mglur5 agc 007  (Alomone Labs)


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    Alomone Labs mglur5 agc 007
    Responses are plotted as percent change from the baseline fEPSPs as a function of time. Numbers on the representative traces show the time on the graph at which they were recorded. A) SKF81297-induced LTP in the cocaine CPP group (clear triangles, 151.4±8.8%, * p <0.05, n = 6) is completely blocked by the PLD-linked mGluR antagonist (PCCG-13, filled triangles, 95.0±9.2%, n = 6). B) mGluR1 receptor antagonist (LY367385, filled triangles, 106.0±6.7%, n = 6) blocks the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). C) The <t>mGluR5</t> antagonist (MPEP, filled triangles, 122.7±5.6%, n = 6) significantly reduces but does not abolish the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). D) PLC antagonist (U-73122, filled triangles, 128.2±6.1%, n = 6), reduces but does not eliminate the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). For comparison, panels A and B use same data graphs and fEPSP traces for the slices from cocaine CPP group superfused with SKF81297 as shown in , and .
    Mglur5 Agc 007, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mglur5 agc 007/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mglur5 agc 007 - by Bioz Stars, 2023-01
    94/100 stars

    Images

    1) Product Images from "Dopamine-Induced Plasticity, Phospholipase D (PLD) Activity and Cocaine-Cue Behavior Depend on PLD-Linked Metabotropic Glutamate Receptors in Amygdala"

    Article Title: Dopamine-Induced Plasticity, Phospholipase D (PLD) Activity and Cocaine-Cue Behavior Depend on PLD-Linked Metabotropic Glutamate Receptors in Amygdala

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0025639

    Responses are plotted as percent change from the baseline fEPSPs as a function of time. Numbers on the representative traces show the time on the graph at which they were recorded. A) SKF81297-induced LTP in the cocaine CPP group (clear triangles, 151.4±8.8%, * p <0.05, n = 6) is completely blocked by the PLD-linked mGluR antagonist (PCCG-13, filled triangles, 95.0±9.2%, n = 6). B) mGluR1 receptor antagonist (LY367385, filled triangles, 106.0±6.7%, n = 6) blocks the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). C) The mGluR5 antagonist (MPEP, filled triangles, 122.7±5.6%, n = 6) significantly reduces but does not abolish the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). D) PLC antagonist (U-73122, filled triangles, 128.2±6.1%, n = 6), reduces but does not eliminate the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). For comparison, panels A and B use same data graphs and fEPSP traces for the slices from cocaine CPP group superfused with SKF81297 as shown in , and .
    Figure Legend Snippet: Responses are plotted as percent change from the baseline fEPSPs as a function of time. Numbers on the representative traces show the time on the graph at which they were recorded. A) SKF81297-induced LTP in the cocaine CPP group (clear triangles, 151.4±8.8%, * p <0.05, n = 6) is completely blocked by the PLD-linked mGluR antagonist (PCCG-13, filled triangles, 95.0±9.2%, n = 6). B) mGluR1 receptor antagonist (LY367385, filled triangles, 106.0±6.7%, n = 6) blocks the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). C) The mGluR5 antagonist (MPEP, filled triangles, 122.7±5.6%, n = 6) significantly reduces but does not abolish the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). D) PLC antagonist (U-73122, filled triangles, 128.2±6.1%, n = 6), reduces but does not eliminate the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). For comparison, panels A and B use same data graphs and fEPSP traces for the slices from cocaine CPP group superfused with SKF81297 as shown in , and .

    Techniques Used:

    The dotted line indicates PLD activity associated with control slices (no EtOH added) which was determined for each animal and used to calculate the change in PLD activity levels with EtOH and/or drug application. Basal levels represent the increase in PLD activity observed in the EtOH-treated slices compared to the no EtOH controls; * p <0.05 compared to the corresponding saline control and # p <0.05 compared to the cocaine CPP group basal PLD activity. Basal PLD activity was significantly increased (*** p <0.001, n = 50) in the cocaine CPP group (dark bars, 527.3±94.3) compared to the saline-treated group (white bars, 142.6±36.9). SKF81297, the D1/5R agonist, application increased the basal levels in the cocaine CPP group significantly (1722.0±176.9, n = 12, # p <0.05) compared to the basal PLD activity observed with EtOH treatment alone in the same experimental group. The D1/5R antagonist, SCH23390, completely blocked basal PLD activity (91.2±21.9, n = 12, ## p <0.01) in the cocaine CPP group. A similar reduction in PEtOH levels was observed with application of either the PLD-linked mGluR antagonist, PCCG-13 (62.9±10.6, n = 7, ## p <0.01) or the mGluR1 antagonist, LY367385 (75.0±13.9, n = 12, ## p <0.01), while the mGluR5 antagonist, MPEP, did not decrease basal PLD activity (305.7±31.5, n = 7, ns) within the cocaine CPP group but were significantly increased compared to (* p <0.05) the saline treated group. Applications of SKF81297 (184.9±30.5, n = 12), SCH23390 (84.9±38.9, n = 12), MPEP (74.2±16.3, n = 7), LY367385 (94.7±18.9, n = 12) and PCCG-13 (132.5±18.4, n = 7) did not significantly alter the PEtOH levels in the saline-treated group compared to the basal activity levels. Inset is a depiction of the triangular excision performed to isolate amygdala (bilaterally for each animal, each slice) containing the basolateral (BLA), the central (CeA) and the lateral (LA) subregions from three serial coronal slices (350 µm) beginning −2.30 mm to −2.80 mm from Bregma .
    Figure Legend Snippet: The dotted line indicates PLD activity associated with control slices (no EtOH added) which was determined for each animal and used to calculate the change in PLD activity levels with EtOH and/or drug application. Basal levels represent the increase in PLD activity observed in the EtOH-treated slices compared to the no EtOH controls; * p <0.05 compared to the corresponding saline control and # p <0.05 compared to the cocaine CPP group basal PLD activity. Basal PLD activity was significantly increased (*** p <0.001, n = 50) in the cocaine CPP group (dark bars, 527.3±94.3) compared to the saline-treated group (white bars, 142.6±36.9). SKF81297, the D1/5R agonist, application increased the basal levels in the cocaine CPP group significantly (1722.0±176.9, n = 12, # p <0.05) compared to the basal PLD activity observed with EtOH treatment alone in the same experimental group. The D1/5R antagonist, SCH23390, completely blocked basal PLD activity (91.2±21.9, n = 12, ## p <0.01) in the cocaine CPP group. A similar reduction in PEtOH levels was observed with application of either the PLD-linked mGluR antagonist, PCCG-13 (62.9±10.6, n = 7, ## p <0.01) or the mGluR1 antagonist, LY367385 (75.0±13.9, n = 12, ## p <0.01), while the mGluR5 antagonist, MPEP, did not decrease basal PLD activity (305.7±31.5, n = 7, ns) within the cocaine CPP group but were significantly increased compared to (* p <0.05) the saline treated group. Applications of SKF81297 (184.9±30.5, n = 12), SCH23390 (84.9±38.9, n = 12), MPEP (74.2±16.3, n = 7), LY367385 (94.7±18.9, n = 12) and PCCG-13 (132.5±18.4, n = 7) did not significantly alter the PEtOH levels in the saline-treated group compared to the basal activity levels. Inset is a depiction of the triangular excision performed to isolate amygdala (bilaterally for each animal, each slice) containing the basolateral (BLA), the central (CeA) and the lateral (LA) subregions from three serial coronal slices (350 µm) beginning −2.30 mm to −2.80 mm from Bregma .

