of the rat brains. They were assessed in extracts from 6-OHDA-lesioned rats treated with pulsatile l -dopa plus intrastriatal administration of Tat-D1Rc or Tat-D1Ri. ( A ) Representative Western blot analysis of D1R in the membrane fraction; ( B ) densitometric analysis of two blots with specific protein signals normalized to the corresponding GAPDH levels. Data are expressed as means ± SEM. Statistical analysis was conducted by independent-samples t -test. * P =0.05 versus LID + Tat-D1Rc. Abbreviations: 6-OHDA, 6-hydroxydopamine; l -dopa, L-3,4-dihydroxyphenylalanine; LID, l -dopa-induced dyskinesia; SEM, standard error of mean; Tat-D1Ri, Tat-fusion interfering peptide; Tat-D1Rc, Tat-fusion control peptide; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

    Techniques Used: Expressing, Western Blot

    antibodies against d1r  (Millipore)

     
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    Millipore antibodies against d1r
    A , comparison of DAR expression in human pituitary (P), striatum (S) and sc adipose tissue (A), as determined by conventional RT-PCR. B , expression of selected DAR in the stromo-vascular cell (SVC) fraction and mature adipocytes, as determined by real-time PCR. Data are expressed as relative changes over SVC. Each value is a mean±SEM of 3 determinations; *, p<0.05. C , Immunoblot of selected DAR proteins in tissues and cells. Lanes: 1, pituitary; 2, proliferating primary preadipocytes; 3, proliferating LS14; 4, proliferating SW872; 5, differentiated primary adipocytes; 6, differentiated LS14; 7, differentiated SW872. Each lane was loaded with 40 µg proteins, except for the pituitary (30 µg proteins). β-actin (β-Act) was used as a loading control. Expression of <t>D1R,</t> D2R and D4R ( panel D ), and PRL vs PRLR ( panel E ) during adipogenesis in LS14 cells was determined by qPCR. Data are expressed as relative changes over day 0, and were calculated from the cycle threshold and efficiency measurements (Mean±SEM of 3 determinations).
    Antibodies Against D1r, supplied by Millipore, 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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    Images

    1) Product Images from "Dopamine Receptors in Human Adipocytes: Expression and Functions"

    Article Title: Dopamine Receptors in Human Adipocytes: Expression and Functions

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0025537

    A , comparison of DAR expression in human pituitary (P), striatum (S) and sc adipose tissue (A), as determined by conventional RT-PCR. B , expression of selected DAR in the stromo-vascular cell (SVC) fraction and mature adipocytes, as determined by real-time PCR. Data are expressed as relative changes over SVC. Each value is a mean±SEM of 3 determinations; *, p<0.05. C , Immunoblot of selected DAR proteins in tissues and cells. Lanes: 1, pituitary; 2, proliferating primary preadipocytes; 3, proliferating LS14; 4, proliferating SW872; 5, differentiated primary adipocytes; 6, differentiated LS14; 7, differentiated SW872. Each lane was loaded with 40 µg proteins, except for the pituitary (30 µg proteins). β-actin (β-Act) was used as a loading control. Expression of D1R, D2R and D4R ( panel D ), and PRL vs PRLR ( panel E ) during adipogenesis in LS14 cells was determined by qPCR. Data are expressed as relative changes over day 0, and were calculated from the cycle threshold and efficiency measurements (Mean±SEM of 3 determinations).
    Figure Legend Snippet: A , comparison of DAR expression in human pituitary (P), striatum (S) and sc adipose tissue (A), as determined by conventional RT-PCR. B , expression of selected DAR in the stromo-vascular cell (SVC) fraction and mature adipocytes, as determined by real-time PCR. Data are expressed as relative changes over SVC. Each value is a mean±SEM of 3 determinations; *, p<0.05. C , Immunoblot of selected DAR proteins in tissues and cells. Lanes: 1, pituitary; 2, proliferating primary preadipocytes; 3, proliferating LS14; 4, proliferating SW872; 5, differentiated primary adipocytes; 6, differentiated LS14; 7, differentiated SW872. Each lane was loaded with 40 µg proteins, except for the pituitary (30 µg proteins). β-actin (β-Act) was used as a loading control. Expression of D1R, D2R and D4R ( panel D ), and PRL vs PRLR ( panel E ) during adipogenesis in LS14 cells was determined by qPCR. Data are expressed as relative changes over day 0, and were calculated from the cycle threshold and efficiency measurements (Mean±SEM of 3 determinations).

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Real-time Polymerase Chain Reaction, Western Blot

    Sc explants ( panel A ), isolated mature adipocytes ( Panel B ) or differentiated primary adipocytes ( panel C ) were incubated with 1 or 100 nM DA or with 10 nM of SKF38393, a D1R/D5R agonist, for 24 hr. Leptin concentration in CM was determined by ELISA. Each value is a mean±SEM of 5 determinations; *, p<0.05. D , differentiated primary adipocytes were incubated as above and adiponectin release was determined by ELISA. E , proliferating primary adipocytes were incubated with 1 or 100 nM DA or with 10 nM of SKF for 6 hr and IL-6 release was determined by ELISA.
    Figure Legend Snippet: Sc explants ( panel A ), isolated mature adipocytes ( Panel B ) or differentiated primary adipocytes ( panel C ) were incubated with 1 or 100 nM DA or with 10 nM of SKF38393, a D1R/D5R agonist, for 24 hr. Leptin concentration in CM was determined by ELISA. Each value is a mean±SEM of 5 determinations; *, p<0.05. D , differentiated primary adipocytes were incubated as above and adiponectin release was determined by ELISA. E , proliferating primary adipocytes were incubated with 1 or 100 nM DA or with 10 nM of SKF for 6 hr and IL-6 release was determined by ELISA.