    Techniques Used: Activity Assay

    mglur5 agc 007  (Alomone Labs)


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    Alomone Labs mglur5 agc 007
    Responses are plotted as percent change from the baseline fEPSPs as a function of time. Numbers on the representative traces show the time on the graph at which they were recorded. A) SKF81297-induced LTP in the cocaine CPP group (clear triangles, 151.4±8.8%, * p <0.05, n = 6) is completely blocked by the PLD-linked mGluR antagonist (PCCG-13, filled triangles, 95.0±9.2%, n = 6). B) mGluR1 receptor antagonist (LY367385, filled triangles, 106.0±6.7%, n = 6) blocks the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). C) The <t>mGluR5</t> antagonist (MPEP, filled triangles, 122.7±5.6%, n = 6) significantly reduces but does not abolish the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). D) PLC antagonist (U-73122, filled triangles, 128.2±6.1%, n = 6), reduces but does not eliminate the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). For comparison, panels A and B use same data graphs and fEPSP traces for the slices from cocaine CPP group superfused with SKF81297 as shown in , and .
    Mglur5 Agc 007, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mglur5 agc 007/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mglur5 agc 007 - by Bioz Stars, 2023-01
    94/100 stars

    Images

    1) Product Images from "Dopamine-Induced Plasticity, Phospholipase D (PLD) Activity and Cocaine-Cue Behavior Depend on PLD-Linked Metabotropic Glutamate Receptors in Amygdala"

    Article Title: Dopamine-Induced Plasticity, Phospholipase D (PLD) Activity and Cocaine-Cue Behavior Depend on PLD-Linked Metabotropic Glutamate Receptors in Amygdala

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0025639

    Responses are plotted as percent change from the baseline fEPSPs as a function of time. Numbers on the representative traces show the time on the graph at which they were recorded. A) SKF81297-induced LTP in the cocaine CPP group (clear triangles, 151.4±8.8%, * p <0.05, n = 6) is completely blocked by the PLD-linked mGluR antagonist (PCCG-13, filled triangles, 95.0±9.2%, n = 6). B) mGluR1 receptor antagonist (LY367385, filled triangles, 106.0±6.7%, n = 6) blocks the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). C) The mGluR5 antagonist (MPEP, filled triangles, 122.7±5.6%, n = 6) significantly reduces but does not abolish the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). D) PLC antagonist (U-73122, filled triangles, 128.2±6.1%, n = 6), reduces but does not eliminate the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). For comparison, panels A and B use same data graphs and fEPSP traces for the slices from cocaine CPP group superfused with SKF81297 as shown in , and .
    Figure Legend Snippet: Responses are plotted as percent change from the baseline fEPSPs as a function of time. Numbers on the representative traces show the time on the graph at which they were recorded. A) SKF81297-induced LTP in the cocaine CPP group (clear triangles, 151.4±8.8%, * p <0.05, n = 6) is completely blocked by the PLD-linked mGluR antagonist (PCCG-13, filled triangles, 95.0±9.2%, n = 6). B) mGluR1 receptor antagonist (LY367385, filled triangles, 106.0±6.7%, n = 6) blocks the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). C) The mGluR5 antagonist (MPEP, filled triangles, 122.7±5.6%, n = 6) significantly reduces but does not abolish the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). D) PLC antagonist (U-73122, filled triangles, 128.2±6.1%, n = 6), reduces but does not eliminate the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). For comparison, panels A and B use same data graphs and fEPSP traces for the slices from cocaine CPP group superfused with SKF81297 as shown in , and .

    Techniques Used:

    The dotted line indicates PLD activity associated with control slices (no EtOH added) which was determined for each animal and used to calculate the change in PLD activity levels with EtOH and/or drug application. Basal levels represent the increase in PLD activity observed in the EtOH-treated slices compared to the no EtOH controls; * p <0.05 compared to the corresponding saline control and # p <0.05 compared to the cocaine CPP group basal PLD activity. Basal PLD activity was significantly increased (*** p <0.001, n = 50) in the cocaine CPP group (dark bars, 527.3±94.3) compared to the saline-treated group (white bars, 142.6±36.9). SKF81297, the D1/5R agonist, application increased the basal levels in the cocaine CPP group significantly (1722.0±176.9, n = 12, # p <0.05) compared to the basal PLD activity observed with EtOH treatment alone in the same experimental group. The D1/5R antagonist, SCH23390, completely blocked basal PLD activity (91.2±21.9, n = 12, ## p <0.01) in the cocaine CPP group. A similar reduction in PEtOH levels was observed with application of either the PLD-linked mGluR antagonist, PCCG-13 (62.9±10.6, n = 7, ## p <0.01) or the mGluR1 antagonist, LY367385 (75.0±13.9, n = 12, ## p <0.01), while the mGluR5 antagonist, MPEP, did not decrease basal PLD activity (305.7±31.5, n = 7, ns) within the cocaine CPP group but were significantly increased compared to (* p <0.05) the saline treated group. Applications of SKF81297 (184.9±30.5, n = 12), SCH23390 (84.9±38.9, n = 12), MPEP (74.2±16.3, n = 7), LY367385 (94.7±18.9, n = 12) and PCCG-13 (132.5±18.4, n = 7) did not significantly alter the PEtOH levels in the saline-treated group compared to the basal activity levels. Inset is a depiction of the triangular excision performed to isolate amygdala (bilaterally for each animal, each slice) containing the basolateral (BLA), the central (CeA) and the lateral (LA) subregions from three serial coronal slices (350 µm) beginning −2.30 mm to −2.80 mm from Bregma .
    Figure Legend Snippet: The dotted line indicates PLD activity associated with control slices (no EtOH added) which was determined for each animal and used to calculate the change in PLD activity levels with EtOH and/or drug application. Basal levels represent the increase in PLD activity observed in the EtOH-treated slices compared to the no EtOH controls; * p <0.05 compared to the corresponding saline control and # p <0.05 compared to the cocaine CPP group basal PLD activity. Basal PLD activity was significantly increased (*** p <0.001, n = 50) in the cocaine CPP group (dark bars, 527.3±94.3) compared to the saline-treated group (white bars, 142.6±36.9). SKF81297, the D1/5R agonist, application increased the basal levels in the cocaine CPP group significantly (1722.0±176.9, n = 12, # p <0.05) compared to the basal PLD activity observed with EtOH treatment alone in the same experimental group. The D1/5R antagonist, SCH23390, completely blocked basal PLD activity (91.2±21.9, n = 12, ## p <0.01) in the cocaine CPP group. A similar reduction in PEtOH levels was observed with application of either the PLD-linked mGluR antagonist, PCCG-13 (62.9±10.6, n = 7, ## p <0.01) or the mGluR1 antagonist, LY367385 (75.0±13.9, n = 12, ## p <0.01), while the mGluR5 antagonist, MPEP, did not decrease basal PLD activity (305.7±31.5, n = 7, ns) within the cocaine CPP group but were significantly increased compared to (* p <0.05) the saline treated group. Applications of SKF81297 (184.9±30.5, n = 12), SCH23390 (84.9±38.9, n = 12), MPEP (74.2±16.3, n = 7), LY367385 (94.7±18.9, n = 12) and PCCG-13 (132.5±18.4, n = 7) did not significantly alter the PEtOH levels in the saline-treated group compared to the basal activity levels. Inset is a depiction of the triangular excision performed to isolate amygdala (bilaterally for each animal, each slice) containing the basolateral (BLA), the central (CeA) and the lateral (LA) subregions from three serial coronal slices (350 µm) beginning −2.30 mm to −2.80 mm from Bregma .

    Techniques Used: Activity Assay

    anti mglur5 antibody  (Alomone Labs)


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    Alomone Labs anti mglur5 antibody
    Transcripts encoding metabotropic glutamate receptors are expressed in mouse blastocysts and oocytes. Metabotropic glutamate receptor types are listed in the tables on the left. In transcripts which were consistently expressed in both blastocysts and oocytes, fold regulation values (“+Grm5 , Glutamate receptor, metabotropic 5; Grm6 , Glutamate receptor, metabotropic 6; Grm7 , Glutamate receptor, metabotropic 7; Grm8 , Glutamate receptor, metabotropic 8; MW, molecular weight markers; A, positive control tissue; B, ovulated oocytes; C, blastocysts. The MWs in base pairs (bp) are indicated to the right of the panels. * Primers for Grm5 receptor type were designed in this study. " width="250" height="auto" />
    Anti Mglur5 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti mglur5 antibody/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
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    94/100 stars

    Images

    1) Product Images from "Glutamate can act as a signaling molecule in mouse preimplantation embryos"

    Article Title: Glutamate can act as a signaling molecule in mouse preimplantation embryos

    Journal: Biology of Reproduction

    doi: 10.1093/biolre/ioac126

    Transcripts encoding metabotropic glutamate receptors are expressed in mouse blastocysts and oocytes. Metabotropic glutamate receptor types are listed in the tables on the left. In transcripts which were consistently expressed in both blastocysts and oocytes, fold regulation values (“+
    Figure Legend Snippet: Transcripts encoding metabotropic glutamate receptors are expressed in mouse blastocysts and oocytes. Metabotropic glutamate receptor types are listed in the tables on the left. In transcripts which were consistently expressed in both blastocysts and oocytes, fold regulation values (“+" means upregulation and “−" means downregulation in blastocysts compared to oocytes) and corresponding P -values are shown. Transcripts were detected by RT-PCR and representative agarose gels with separated PCR products are shown in the panels on the right. Lanes: Grm1 , Glutamate receptor, metabotropic 1; Grm2 , Glutamate receptor, metabotropic 2; Grm3 , Glutamate receptor, metabotropic 3; Grm4 , Glutamate receptor, metabotropic 4; Grm5 , Glutamate receptor, metabotropic 5; Grm6 , Glutamate receptor, metabotropic 6; Grm7 , Glutamate receptor, metabotropic 7; Grm8 , Glutamate receptor, metabotropic 8; MW, molecular weight markers; A, positive control tissue; B, ovulated oocytes; C, blastocysts. The MWs in base pairs (bp) are indicated to the right of the panels. * Primers for Grm5 receptor type were designed in this study.