    Techniques Used: Isolation, Incubation, Concentration Assay, Enzyme-linked Immunosorbent Assay

    DA can reach the adipocytes from infiltrating lymphocyte/macrophages, sympathetic nerve endings or via the circulation in the form of DA-S. DA-S can become de-conjugated to bioactive DA by ARSA which is secreted from the lysosomes. DA binds to either D2R-like or D1R-like membrane receptors. Activation of D2R causes suppression of cAMP and inhibition of PRL gene expression and release. Activation of D1R-like receptors results in the inhibition of leptin release and stimulation of adiponectin and IL-6, an effect which may be mediated via the cGMP or MAPK signaling. Other catecholamines (i.e. NE and Epi) from the circulation or sympathetic neurons activate β-AR and modulate, by yet an unknown fashion, adipokine release. See text for additional explanations. ARSA, arylsulfatase A; β-AR, β-adrenergic receptors; D2R/D1R, type 1 or type 2 dopamine receptors; DA, dopamine; DA-S, dopamine sulfate; Epi, epinephrine; NE, norepinephrine; MAPK, mitogen-activated protein kinase; PRL, prolactin.
    Figure Legend Snippet: DA can reach the adipocytes from infiltrating lymphocyte/macrophages, sympathetic nerve endings or via the circulation in the form of DA-S. DA-S can become de-conjugated to bioactive DA by ARSA which is secreted from the lysosomes. DA binds to either D2R-like or D1R-like membrane receptors. Activation of D2R causes suppression of cAMP and inhibition of PRL gene expression and release. Activation of D1R-like receptors results in the inhibition of leptin release and stimulation of adiponectin and IL-6, an effect which may be mediated via the cGMP or MAPK signaling. Other catecholamines (i.e. NE and Epi) from the circulation or sympathetic neurons activate β-AR and modulate, by yet an unknown fashion, adipokine release. See text for additional explanations. ARSA, arylsulfatase A; β-AR, β-adrenergic receptors; D2R/D1R, type 1 or type 2 dopamine receptors; DA, dopamine; DA-S, dopamine sulfate; Epi, epinephrine; NE, norepinephrine; MAPK, mitogen-activated protein kinase; PRL, prolactin.

    Techniques Used: Activation Assay, Inhibition, Expressing

    mouse antibody against d1r  (Millipore)

     
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    Millipore mouse antibody against d1r
    PD rats show different AIMs scores after the administration of l -DOPA, <t>D1R</t> antagonist or agonist. Notes: Axial ( A ), limb ( B ), orolingual ( C ) and locomotor ( D ). AIMs scores were observed at 2, 7, 12, 17 and 22 days. Increased AIMs scores in PD rats were observed after the administration of l -DOPA. Meanwhile, the group treated with l -DOPA and D1R agonist showed increasing AIMs scores; however, rats treated with D1R antagonist, SCH23390, plus l -DOPA showed no increasing AIMs scores compared to rats peritoneally injected with l -DOPA alone. Data are presented as mean ± SD. # p < 0.05, versus day 2; * p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: AIMs, abnormal involuntary movements; ANOVA, analysis of variance; d, days; D1R, D1 dopamine receptor; l -DOPA, L-3,4-dihydroxyphenylalanine; PD, Parkinson’s disease.
    Mouse Antibody Against D1r, supplied by Millipore, 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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    Images

    1) Product Images from "The abnormal activation of D1R/Shp-2 complex involved in levodopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats"

    Article Title: The abnormal activation of D1R/Shp-2 complex involved in levodopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    Journal: Neuropsychiatric Disease and Treatment

    doi: 10.2147/NDT.S162562

    PD rats show different AIMs scores after the administration of l -DOPA, D1R antagonist or agonist. Notes: Axial ( A ), limb ( B ), orolingual ( C ) and locomotor ( D ). AIMs scores were observed at 2, 7, 12, 17 and 22 days. Increased AIMs scores in PD rats were observed after the administration of l -DOPA. Meanwhile, the group treated with l -DOPA and D1R agonist showed increasing AIMs scores; however, rats treated with D1R antagonist, SCH23390, plus l -DOPA showed no increasing AIMs scores compared to rats peritoneally injected with l -DOPA alone. Data are presented as mean ± SD. # p < 0.05, versus day 2; * p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: AIMs, abnormal involuntary movements; ANOVA, analysis of variance; d, days; D1R, D1 dopamine receptor; l -DOPA, L-3,4-dihydroxyphenylalanine; PD, Parkinson’s disease.
    Figure Legend Snippet: PD rats show different AIMs scores after the administration of l -DOPA, D1R antagonist or agonist. Notes: Axial ( A ), limb ( B ), orolingual ( C ) and locomotor ( D ). AIMs scores were observed at 2, 7, 12, 17 and 22 days. Increased AIMs scores in PD rats were observed after the administration of l -DOPA. Meanwhile, the group treated with l -DOPA and D1R agonist showed increasing AIMs scores; however, rats treated with D1R antagonist, SCH23390, plus l -DOPA showed no increasing AIMs scores compared to rats peritoneally injected with l -DOPA alone. Data are presented as mean ± SD. # p < 0.05, versus day 2; * p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: AIMs, abnormal involuntary movements; ANOVA, analysis of variance; d, days; D1R, D1 dopamine receptor; l -DOPA, L-3,4-dihydroxyphenylalanine; PD, Parkinson’s disease.

    Techniques Used: Injection

    D1R interacts with Shp-2 in the striatal neurons. Notes: Striatal proteins were coimmunoprecipitated with anti-D1R and anti-Shp-2 antibodies ( A and B ). Representative immunoblots showing D1R and Shp-2 interactions in striatal neurons as detected by coimmunoprecipitation. No precipitating antibody, an irrelevant IgG was used in L2, L3, respectively. The D1R antibody (L4A) or Shp-2 antibody (L4B) was used in L4 for normal rats and L5 for LID rats, respectively. No striatal proteins and antibodies were used in L1. Abbreviations: IP, immunoprecipitation; D1R, D1 dopamine receptor; L1, lane 1; L2, lane 2; L3, lane 3; L4, lane 4; L5, lane 5; LID, levodopa-induced dyskinesia.
    Figure Legend Snippet: D1R interacts with Shp-2 in the striatal neurons. Notes: Striatal proteins were coimmunoprecipitated with anti-D1R and anti-Shp-2 antibodies ( A and B ). Representative immunoblots showing D1R and Shp-2 interactions in striatal neurons as detected by coimmunoprecipitation. No precipitating antibody, an irrelevant IgG was used in L2, L3, respectively. The D1R antibody (L4A) or Shp-2 antibody (L4B) was used in L4 for normal rats and L5 for LID rats, respectively. No striatal proteins and antibodies were used in L1. Abbreviations: IP, immunoprecipitation; D1R, D1 dopamine receptor; L1, lane 1; L2, lane 2; L3, lane 3; L4, lane 4; L5, lane 5; LID, levodopa-induced dyskinesia.

    Techniques Used: Western Blot, Immunoprecipitation

    Molecular events underlying LID involving D1R/Shp-2 complex and its downstream signaling factors, such as ERK1/2 and mTOR. Notes: The bands represent immunoblot images detected by antibodies against p-Shp-2 ( A ), p-ERK ( B ) and p-mTOR ( C ). Proteins were analyzed from the sham group (1), l -DOPA group (2), SCH23390 + l -DOPA group (3), SKF38393 group (4). Repeated administration of l -DOPA increased the level of p-Shp-2, p-ERK1/2 and p-mTOR. SKF38393 increased the levels similarly. Conversely, SCH23390 plus L-DOPA prevented the increase. Data are presented as mean ± SD. * p < 0.05, versus sham group; # p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: ANOVA, analysis of variance; D1R, D1 dopamine receptor; ERK1/2, extracellular signal-regulated kinases 1 and 2; l -DOPA, l -3,4-dihydroxyphenylalanine; LID, levodopa-induced dyskinesia.
    Figure Legend Snippet: Molecular events underlying LID involving D1R/Shp-2 complex and its downstream signaling factors, such as ERK1/2 and mTOR. Notes: The bands represent immunoblot images detected by antibodies against p-Shp-2 ( A ), p-ERK ( B ) and p-mTOR ( C ). Proteins were analyzed from the sham group (1), l -DOPA group (2), SCH23390 + l -DOPA group (3), SKF38393 group (4). Repeated administration of l -DOPA increased the level of p-Shp-2, p-ERK1/2 and p-mTOR. SKF38393 increased the levels similarly. Conversely, SCH23390 plus L-DOPA prevented the increase. Data are presented as mean ± SD. * p < 0.05, versus sham group; # p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: ANOVA, analysis of variance; D1R, D1 dopamine receptor; ERK1/2, extracellular signal-regulated kinases 1 and 2; l -DOPA, l -3,4-dihydroxyphenylalanine; LID, levodopa-induced dyskinesia.

    Techniques Used: Western Blot

    mouse primary antibody against d1r  (Millipore)

     
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    Millipore mouse primary antibody against d1r
    PD rats show different AIMs scores after the administration of l -DOPA, <t>D1R</t> antagonist or agonist. Notes: Axial ( A ), limb ( B ), orolingual ( C ) and locomotor ( D ). AIMs scores were observed at 2, 7, 12, 17 and 22 days. Increased AIMs scores in PD rats were observed after the administration of l -DOPA. Meanwhile, the group treated with l -DOPA and D1R agonist showed increasing AIMs scores; however, rats treated with D1R antagonist, SCH23390, plus l -DOPA showed no increasing AIMs scores compared to rats peritoneally injected with l -DOPA alone. Data are presented as mean ± SD. # p < 0.05, versus day 2; * p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: AIMs, abnormal involuntary movements; ANOVA, analysis of variance; d, days; D1R, D1 dopamine receptor; l -DOPA, L-3,4-dihydroxyphenylalanine; PD, Parkinson’s disease.
    Mouse Primary Antibody Against D1r, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse primary antibody against d1r/product/Millipore
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    Images

    1) Product Images from "The abnormal activation of D1R/Shp-2 complex involved in levodopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats"

    Article Title: The abnormal activation of D1R/Shp-2 complex involved in levodopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    Journal: Neuropsychiatric Disease and Treatment

    doi: 10.2147/NDT.S162562

    PD rats show different AIMs scores after the administration of l -DOPA, D1R antagonist or agonist. Notes: Axial ( A ), limb ( B ), orolingual ( C ) and locomotor ( D ). AIMs scores were observed at 2, 7, 12, 17 and 22 days. Increased AIMs scores in PD rats were observed after the administration of l -DOPA. Meanwhile, the group treated with l -DOPA and D1R agonist showed increasing AIMs scores; however, rats treated with D1R antagonist, SCH23390, plus l -DOPA showed no increasing AIMs scores compared to rats peritoneally injected with l -DOPA alone. Data are presented as mean ± SD. # p < 0.05, versus day 2; * p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: AIMs, abnormal involuntary movements; ANOVA, analysis of variance; d, days; D1R, D1 dopamine receptor; l -DOPA, L-3,4-dihydroxyphenylalanine; PD, Parkinson’s disease.
    Figure Legend Snippet: PD rats show different AIMs scores after the administration of l -DOPA, D1R antagonist or agonist. Notes: Axial ( A ), limb ( B ), orolingual ( C ) and locomotor ( D ). AIMs scores were observed at 2, 7, 12, 17 and 22 days. Increased AIMs scores in PD rats were observed after the administration of l -DOPA. Meanwhile, the group treated with l -DOPA and D1R agonist showed increasing AIMs scores; however, rats treated with D1R antagonist, SCH23390, plus l -DOPA showed no increasing AIMs scores compared to rats peritoneally injected with l -DOPA alone. Data are presented as mean ± SD. # p < 0.05, versus day 2; * p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: AIMs, abnormal involuntary movements; ANOVA, analysis of variance; d, days; D1R, D1 dopamine receptor; l -DOPA, L-3,4-dihydroxyphenylalanine; PD, Parkinson’s disease.

    Techniques Used: Injection

    D1R interacts with Shp-2 in the striatal neurons. Notes: Striatal proteins were coimmunoprecipitated with anti-D1R and anti-Shp-2 antibodies ( A and B ). Representative immunoblots showing D1R and Shp-2 interactions in striatal neurons as detected by coimmunoprecipitation. No precipitating antibody, an irrelevant IgG was used in L2, L3, respectively. The D1R antibody (L4A) or Shp-2 antibody (L4B) was used in L4 for normal rats and L5 for LID rats, respectively. No striatal proteins and antibodies were used in L1. Abbreviations: IP, immunoprecipitation; D1R, D1 dopamine receptor; L1, lane 1; L2, lane 2; L3, lane 3; L4, lane 4; L5, lane 5; LID, levodopa-induced dyskinesia.
    Figure Legend Snippet: D1R interacts with Shp-2 in the striatal neurons. Notes: Striatal proteins were coimmunoprecipitated with anti-D1R and anti-Shp-2 antibodies ( A and B ). Representative immunoblots showing D1R and Shp-2 interactions in striatal neurons as detected by coimmunoprecipitation. No precipitating antibody, an irrelevant IgG was used in L2, L3, respectively. The D1R antibody (L4A) or Shp-2 antibody (L4B) was used in L4 for normal rats and L5 for LID rats, respectively. No striatal proteins and antibodies were used in L1. Abbreviations: IP, immunoprecipitation; D1R, D1 dopamine receptor; L1, lane 1; L2, lane 2; L3, lane 3; L4, lane 4; L5, lane 5; LID, levodopa-induced dyskinesia.