    Techniques Used: Reverse Transcription Polymerase Chain Reaction, Molecular Weight, Positive Control

    Glutamate effects are blocked with AMPA/kainate and GRM5 receptor antagonists. Cell numbers and proportions of dead cells in blastocysts pretreated with the mixture of AMPA, kainate, and GRM5 receptor antagonists (CNQX and MPEP) prior to L-glutamic acid exposure. GlAc 5 mM, blastocysts incubated with L-glutamic acid (at 5 mM final concentration) for 24 h; CNQX + MPEP, blastocysts incubated with CNQX and MPEP (at 300 μM and 10 μM final concentrations, respectively) for 24 h; GlAc 5 mM + (CNQX + MPEP), blastocysts incubated with CNQX + MPEP antagonists for 20 min prior to addition of L-glutamic acid (for the following 24 h incubation). TE, trophectoderm, ICM, inner cell mass. The number of blastocysts in the groups ( n ): Control, n = 32; GlAc 5 mM, n = 33; CNQX + MPEP, n = 28; GlAc 5 mM + (CNQX + MPEP), n = 34. The values are arithmetical mean + SEM. Statistical significance of differences: * P < 0.05, * * P < 0.01, * * * P < 0.001.
    Figure Legend Snippet: Glutamate effects are blocked with AMPA/kainate and GRM5 receptor antagonists. Cell numbers and proportions of dead cells in blastocysts pretreated with the mixture of AMPA, kainate, and GRM5 receptor antagonists (CNQX and MPEP) prior to L-glutamic acid exposure. GlAc 5 mM, blastocysts incubated with L-glutamic acid (at 5 mM final concentration) for 24 h; CNQX + MPEP, blastocysts incubated with CNQX and MPEP (at 300 μM and 10 μM final concentrations, respectively) for 24 h; GlAc 5 mM + (CNQX + MPEP), blastocysts incubated with CNQX + MPEP antagonists for 20 min prior to addition of L-glutamic acid (for the following 24 h incubation). TE, trophectoderm, ICM, inner cell mass. The number of blastocysts in the groups ( n ): Control, n = 32; GlAc 5 mM, n = 33; CNQX + MPEP, n = 28; GlAc 5 mM + (CNQX + MPEP), n = 34. The values are arithmetical mean + SEM. Statistical significance of differences: * P < 0.05, * * P < 0.01, * * * P < 0.001.

    Techniques Used: Incubation, Concentration Assay

    rabbit polyclonal anti mglur5  (Alomone Labs)


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    Alomone Labs rabbit polyclonal anti mglur5
    KEY RESOURCES TABLE
    Rabbit Polyclonal Anti Mglur5, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit polyclonal anti mglur5/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
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    94/100 stars

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    1) Product Images from "Alzheimer’s vulnerable brain region relies on a distinct retromer core dedicated to endosomal recycling"

    Article Title: Alzheimer’s vulnerable brain region relies on a distinct retromer core dedicated to endosomal recycling

    Journal: Cell reports

    doi: 10.1016/j.celrep.2021.110182

    KEY RESOURCES TABLE
    Figure Legend Snippet: KEY RESOURCES TABLE

    Techniques Used: Recombinant, Bicinchoninic Acid Protein Assay, Enzyme-linked Immunosorbent Assay, Construct, Plasmid Preparation, Software

    guinea pig polyclonal  (Alomone Labs)


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    Alomone Labs guinea pig polyclonal
    List of TRPV1 antibodies tested on sheep DRGs
    Guinea Pig Polyclonal, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 1 article reviews
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    1) Product Images from "Functional Characterization of Ovine Dorsal Root Ganglion Neurons Reveal Peripheral Sensitization after Osteochondral Defect"

    Article Title: Functional Characterization of Ovine Dorsal Root Ganglion Neurons Reveal Peripheral Sensitization after Osteochondral Defect

    Journal: eNeuro

    doi: 10.1523/ENEURO.0237-21.2021

    List of TRPV1 antibodies tested on sheep DRGs
    Figure Legend Snippet: List of TRPV1 antibodies tested on sheep DRGs

    Techniques Used:

    anti mglur5  (Alomone Labs)


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    Alomone Labs anti mglur5
    Anti Mglur5, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti mglur5/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
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    anti mglur5 - by Bioz Stars, 2023-01
    94/100 stars

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    anti mglur5  (Alomone Labs)


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    Alomone Labs anti mglur5
    Anti Mglur5, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    rabbit anti mglur5  (Alomone Labs)


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    Alomone Labs rabbit anti mglur5
    A. Example responses of the CINs to a positive current pulse in the control and the Er81 cKO conditions. B. Average action potential rate during across all positive current pulses. The inset shows a time-expanded view of the early response (0-0.1 s; p = 0.280, n = 16 cells from 5 control mice and 18 cells from 2 Er81 cKO mice). C. Average action potential rate during positive current steps (sample size as in B). D. Adaptation index as a function of the current step amplitude (sample size as in B). E. Example trace of the putative I Kr following a depolarising voltage pulse. F. Mean traces of I Kr as a function of time at different holding potentials (-50 to −20 mV, 10 mV steps). G. Average I Kr as a function of the holding potential (control; n = 14, 3 mice and cKO; n = 16, 2 mice, -30 mV; p = 0.138, −20 mV; p = 0.272). H-J . Expression of KCNQ2 mRNA ( H , n = 6 control and n = 5 Er81 cKO), examples of CINs ( I , green) stained for KCNQ2 protein ( I , red) and the summary of the protein expression ( J , n = 5 control mice and n = 4 Er81 cKO mice, p = 0.302). K-M. Expression of <t>mGluR5</t> mRNA ( K , n = 7 control and n = 6 Er81 cKO), examples of CINs ( L , green) stained for <t>mGluR5</t> <t>protein</t> ( L , red) and the summary of the protein expression ( M , n = 5 control mice and n = 4 Er81 cKO mice). Data are presented as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Rabbit Anti Mglur5, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    1) Product Images from "Loss of the Er81 Transcription Factor in Cholinergic Cells Alters Striatal Activity and Habit Formation"

    Article Title: Loss of the Er81 Transcription Factor in Cholinergic Cells Alters Striatal Activity and Habit Formation

    Journal: bioRxiv

    doi: 10.1101/2020.01.14.905497

    A. Example responses of the CINs to a positive current pulse in the control and the Er81 cKO conditions. B. Average action potential rate during across all positive current pulses. The inset shows a time-expanded view of the early response (0-0.1 s; p = 0.280, n = 16 cells from 5 control mice and 18 cells from 2 Er81 cKO mice). C. Average action potential rate during positive current steps (sample size as in B). D. Adaptation index as a function of the current step amplitude (sample size as in B). E. Example trace of the putative I Kr following a depolarising voltage pulse. F. Mean traces of I Kr as a function of time at different holding potentials (-50 to −20 mV, 10 mV steps). G. Average I Kr as a function of the holding potential (control; n = 14, 3 mice and cKO; n = 16, 2 mice, -30 mV; p = 0.138, −20 mV; p = 0.272). H-J . Expression of KCNQ2 mRNA ( H , n = 6 control and n = 5 Er81 cKO), examples of CINs ( I , green) stained for KCNQ2 protein ( I , red) and the summary of the protein expression ( J , n = 5 control mice and n = 4 Er81 cKO mice, p = 0.302). K-M. Expression of mGluR5 mRNA ( K , n = 7 control and n = 6 Er81 cKO), examples of CINs ( L , green) stained for mGluR5 protein ( L , red) and the summary of the protein expression ( M , n = 5 control mice and n = 4 Er81 cKO mice). Data are presented as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: A. Example responses of the CINs to a positive current pulse in the control and the Er81 cKO conditions. B. Average action potential rate during across all positive current pulses. The inset shows a time-expanded view of the early response (0-0.1 s; p = 0.280, n = 16 cells from 5 control mice and 18 cells from 2 Er81 cKO mice). C. Average action potential rate during positive current steps (sample size as in B). D. Adaptation index as a function of the current step amplitude (sample size as in B). E. Example trace of the putative I Kr following a depolarising voltage pulse. F. Mean traces of I Kr as a function of time at different holding potentials (-50 to −20 mV, 10 mV steps). G. Average I Kr as a function of the holding potential (control; n = 14, 3 mice and cKO; n = 16, 2 mice, -30 mV; p = 0.138, −20 mV; p = 0.272). H-J . Expression of KCNQ2 mRNA ( H , n = 6 control and n = 5 Er81 cKO), examples of CINs ( I , green) stained for KCNQ2 protein ( I , red) and the summary of the protein expression ( J , n = 5 control mice and n = 4 Er81 cKO mice, p = 0.302). K-M. Expression of mGluR5 mRNA ( K , n = 7 control and n = 6 Er81 cKO), examples of CINs ( L , green) stained for mGluR5 protein ( L , red) and the summary of the protein expression ( M , n = 5 control mice and n = 4 Er81 cKO mice). Data are presented as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Expressing, Staining

    mglur5 antibody  (Alomone Labs)


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    Alomone Labs mglur5 antibody
    Mglur5 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    rabbit polyclonal mglur5 antibody  (Alomone Labs)


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    Alomone Labs rabbit polyclonal mglur5 antibody
    a, Upper: schematic of the injection process for <t>mGluR5–CRISPR</t> into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b, RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., ***P < 0.001, ****p < 0.0001, one-way ANOVA. c, Left: immunostaining of mGluR5 (cyan) 5 weeks after stereotaxic injection of saline (control) or mGluR5–CRISPR into the striatum of WT or Fmr1 KO mice. Scale bar, 100 μm. Right: the number of mGluR5+ cells in WT control, WT mGluR5–CRISPR, Fmr1 KO control and Fmr1 KO mGluR5–CRISPR groups were counted and normalized to the number of DAPI+ cells. n = 8–10, mean ± s.e.m., ****P < 0.0001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.
    Rabbit Polyclonal Mglur5 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Nanoparticle delivery of CRISPR into the brain rescues a mouse model of fragile X syndrome from exaggerated repetitive behaviours"

    Article Title: Nanoparticle delivery of CRISPR into the brain rescues a mouse model of fragile X syndrome from exaggerated repetitive behaviours

    Journal: Nature biomedical engineering

    doi: 10.1038/s41551-018-0252-8

    a, Upper: schematic of the injection process for mGluR5–CRISPR into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b, RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., ***P < 0.001, ****p < 0.0001, one-way ANOVA. c, Left: immunostaining of mGluR5 (cyan) 5 weeks after stereotaxic injection of saline (control) or mGluR5–CRISPR into the striatum of WT or Fmr1 KO mice. Scale bar, 100 μm. Right: the number of mGluR5+ cells in WT control, WT mGluR5–CRISPR, Fmr1 KO control and Fmr1 KO mGluR5–CRISPR groups were counted and normalized to the number of DAPI+ cells. n = 8–10, mean ± s.e.m., ****P < 0.0001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.
    Figure Legend Snippet: a, Upper: schematic of the injection process for mGluR5–CRISPR into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b, RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., ***P < 0.001, ****p < 0.0001, one-way ANOVA. c, Left: immunostaining of mGluR5 (cyan) 5 weeks after stereotaxic injection of saline (control) or mGluR5–CRISPR into the striatum of WT or Fmr1 KO mice. Scale bar, 100 μm. Right: the number of mGluR5+ cells in WT control, WT mGluR5–CRISPR, Fmr1 KO control and Fmr1 KO mGluR5–CRISPR groups were counted and normalized to the number of DAPI+ cells. n = 8–10, mean ± s.e.m., ****P < 0.0001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.

    Techniques Used: Injection, CRISPR, Knock-Out, Amplification, Quantitative RT-PCR, Immunostaining

    a–c, Three weeks after stereotaxic injection of either saline (control) or mGluR5–CRISPR into the striatum of WT and Fmr1 KO mice, the marble-burying assay (a) or the empty cage observation test (b,c) was performed. a, Left: percentage of marbles buried after 30 min of the marble-burying test. Right: representative images after marble-burying assay for 30 min. Jumping (b) and line crossing behaviours (c) were scored during 10 min of an empty cage observation test. n = 10–12 for each group, mean ± s.e.m., *P < 0.05, **P < 0.01, ***P < 0.001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.
    Figure Legend Snippet: a–c, Three weeks after stereotaxic injection of either saline (control) or mGluR5–CRISPR into the striatum of WT and Fmr1 KO mice, the marble-burying assay (a) or the empty cage observation test (b,c) was performed. a, Left: percentage of marbles buried after 30 min of the marble-burying test. Right: representative images after marble-burying assay for 30 min. Jumping (b) and line crossing behaviours (c) were scored during 10 min of an empty cage observation test. n = 10–12 for each group, mean ± s.e.m., *P < 0.05, **P < 0.01, ***P < 0.001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.