    Techniques Used: Western Blot, Immunoprecipitation

    Molecular events underlying LID involving D1R/Shp-2 complex and its downstream signaling factors, such as ERK1/2 and mTOR. Notes: The bands represent immunoblot images detected by antibodies against p-Shp-2 ( A ), p-ERK ( B ) and p-mTOR ( C ). Proteins were analyzed from the sham group (1), l -DOPA group (2), SCH23390 + l -DOPA group (3), SKF38393 group (4). Repeated administration of l -DOPA increased the level of p-Shp-2, p-ERK1/2 and p-mTOR. SKF38393 increased the levels similarly. Conversely, SCH23390 plus L-DOPA prevented the increase. Data are presented as mean ± SD. * p < 0.05, versus sham group; # p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: ANOVA, analysis of variance; D1R, D1 dopamine receptor; ERK1/2, extracellular signal-regulated kinases 1 and 2; l -DOPA, l -3,4-dihydroxyphenylalanine; LID, levodopa-induced dyskinesia.
    Figure Legend Snippet: Molecular events underlying LID involving D1R/Shp-2 complex and its downstream signaling factors, such as ERK1/2 and mTOR. Notes: The bands represent immunoblot images detected by antibodies against p-Shp-2 ( A ), p-ERK ( B ) and p-mTOR ( C ). Proteins were analyzed from the sham group (1), l -DOPA group (2), SCH23390 + l -DOPA group (3), SKF38393 group (4). Repeated administration of l -DOPA increased the level of p-Shp-2, p-ERK1/2 and p-mTOR. SKF38393 increased the levels similarly. Conversely, SCH23390 plus L-DOPA prevented the increase. Data are presented as mean ± SD. * p < 0.05, versus sham group; # p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: ANOVA, analysis of variance; D1R, D1 dopamine receptor; ERK1/2, extracellular signal-regulated kinases 1 and 2; l -DOPA, l -3,4-dihydroxyphenylalanine; LID, levodopa-induced dyskinesia.

    Techniques Used: Western Blot

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    antibodies against d1r  (Millipore)
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    Pain relief increased dopaminergic D2 receptor expression in injured mice. D2 receptor expression in the CeA was significantly decreased in incised mice treated with PNB compared with incised mice treated with saline (n = 6; * p < 0.05 vs the incision+saline group; one-way ANOVA,Interaction::F (3, 20) = 6.274). The expression of <t>D1</t> <t>receptor</t> was not significantly changed. (b) In the CeA, D1 receptor was mainly expressed in glutamatergic excitatory neurons (positive for glutaminase). In the CeA, D2 receptor was predominantly expressed in GABAergic inhibitory neurons (positive for GABA). Scale bar, 50 μm.
    Antibodies Against D1r, supplied by Millipore, 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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    rabbit antibody against d1r  (Millipore)
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    Effects of intrastriatal administration of Tat-fusion interfering peptide (Tat-D1Ri) on <t>D1R–GluN1</t> interactions. Notes: Tat-D1Ri, Tat-D1Rc, or saline were locally injected into the striatum of the normal adult rat at a rate of 0.2 µL/min. Rat striatal tissues were then used for coimmunoprecipitation experiments to validate the efficacy and selectivity of interfering peptide. The intrastriatal injection of Tat-D1Ri rather than Tat-D1Rc caused reduction of <t>D1R–GluN1</t> interactions, which demonstrated the effectiveness of Tat-D1Ri. Abbreviations: Tat-D1Rc, Tat-fusion control peptide; Ig, Immunoglobulin; IP, immunoprecipitation; IB, immunoblot.
    Rabbit Antibody Against D1r, supplied by Millipore, 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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    rabbit primary antibody against d1r  (Millipore)
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    Effects of intrastriatal administration of Tat-fusion interfering peptide (Tat-D1Ri) on <t>D1R–GluN1</t> interactions. Notes: Tat-D1Ri, Tat-D1Rc, or saline were locally injected into the striatum of the normal adult rat at a rate of 0.2 µL/min. Rat striatal tissues were then used for coimmunoprecipitation experiments to validate the efficacy and selectivity of interfering peptide. The intrastriatal injection of Tat-D1Ri rather than Tat-D1Rc caused reduction of <t>D1R–GluN1</t> interactions, which demonstrated the effectiveness of Tat-D1Ri. Abbreviations: Tat-D1Rc, Tat-fusion control peptide; Ig, Immunoglobulin; IP, immunoprecipitation; IB, immunoblot.
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    PD rats show different AIMs scores after the administration of l -DOPA, <t>D1R</t> antagonist or agonist. Notes: Axial ( A ), limb ( B ), orolingual ( C ) and locomotor ( D ). AIMs scores were observed at 2, 7, 12, 17 and 22 days. Increased AIMs scores in PD rats were observed after the administration of l -DOPA. Meanwhile, the group treated with l -DOPA and D1R agonist showed increasing AIMs scores; however, rats treated with D1R antagonist, SCH23390, plus l -DOPA showed no increasing AIMs scores compared to rats peritoneally injected with l -DOPA alone. Data are presented as mean ± SD. # p < 0.05, versus day 2; * p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: AIMs, abnormal involuntary movements; ANOVA, analysis of variance; d, days; D1R, D1 dopamine receptor; l -DOPA, L-3,4-dihydroxyphenylalanine; PD, Parkinson’s disease.
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    mouse primary antibody against d1r  (Millipore)
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    PD rats show different AIMs scores after the administration of l -DOPA, <t>D1R</t> antagonist or agonist. Notes: Axial ( A ), limb ( B ), orolingual ( C ) and locomotor ( D ). AIMs scores were observed at 2, 7, 12, 17 and 22 days. Increased AIMs scores in PD rats were observed after the administration of l -DOPA. Meanwhile, the group treated with l -DOPA and D1R agonist showed increasing AIMs scores; however, rats treated with D1R antagonist, SCH23390, plus l -DOPA showed no increasing AIMs scores compared to rats peritoneally injected with l -DOPA alone. Data are presented as mean ± SD. # p < 0.05, versus day 2; * p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: AIMs, abnormal involuntary movements; ANOVA, analysis of variance; d, days; D1R, D1 dopamine receptor; l -DOPA, L-3,4-dihydroxyphenylalanine; PD, Parkinson’s disease.
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    Image Search Results