    Techniques Used: Injection, CRISPR

    rabbit polyclonal mglur5 antibody  (Alomone Labs)


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    Structured Review

    Alomone Labs rabbit polyclonal mglur5 antibody
    a, Upper: schematic of the injection process for <t>mGluR5–CRISPR</t> into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b, RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., ***P < 0.001, ****p < 0.0001, one-way ANOVA. c, Left: immunostaining of mGluR5 (cyan) 5 weeks after stereotaxic injection of saline (control) or mGluR5–CRISPR into the striatum of WT or Fmr1 KO mice. Scale bar, 100 μm. Right: the number of mGluR5+ cells in WT control, WT mGluR5–CRISPR, Fmr1 KO control and Fmr1 KO mGluR5–CRISPR groups were counted and normalized to the number of DAPI+ cells. n = 8–10, mean ± s.e.m., ****P < 0.0001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.
    Rabbit Polyclonal Mglur5 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit polyclonal mglur5 antibody/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
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    1) Product Images from "Nanoparticle delivery of CRISPR into the brain rescues a mouse model of fragile X syndrome from exaggerated repetitive behaviours"

    Article Title: Nanoparticle delivery of CRISPR into the brain rescues a mouse model of fragile X syndrome from exaggerated repetitive behaviours

    Journal: Nature biomedical engineering

    doi: 10.1038/s41551-018-0252-8

    a, Upper: schematic of the injection process for mGluR5–CRISPR into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b, RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., ***P < 0.001, ****p < 0.0001, one-way ANOVA. c, Left: immunostaining of mGluR5 (cyan) 5 weeks after stereotaxic injection of saline (control) or mGluR5–CRISPR into the striatum of WT or Fmr1 KO mice. Scale bar, 100 μm. Right: the number of mGluR5+ cells in WT control, WT mGluR5–CRISPR, Fmr1 KO control and Fmr1 KO mGluR5–CRISPR groups were counted and normalized to the number of DAPI+ cells. n = 8–10, mean ± s.e.m., ****P < 0.0001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.
    Figure Legend Snippet: a, Upper: schematic of the injection process for mGluR5–CRISPR into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b, RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., ***P < 0.001, ****p < 0.0001, one-way ANOVA. c, Left: immunostaining of mGluR5 (cyan) 5 weeks after stereotaxic injection of saline (control) or mGluR5–CRISPR into the striatum of WT or Fmr1 KO mice. Scale bar, 100 μm. Right: the number of mGluR5+ cells in WT control, WT mGluR5–CRISPR, Fmr1 KO control and Fmr1 KO mGluR5–CRISPR groups were counted and normalized to the number of DAPI+ cells. n = 8–10, mean ± s.e.m., ****P < 0.0001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.

    Techniques Used: Injection, CRISPR, Knock-Out, Amplification, Quantitative RT-PCR, Immunostaining

    a–c, Three weeks after stereotaxic injection of either saline (control) or mGluR5–CRISPR into the striatum of WT and Fmr1 KO mice, the marble-burying assay (a) or the empty cage observation test (b,c) was performed. a, Left: percentage of marbles buried after 30 min of the marble-burying test. Right: representative images after marble-burying assay for 30 min. Jumping (b) and line crossing behaviours (c) were scored during 10 min of an empty cage observation test. n = 10–12 for each group, mean ± s.e.m., *P < 0.05, **P < 0.01, ***P < 0.001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.
    Figure Legend Snippet: a–c, Three weeks after stereotaxic injection of either saline (control) or mGluR5–CRISPR into the striatum of WT and Fmr1 KO mice, the marble-burying assay (a) or the empty cage observation test (b,c) was performed. a, Left: percentage of marbles buried after 30 min of the marble-burying test. Right: representative images after marble-burying assay for 30 min. Jumping (b) and line crossing behaviours (c) were scored during 10 min of an empty cage observation test. n = 10–12 for each group, mean ± s.e.m., *P < 0.05, **P < 0.01, ***P < 0.001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.