    Pain relief increased dopaminergic D2 receptor expression in injured mice. D2 receptor expression in the CeA was significantly decreased in incised mice treated with PNB compared with incised mice treated with saline (n = 6; * p < 0.05 vs the incision+saline group; one-way ANOVA,Interaction::F (3, 20) = 6.274). The expression of D1 receptor was not significantly changed. (b) In the CeA, D1 receptor was mainly expressed in glutamatergic excitatory neurons (positive for glutaminase). In the CeA, D2 receptor was predominantly expressed in GABAergic inhibitory neurons (positive for GABA). Scale bar, 50 μm.

    Journal: Molecular Pain

    Article Title: Dopamine receptor D2, but not D1, mediates the reward circuit from the ventral tegmental area to the central amygdala, which is involved in pain relief

    doi: 10.1177/17448069221145096

    Figure Lengend Snippet: Pain relief increased dopaminergic D2 receptor expression in injured mice. D2 receptor expression in the CeA was significantly decreased in incised mice treated with PNB compared with incised mice treated with saline (n = 6; * p < 0.05 vs the incision+saline group; one-way ANOVA,Interaction::F (3, 20) = 6.274). The expression of D1 receptor was not significantly changed. (b) In the CeA, D1 receptor was mainly expressed in glutamatergic excitatory neurons (positive for glutaminase). In the CeA, D2 receptor was predominantly expressed in GABAergic inhibitory neurons (positive for GABA). Scale bar, 50 μm.

    Article Snippet: After being blocked with 3% bovine serum albumin (BSA) (Solarbio, Beijing, China) and incubated overnight at 4°C with primary antibodies against D1R (1:1000; catalog No. MAB5290, Millipore), D2R (1:1000 catalog No. AB5084P, Millipore), and GAPDH (catalog No. RM2002 L, Beijing Ray), the membranes were washed six times for 10 min each in Tris-buffered saline and 1% Tween.

    Techniques: Expressing

    Journal: Molecular Pain

    Article Title: Dopamine receptor D2, but not D1, mediates the reward circuit from the ventral tegmental area to the central amygdala, which is involved in pain relief

    doi: 10.1177/17448069221145096

    Figure Lengend Snippet:

    Article Snippet: After being blocked with 3% bovine serum albumin (BSA) (Solarbio, Beijing, China) and incubated overnight at 4°C with primary antibodies against D1R (1:1000; catalog No. MAB5290, Millipore), D2R (1:1000 catalog No. AB5084P, Millipore), and GAPDH (catalog No. RM2002 L, Beijing Ray), the membranes were washed six times for 10 min each in Tris-buffered saline and 1% Tween.

    Techniques:

    Effects of intrastriatal administration of Tat-fusion interfering peptide (Tat-D1Ri) on D1R–GluN1 interactions. Notes: Tat-D1Ri, Tat-D1Rc, or saline were locally injected into the striatum of the normal adult rat at a rate of 0.2 µL/min. Rat striatal tissues were then used for coimmunoprecipitation experiments to validate the efficacy and selectivity of interfering peptide. The intrastriatal injection of Tat-D1Ri rather than Tat-D1Rc caused reduction of D1R–GluN1 interactions, which demonstrated the effectiveness of Tat-D1Ri. Abbreviations: Tat-D1Rc, Tat-fusion control peptide; Ig, Immunoglobulin; IP, immunoprecipitation; IB, immunoblot.

    Journal: Drug Design, Development and Therapy

    Article Title: Targeting the D1-N-methyl- d -aspartate receptor complex reduces l -dopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    doi: 10.2147/DDDT.S93487

    Figure Lengend Snippet: Effects of intrastriatal administration of Tat-fusion interfering peptide (Tat-D1Ri) on D1R–GluN1 interactions. Notes: Tat-D1Ri, Tat-D1Rc, or saline were locally injected into the striatum of the normal adult rat at a rate of 0.2 µL/min. Rat striatal tissues were then used for coimmunoprecipitation experiments to validate the efficacy and selectivity of interfering peptide. The intrastriatal injection of Tat-D1Ri rather than Tat-D1Rc caused reduction of D1R–GluN1 interactions, which demonstrated the effectiveness of Tat-D1Ri. Abbreviations: Tat-D1Rc, Tat-fusion control peptide; Ig, Immunoglobulin; IP, immunoprecipitation; IB, immunoblot.

    Article Snippet: Samples were incubated with a rabbit antibody against D1R (EMD Millipore, Billerica, MA, USA) or a mouse antibody against GluN1 (Millipore) overnight at 4°C.

    Techniques: Injection, Immunoprecipitation, Western Blot

    Effects of intrastriatal administration of Tat-D1Ri on membrane D1R subunit expression. Notes: Protein levels were evaluated by Western blotting of proteins extracted from the lesioned striatum of the rat brains. They were assessed in extracts from 6-OHDA-lesioned rats treated with pulsatile l -dopa plus intrastriatal administration of Tat-D1Rc or Tat-D1Ri. ( A ) Representative Western blot analysis of D1R in the membrane fraction; ( B ) densitometric analysis of two blots with specific protein signals normalized to the corresponding GAPDH levels. Data are expressed as means ± SEM. Statistical analysis was conducted by independent-samples t -test. * P =0.05 versus LID + Tat-D1Rc. Abbreviations: 6-OHDA, 6-hydroxydopamine; l -dopa, L-3,4-dihydroxyphenylalanine; LID, l -dopa-induced dyskinesia; SEM, standard error of mean; Tat-D1Ri, Tat-fusion interfering peptide; Tat-D1Rc, Tat-fusion control peptide; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

    Journal: Drug Design, Development and Therapy

    Article Title: Targeting the D1-N-methyl- d -aspartate receptor complex reduces l -dopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    doi: 10.2147/DDDT.S93487

    Figure Lengend Snippet: Effects of intrastriatal administration of Tat-D1Ri on membrane D1R subunit expression. Notes: Protein levels were evaluated by Western blotting of proteins extracted from the lesioned striatum of the rat brains. They were assessed in extracts from 6-OHDA-lesioned rats treated with pulsatile l -dopa plus intrastriatal administration of Tat-D1Rc or Tat-D1Ri. ( A ) Representative Western blot analysis of D1R in the membrane fraction; ( B ) densitometric analysis of two blots with specific protein signals normalized to the corresponding GAPDH levels. Data are expressed as means ± SEM. Statistical analysis was conducted by independent-samples t -test. * P =0.05 versus LID + Tat-D1Rc. Abbreviations: 6-OHDA, 6-hydroxydopamine; l -dopa, L-3,4-dihydroxyphenylalanine; LID, l -dopa-induced dyskinesia; SEM, standard error of mean; Tat-D1Ri, Tat-fusion interfering peptide; Tat-D1Rc, Tat-fusion control peptide; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

    Article Snippet: Samples were incubated with a rabbit antibody against D1R (EMD Millipore, Billerica, MA, USA) or a mouse antibody against GluN1 (Millipore) overnight at 4°C.

    Techniques: Expressing, Western Blot

    Effects of intrastriatal administration of Tat-fusion interfering peptide (Tat-D1Ri) on D1R–GluN1 interactions. Notes: Tat-D1Ri, Tat-D1Rc, or saline were locally injected into the striatum of the normal adult rat at a rate of 0.2 µL/min. Rat striatal tissues were then used for coimmunoprecipitation experiments to validate the efficacy and selectivity of interfering peptide. The intrastriatal injection of Tat-D1Ri rather than Tat-D1Rc caused reduction of D1R–GluN1 interactions, which demonstrated the effectiveness of Tat-D1Ri. Abbreviations: Tat-D1Rc, Tat-fusion control peptide; Ig, Immunoglobulin; IP, immunoprecipitation; IB, immunoblot.

    Journal: Drug Design, Development and Therapy

    Article Title: Targeting the D1-N-methyl- d -aspartate receptor complex reduces l -dopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    doi: 10.2147/DDDT.S93487

    Figure Lengend Snippet: Effects of intrastriatal administration of Tat-fusion interfering peptide (Tat-D1Ri) on D1R–GluN1 interactions. Notes: Tat-D1Ri, Tat-D1Rc, or saline were locally injected into the striatum of the normal adult rat at a rate of 0.2 µL/min. Rat striatal tissues were then used for coimmunoprecipitation experiments to validate the efficacy and selectivity of interfering peptide. The intrastriatal injection of Tat-D1Ri rather than Tat-D1Rc caused reduction of D1R–GluN1 interactions, which demonstrated the effectiveness of Tat-D1Ri. Abbreviations: Tat-D1Rc, Tat-fusion control peptide; Ig, Immunoglobulin; IP, immunoprecipitation; IB, immunoblot.

    Article Snippet: Membranes were blocked in 5% nonfat milk for 1 hour at room temperature and incubated with a rabbit primary antibody against D1R (Millipore) or a mouse primary antibody against GluN1 (Millipore) overnight at 4°C.

    Techniques: Injection, Immunoprecipitation, Western Blot

    Effects of intrastriatal administration of Tat-D1Ri on membrane D1R subunit expression. Notes: Protein levels were evaluated by Western blotting of proteins extracted from the lesioned striatum of the rat brains. They were assessed in extracts from 6-OHDA-lesioned rats treated with pulsatile l -dopa plus intrastriatal administration of Tat-D1Rc or Tat-D1Ri. ( A ) Representative Western blot analysis of D1R in the membrane fraction; ( B ) densitometric analysis of two blots with specific protein signals normalized to the corresponding GAPDH levels. Data are expressed as means ± SEM. Statistical analysis was conducted by independent-samples t -test. * P =0.05 versus LID + Tat-D1Rc. Abbreviations: 6-OHDA, 6-hydroxydopamine; l -dopa, L-3,4-dihydroxyphenylalanine; LID, l -dopa-induced dyskinesia; SEM, standard error of mean; Tat-D1Ri, Tat-fusion interfering peptide; Tat-D1Rc, Tat-fusion control peptide; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

    Journal: Drug Design, Development and Therapy

    Article Title: Targeting the D1-N-methyl- d -aspartate receptor complex reduces l -dopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    doi: 10.2147/DDDT.S93487

    Figure Lengend Snippet: Effects of intrastriatal administration of Tat-D1Ri on membrane D1R subunit expression. Notes: Protein levels were evaluated by Western blotting of proteins extracted from the lesioned striatum of the rat brains. They were assessed in extracts from 6-OHDA-lesioned rats treated with pulsatile l -dopa plus intrastriatal administration of Tat-D1Rc or Tat-D1Ri. ( A ) Representative Western blot analysis of D1R in the membrane fraction; ( B ) densitometric analysis of two blots with specific protein signals normalized to the corresponding GAPDH levels. Data are expressed as means ± SEM. Statistical analysis was conducted by independent-samples t -test. * P =0.05 versus LID + Tat-D1Rc. Abbreviations: 6-OHDA, 6-hydroxydopamine; l -dopa, L-3,4-dihydroxyphenylalanine; LID, l -dopa-induced dyskinesia; SEM, standard error of mean; Tat-D1Ri, Tat-fusion interfering peptide; Tat-D1Rc, Tat-fusion control peptide; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

    Article Snippet: Membranes were blocked in 5% nonfat milk for 1 hour at room temperature and incubated with a rabbit primary antibody against D1R (Millipore) or a mouse primary antibody against GluN1 (Millipore) overnight at 4°C.

    Techniques: Expressing, Western Blot

    PD rats show different AIMs scores after the administration of l -DOPA, D1R antagonist or agonist. Notes: Axial ( A ), limb ( B ), orolingual ( C ) and locomotor ( D ). AIMs scores were observed at 2, 7, 12, 17 and 22 days. Increased AIMs scores in PD rats were observed after the administration of l -DOPA. Meanwhile, the group treated with l -DOPA and D1R agonist showed increasing AIMs scores; however, rats treated with D1R antagonist, SCH23390, plus l -DOPA showed no increasing AIMs scores compared to rats peritoneally injected with l -DOPA alone. Data are presented as mean ± SD. # p < 0.05, versus day 2; * p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: AIMs, abnormal involuntary movements; ANOVA, analysis of variance; d, days; D1R, D1 dopamine receptor; l -DOPA, L-3,4-dihydroxyphenylalanine; PD, Parkinson’s disease.