    Techniques Used: Injection, CRISPR

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    Alomone Labs mglur5 agc 007
    Responses are plotted as percent change from the baseline fEPSPs as a function of time. Numbers on the representative traces show the time on the graph at which they were recorded. A) SKF81297-induced LTP in the cocaine CPP group (clear triangles, 151.4±8.8%, * p <0.05, n = 6) is completely blocked by the PLD-linked mGluR antagonist (PCCG-13, filled triangles, 95.0±9.2%, n = 6). B) mGluR1 receptor antagonist (LY367385, filled triangles, 106.0±6.7%, n = 6) blocks the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). C) The <t>mGluR5</t> antagonist (MPEP, filled triangles, 122.7±5.6%, n = 6) significantly reduces but does not abolish the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). D) PLC antagonist (U-73122, filled triangles, 128.2±6.1%, n = 6), reduces but does not eliminate the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). For comparison, panels A and B use same data graphs and fEPSP traces for the slices from cocaine CPP group superfused with SKF81297 as shown in , and .
    Mglur5 Agc 007, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Transcripts encoding metabotropic glutamate receptors are expressed in mouse blastocysts and oocytes. Metabotropic glutamate receptor types are listed in the tables on the left. In transcripts which were consistently expressed in both blastocysts and oocytes, fold regulation values (“+Grm5 , Glutamate receptor, metabotropic 5; Grm6 , Glutamate receptor, metabotropic 6; Grm7 , Glutamate receptor, metabotropic 7; Grm8 , Glutamate receptor, metabotropic 8; MW, molecular weight markers; A, positive control tissue; B, ovulated oocytes; C, blastocysts. The MWs in base pairs (bp) are indicated to the right of the panels. * Primers for Grm5 receptor type were designed in this study. " width="250" height="auto" />
    Anti Mglur5 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    List of TRPV1 antibodies tested on sheep DRGs
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    A. Example responses of the CINs to a positive current pulse in the control and the Er81 cKO conditions. B. Average action potential rate during across all positive current pulses. The inset shows a time-expanded view of the early response (0-0.1 s; p = 0.280, n = 16 cells from 5 control mice and 18 cells from 2 Er81 cKO mice). C. Average action potential rate during positive current steps (sample size as in B). D. Adaptation index as a function of the current step amplitude (sample size as in B). E. Example trace of the putative I Kr following a depolarising voltage pulse. F. Mean traces of I Kr as a function of time at different holding potentials (-50 to −20 mV, 10 mV steps). G. Average I Kr as a function of the holding potential (control; n = 14, 3 mice and cKO; n = 16, 2 mice, -30 mV; p = 0.138, −20 mV; p = 0.272). H-J . Expression of KCNQ2 mRNA ( H , n = 6 control and n = 5 Er81 cKO), examples of CINs ( I , green) stained for KCNQ2 protein ( I , red) and the summary of the protein expression ( J , n = 5 control mice and n = 4 Er81 cKO mice, p = 0.302). K-M. Expression of <t>mGluR5</t> mRNA ( K , n = 7 control and n = 6 Er81 cKO), examples of CINs ( L , green) stained for <t>mGluR5</t> <t>protein</t> ( L , red) and the summary of the protein expression ( M , n = 5 control mice and n = 4 Er81 cKO mice). Data are presented as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
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    Alomone Labs mglur5 antibody
    A. Example responses of the CINs to a positive current pulse in the control and the Er81 cKO conditions. B. Average action potential rate during across all positive current pulses. The inset shows a time-expanded view of the early response (0-0.1 s; p = 0.280, n = 16 cells from 5 control mice and 18 cells from 2 Er81 cKO mice). C. Average action potential rate during positive current steps (sample size as in B). D. Adaptation index as a function of the current step amplitude (sample size as in B). E. Example trace of the putative I Kr following a depolarising voltage pulse. F. Mean traces of I Kr as a function of time at different holding potentials (-50 to −20 mV, 10 mV steps). G. Average I Kr as a function of the holding potential (control; n = 14, 3 mice and cKO; n = 16, 2 mice, -30 mV; p = 0.138, −20 mV; p = 0.272). H-J . Expression of KCNQ2 mRNA ( H , n = 6 control and n = 5 Er81 cKO), examples of CINs ( I , green) stained for KCNQ2 protein ( I , red) and the summary of the protein expression ( J , n = 5 control mice and n = 4 Er81 cKO mice, p = 0.302). K-M. Expression of <t>mGluR5</t> mRNA ( K , n = 7 control and n = 6 Er81 cKO), examples of CINs ( L , green) stained for <t>mGluR5</t> <t>protein</t> ( L , red) and the summary of the protein expression ( M , n = 5 control mice and n = 4 Er81 cKO mice). Data are presented as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Mglur5 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Alomone Labs rabbit polyclonal mglur5 antibody
    a, Upper: schematic of the injection process for <t>mGluR5–CRISPR</t> into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b, RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., ***P < 0.001, ****p < 0.0001, one-way ANOVA. c, Left: immunostaining of mGluR5 (cyan) 5 weeks after stereotaxic injection of saline (control) or mGluR5–CRISPR into the striatum of WT or Fmr1 KO mice. Scale bar, 100 μm. Right: the number of mGluR5+ cells in WT control, WT mGluR5–CRISPR, Fmr1 KO control and Fmr1 KO mGluR5–CRISPR groups were counted and normalized to the number of DAPI+ cells. n = 8–10, mean ± s.e.m., ****P < 0.0001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.
    Rabbit Polyclonal Mglur5 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit polyclonal mglur5 antibody/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal mglur5 antibody - by Bioz Stars, 2023-01
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    Image Search Results


    Responses are plotted as percent change from the baseline fEPSPs as a function of time. Numbers on the representative traces show the time on the graph at which they were recorded. A) SKF81297-induced LTP in the cocaine CPP group (clear triangles, 151.4±8.8%, * p <0.05, n = 6) is completely blocked by the PLD-linked mGluR antagonist (PCCG-13, filled triangles, 95.0±9.2%, n = 6). B) mGluR1 receptor antagonist (LY367385, filled triangles, 106.0±6.7%, n = 6) blocks the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). C) The mGluR5 antagonist (MPEP, filled triangles, 122.7±5.6%, n = 6) significantly reduces but does not abolish the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). D) PLC antagonist (U-73122, filled triangles, 128.2±6.1%, n = 6), reduces but does not eliminate the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). For comparison, panels A and B use same data graphs and fEPSP traces for the slices from cocaine CPP group superfused with SKF81297 as shown in , and .

    Journal: PLoS ONE

    Article Title: Dopamine-Induced Plasticity, Phospholipase D (PLD) Activity and Cocaine-Cue Behavior Depend on PLD-Linked Metabotropic Glutamate Receptors in Amygdala

    doi: 10.1371/journal.pone.0025639

    Figure Lengend Snippet: Responses are plotted as percent change from the baseline fEPSPs as a function of time. Numbers on the representative traces show the time on the graph at which they were recorded. A) SKF81297-induced LTP in the cocaine CPP group (clear triangles, 151.4±8.8%, * p <0.05, n = 6) is completely blocked by the PLD-linked mGluR antagonist (PCCG-13, filled triangles, 95.0±9.2%, n = 6). B) mGluR1 receptor antagonist (LY367385, filled triangles, 106.0±6.7%, n = 6) blocks the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). C) The mGluR5 antagonist (MPEP, filled triangles, 122.7±5.6%, n = 6) significantly reduces but does not abolish the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). D) PLC antagonist (U-73122, filled triangles, 128.2±6.1%, n = 6), reduces but does not eliminate the SKF81297-induced LTP (clear triangles, * p <0.05, n = 6). For comparison, panels A and B use same data graphs and fEPSP traces for the slices from cocaine CPP group superfused with SKF81297 as shown in , and .

    Article Snippet: Primary antibodies (with the references provided where the antibodies were tested for specificity) included: metabotropic glutamate receptors [mGluR1 (AGC-006) and mGluR5 (AGC-007) ] from Alomone (Jerusalem, Israel); phospholipase D [PLD1 (sc-25512) and PLD2 (sc-25513), ] and actin (sc-1616) from Santa Cruz Biotechnologies Inc. (Santa Cruz, CA); dopamine receptor D1R (AB20066) from Abcam (Cambridge, MA); D5R (MAB5292) from Millipore (Temecula, CA) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH, Clone 6C5) from Advanced Immunochemicals Inc. (Long Beach, CA).