    Journal: Neuropsychiatric Disease and Treatment

    Article Title: The abnormal activation of D1R/Shp-2 complex involved in levodopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    doi: 10.2147/NDT.S162562

    Figure Lengend Snippet: PD rats show different AIMs scores after the administration of l -DOPA, D1R antagonist or agonist. Notes: Axial ( A ), limb ( B ), orolingual ( C ) and locomotor ( D ). AIMs scores were observed at 2, 7, 12, 17 and 22 days. Increased AIMs scores in PD rats were observed after the administration of l -DOPA. Meanwhile, the group treated with l -DOPA and D1R agonist showed increasing AIMs scores; however, rats treated with D1R antagonist, SCH23390, plus l -DOPA showed no increasing AIMs scores compared to rats peritoneally injected with l -DOPA alone. Data are presented as mean ± SD. # p < 0.05, versus day 2; * p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: AIMs, abnormal involuntary movements; ANOVA, analysis of variance; d, days; D1R, D1 dopamine receptor; l -DOPA, L-3,4-dihydroxyphenylalanine; PD, Parkinson’s disease.

    Article Snippet: Samples were incubated with a mouse antibody against D1R (EMD Millipore, Billerica, MA, USA) or a rabbit antibody against Shp-2 (Proteintech, Rosemont, IL, USA) overnight at 4°C.

    Techniques: Injection

    D1R interacts with Shp-2 in the striatal neurons. Notes: Striatal proteins were coimmunoprecipitated with anti-D1R and anti-Shp-2 antibodies ( A and B ). Representative immunoblots showing D1R and Shp-2 interactions in striatal neurons as detected by coimmunoprecipitation. No precipitating antibody, an irrelevant IgG was used in L2, L3, respectively. The D1R antibody (L4A) or Shp-2 antibody (L4B) was used in L4 for normal rats and L5 for LID rats, respectively. No striatal proteins and antibodies were used in L1. Abbreviations: IP, immunoprecipitation; D1R, D1 dopamine receptor; L1, lane 1; L2, lane 2; L3, lane 3; L4, lane 4; L5, lane 5; LID, levodopa-induced dyskinesia.

    Journal: Neuropsychiatric Disease and Treatment

    Article Title: The abnormal activation of D1R/Shp-2 complex involved in levodopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    doi: 10.2147/NDT.S162562

    Figure Lengend Snippet: D1R interacts with Shp-2 in the striatal neurons. Notes: Striatal proteins were coimmunoprecipitated with anti-D1R and anti-Shp-2 antibodies ( A and B ). Representative immunoblots showing D1R and Shp-2 interactions in striatal neurons as detected by coimmunoprecipitation. No precipitating antibody, an irrelevant IgG was used in L2, L3, respectively. The D1R antibody (L4A) or Shp-2 antibody (L4B) was used in L4 for normal rats and L5 for LID rats, respectively. No striatal proteins and antibodies were used in L1. Abbreviations: IP, immunoprecipitation; D1R, D1 dopamine receptor; L1, lane 1; L2, lane 2; L3, lane 3; L4, lane 4; L5, lane 5; LID, levodopa-induced dyskinesia.

    Article Snippet: Samples were incubated with a mouse antibody against D1R (EMD Millipore, Billerica, MA, USA) or a rabbit antibody against Shp-2 (Proteintech, Rosemont, IL, USA) overnight at 4°C.

    Techniques: Western Blot, Immunoprecipitation

    Molecular events underlying LID involving D1R/Shp-2 complex and its downstream signaling factors, such as ERK1/2 and mTOR. Notes: The bands represent immunoblot images detected by antibodies against p-Shp-2 ( A ), p-ERK ( B ) and p-mTOR ( C ). Proteins were analyzed from the sham group (1), l -DOPA group (2), SCH23390 + l -DOPA group (3), SKF38393 group (4). Repeated administration of l -DOPA increased the level of p-Shp-2, p-ERK1/2 and p-mTOR. SKF38393 increased the levels similarly. Conversely, SCH23390 plus L-DOPA prevented the increase. Data are presented as mean ± SD. * p < 0.05, versus sham group; # p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: ANOVA, analysis of variance; D1R, D1 dopamine receptor; ERK1/2, extracellular signal-regulated kinases 1 and 2; l -DOPA, l -3,4-dihydroxyphenylalanine; LID, levodopa-induced dyskinesia.

    Journal: Neuropsychiatric Disease and Treatment

    Article Title: The abnormal activation of D1R/Shp-2 complex involved in levodopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    doi: 10.2147/NDT.S162562

    Figure Lengend Snippet: Molecular events underlying LID involving D1R/Shp-2 complex and its downstream signaling factors, such as ERK1/2 and mTOR. Notes: The bands represent immunoblot images detected by antibodies against p-Shp-2 ( A ), p-ERK ( B ) and p-mTOR ( C ). Proteins were analyzed from the sham group (1), l -DOPA group (2), SCH23390 + l -DOPA group (3), SKF38393 group (4). Repeated administration of l -DOPA increased the level of p-Shp-2, p-ERK1/2 and p-mTOR. SKF38393 increased the levels similarly. Conversely, SCH23390 plus L-DOPA prevented the increase. Data are presented as mean ± SD. * p < 0.05, versus sham group; # p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: ANOVA, analysis of variance; D1R, D1 dopamine receptor; ERK1/2, extracellular signal-regulated kinases 1 and 2; l -DOPA, l -3,4-dihydroxyphenylalanine; LID, levodopa-induced dyskinesia.

    Article Snippet: Samples were incubated with a mouse antibody against D1R (EMD Millipore, Billerica, MA, USA) or a rabbit antibody against Shp-2 (Proteintech, Rosemont, IL, USA) overnight at 4°C.

    Techniques: Western Blot

    PD rats show different AIMs scores after the administration of l -DOPA, D1R antagonist or agonist. Notes: Axial ( A ), limb ( B ), orolingual ( C ) and locomotor ( D ). AIMs scores were observed at 2, 7, 12, 17 and 22 days. Increased AIMs scores in PD rats were observed after the administration of l -DOPA. Meanwhile, the group treated with l -DOPA and D1R agonist showed increasing AIMs scores; however, rats treated with D1R antagonist, SCH23390, plus l -DOPA showed no increasing AIMs scores compared to rats peritoneally injected with l -DOPA alone. Data are presented as mean ± SD. # p < 0.05, versus day 2; * p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: AIMs, abnormal involuntary movements; ANOVA, analysis of variance; d, days; D1R, D1 dopamine receptor; l -DOPA, L-3,4-dihydroxyphenylalanine; PD, Parkinson’s disease.

    Journal: Neuropsychiatric Disease and Treatment

    Article Title: The abnormal activation of D1R/Shp-2 complex involved in levodopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    doi: 10.2147/NDT.S162562

    Figure Lengend Snippet: PD rats show different AIMs scores after the administration of l -DOPA, D1R antagonist or agonist. Notes: Axial ( A ), limb ( B ), orolingual ( C ) and locomotor ( D ). AIMs scores were observed at 2, 7, 12, 17 and 22 days. Increased AIMs scores in PD rats were observed after the administration of l -DOPA. Meanwhile, the group treated with l -DOPA and D1R agonist showed increasing AIMs scores; however, rats treated with D1R antagonist, SCH23390, plus l -DOPA showed no increasing AIMs scores compared to rats peritoneally injected with l -DOPA alone. Data are presented as mean ± SD. # p < 0.05, versus day 2; * p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: AIMs, abnormal involuntary movements; ANOVA, analysis of variance; d, days; D1R, D1 dopamine receptor; l -DOPA, L-3,4-dihydroxyphenylalanine; PD, Parkinson’s disease.

    Article Snippet: Membranes were blocked in 5% nonfat milk for 1 hour at room temperature and incubated with a mouse primary antibody against D1R (EMD Millipore) or a rabbit primary antibody against Shp-2 (Proteintech) overnight at 4°C.

    Techniques: Injection

    D1R interacts with Shp-2 in the striatal neurons. Notes: Striatal proteins were coimmunoprecipitated with anti-D1R and anti-Shp-2 antibodies ( A and B ). Representative immunoblots showing D1R and Shp-2 interactions in striatal neurons as detected by coimmunoprecipitation. No precipitating antibody, an irrelevant IgG was used in L2, L3, respectively. The D1R antibody (L4A) or Shp-2 antibody (L4B) was used in L4 for normal rats and L5 for LID rats, respectively. No striatal proteins and antibodies were used in L1. Abbreviations: IP, immunoprecipitation; D1R, D1 dopamine receptor; L1, lane 1; L2, lane 2; L3, lane 3; L4, lane 4; L5, lane 5; LID, levodopa-induced dyskinesia.

    Journal: Neuropsychiatric Disease and Treatment

    Article Title: The abnormal activation of D1R/Shp-2 complex involved in levodopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    doi: 10.2147/NDT.S162562

    Figure Lengend Snippet: D1R interacts with Shp-2 in the striatal neurons. Notes: Striatal proteins were coimmunoprecipitated with anti-D1R and anti-Shp-2 antibodies ( A and B ). Representative immunoblots showing D1R and Shp-2 interactions in striatal neurons as detected by coimmunoprecipitation. No precipitating antibody, an irrelevant IgG was used in L2, L3, respectively. The D1R antibody (L4A) or Shp-2 antibody (L4B) was used in L4 for normal rats and L5 for LID rats, respectively. No striatal proteins and antibodies were used in L1. Abbreviations: IP, immunoprecipitation; D1R, D1 dopamine receptor; L1, lane 1; L2, lane 2; L3, lane 3; L4, lane 4; L5, lane 5; LID, levodopa-induced dyskinesia.

    Article Snippet: Membranes were blocked in 5% nonfat milk for 1 hour at room temperature and incubated with a mouse primary antibody against D1R (EMD Millipore) or a rabbit primary antibody against Shp-2 (Proteintech) overnight at 4°C.

    Techniques: Western Blot, Immunoprecipitation

    Molecular events underlying LID involving D1R/Shp-2 complex and its downstream signaling factors, such as ERK1/2 and mTOR. Notes: The bands represent immunoblot images detected by antibodies against p-Shp-2 ( A ), p-ERK ( B ) and p-mTOR ( C ). Proteins were analyzed from the sham group (1), l -DOPA group (2), SCH23390 + l -DOPA group (3), SKF38393 group (4). Repeated administration of l -DOPA increased the level of p-Shp-2, p-ERK1/2 and p-mTOR. SKF38393 increased the levels similarly. Conversely, SCH23390 plus L-DOPA prevented the increase. Data are presented as mean ± SD. * p < 0.05, versus sham group; # p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: ANOVA, analysis of variance; D1R, D1 dopamine receptor; ERK1/2, extracellular signal-regulated kinases 1 and 2; l -DOPA, l -3,4-dihydroxyphenylalanine; LID, levodopa-induced dyskinesia.

    Journal: Neuropsychiatric Disease and Treatment

    Article Title: The abnormal activation of D1R/Shp-2 complex involved in levodopa-induced dyskinesia in 6-hydroxydopamine-lesioned Parkinson’s rats

    doi: 10.2147/NDT.S162562

    Figure Lengend Snippet: Molecular events underlying LID involving D1R/Shp-2 complex and its downstream signaling factors, such as ERK1/2 and mTOR. Notes: The bands represent immunoblot images detected by antibodies against p-Shp-2 ( A ), p-ERK ( B ) and p-mTOR ( C ). Proteins were analyzed from the sham group (1), l -DOPA group (2), SCH23390 + l -DOPA group (3), SKF38393 group (4). Repeated administration of l -DOPA increased the level of p-Shp-2, p-ERK1/2 and p-mTOR. SKF38393 increased the levels similarly. Conversely, SCH23390 plus L-DOPA prevented the increase. Data are presented as mean ± SD. * p < 0.05, versus sham group; # p < 0.05, versus l -DOPA group. Data are statistically analyzed by one-way ANOVA test. Abbreviations: ANOVA, analysis of variance; D1R, D1 dopamine receptor; ERK1/2, extracellular signal-regulated kinases 1 and 2; l -DOPA, l -3,4-dihydroxyphenylalanine; LID, levodopa-induced dyskinesia.

    Article Snippet: Membranes were blocked in 5% nonfat milk for 1 hour at room temperature and incubated with a mouse primary antibody against D1R (EMD Millipore) or a rabbit primary antibody against Shp-2 (Proteintech) overnight at 4°C.

    Techniques: Western Blot