    Techniques:

    The dotted line indicates PLD activity associated with control slices (no EtOH added) which was determined for each animal and used to calculate the change in PLD activity levels with EtOH and/or drug application. Basal levels represent the increase in PLD activity observed in the EtOH-treated slices compared to the no EtOH controls; * p <0.05 compared to the corresponding saline control and # p <0.05 compared to the cocaine CPP group basal PLD activity. Basal PLD activity was significantly increased (*** p <0.001, n = 50) in the cocaine CPP group (dark bars, 527.3±94.3) compared to the saline-treated group (white bars, 142.6±36.9). SKF81297, the D1/5R agonist, application increased the basal levels in the cocaine CPP group significantly (1722.0±176.9, n = 12, # p <0.05) compared to the basal PLD activity observed with EtOH treatment alone in the same experimental group. The D1/5R antagonist, SCH23390, completely blocked basal PLD activity (91.2±21.9, n = 12, ## p <0.01) in the cocaine CPP group. A similar reduction in PEtOH levels was observed with application of either the PLD-linked mGluR antagonist, PCCG-13 (62.9±10.6, n = 7, ## p <0.01) or the mGluR1 antagonist, LY367385 (75.0±13.9, n = 12, ## p <0.01), while the mGluR5 antagonist, MPEP, did not decrease basal PLD activity (305.7±31.5, n = 7, ns) within the cocaine CPP group but were significantly increased compared to (* p <0.05) the saline treated group. Applications of SKF81297 (184.9±30.5, n = 12), SCH23390 (84.9±38.9, n = 12), MPEP (74.2±16.3, n = 7), LY367385 (94.7±18.9, n = 12) and PCCG-13 (132.5±18.4, n = 7) did not significantly alter the PEtOH levels in the saline-treated group compared to the basal activity levels. Inset is a depiction of the triangular excision performed to isolate amygdala (bilaterally for each animal, each slice) containing the basolateral (BLA), the central (CeA) and the lateral (LA) subregions from three serial coronal slices (350 µm) beginning −2.30 mm to −2.80 mm from Bregma .

    Journal: PLoS ONE

    Article Title: Dopamine-Induced Plasticity, Phospholipase D (PLD) Activity and Cocaine-Cue Behavior Depend on PLD-Linked Metabotropic Glutamate Receptors in Amygdala

    doi: 10.1371/journal.pone.0025639

    Figure Lengend Snippet: The dotted line indicates PLD activity associated with control slices (no EtOH added) which was determined for each animal and used to calculate the change in PLD activity levels with EtOH and/or drug application. Basal levels represent the increase in PLD activity observed in the EtOH-treated slices compared to the no EtOH controls; * p <0.05 compared to the corresponding saline control and # p <0.05 compared to the cocaine CPP group basal PLD activity. Basal PLD activity was significantly increased (*** p <0.001, n = 50) in the cocaine CPP group (dark bars, 527.3±94.3) compared to the saline-treated group (white bars, 142.6±36.9). SKF81297, the D1/5R agonist, application increased the basal levels in the cocaine CPP group significantly (1722.0±176.9, n = 12, # p <0.05) compared to the basal PLD activity observed with EtOH treatment alone in the same experimental group. The D1/5R antagonist, SCH23390, completely blocked basal PLD activity (91.2±21.9, n = 12, ## p <0.01) in the cocaine CPP group. A similar reduction in PEtOH levels was observed with application of either the PLD-linked mGluR antagonist, PCCG-13 (62.9±10.6, n = 7, ## p <0.01) or the mGluR1 antagonist, LY367385 (75.0±13.9, n = 12, ## p <0.01), while the mGluR5 antagonist, MPEP, did not decrease basal PLD activity (305.7±31.5, n = 7, ns) within the cocaine CPP group but were significantly increased compared to (* p <0.05) the saline treated group. Applications of SKF81297 (184.9±30.5, n = 12), SCH23390 (84.9±38.9, n = 12), MPEP (74.2±16.3, n = 7), LY367385 (94.7±18.9, n = 12) and PCCG-13 (132.5±18.4, n = 7) did not significantly alter the PEtOH levels in the saline-treated group compared to the basal activity levels. Inset is a depiction of the triangular excision performed to isolate amygdala (bilaterally for each animal, each slice) containing the basolateral (BLA), the central (CeA) and the lateral (LA) subregions from three serial coronal slices (350 µm) beginning −2.30 mm to −2.80 mm from Bregma .

    Article Snippet: Primary antibodies (with the references provided where the antibodies were tested for specificity) included: metabotropic glutamate receptors [mGluR1 (AGC-006) and mGluR5 (AGC-007) ] from Alomone (Jerusalem, Israel); phospholipase D [PLD1 (sc-25512) and PLD2 (sc-25513), ] and actin (sc-1616) from Santa Cruz Biotechnologies Inc. (Santa Cruz, CA); dopamine receptor D1R (AB20066) from Abcam (Cambridge, MA); D5R (MAB5292) from Millipore (Temecula, CA) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH, Clone 6C5) from Advanced Immunochemicals Inc. (Long Beach, CA).

    Techniques: Activity Assay

    Transcripts encoding metabotropic glutamate receptors are expressed in mouse blastocysts and oocytes. Metabotropic glutamate receptor types are listed in the tables on the left. In transcripts which were consistently expressed in both blastocysts and oocytes, fold regulation values (“+

    Journal: Biology of Reproduction

    Article Title: Glutamate can act as a signaling molecule in mouse preimplantation embryos

    doi: 10.1093/biolre/ioac126

    Figure Lengend Snippet: Transcripts encoding metabotropic glutamate receptors are expressed in mouse blastocysts and oocytes. Metabotropic glutamate receptor types are listed in the tables on the left. In transcripts which were consistently expressed in both blastocysts and oocytes, fold regulation values (“+" means upregulation and “−" means downregulation in blastocysts compared to oocytes) and corresponding P -values are shown. Transcripts were detected by RT-PCR and representative agarose gels with separated PCR products are shown in the panels on the right. Lanes: Grm1 , Glutamate receptor, metabotropic 1; Grm2 , Glutamate receptor, metabotropic 2; Grm3 , Glutamate receptor, metabotropic 3; Grm4 , Glutamate receptor, metabotropic 4; Grm5 , Glutamate receptor, metabotropic 5; Grm6 , Glutamate receptor, metabotropic 6; Grm7 , Glutamate receptor, metabotropic 7; Grm8 , Glutamate receptor, metabotropic 8; MW, molecular weight markers; A, positive control tissue; B, ovulated oocytes; C, blastocysts. The MWs in base pairs (bp) are indicated to the right of the panels. * Primers for Grm5 receptor type were designed in this study.

    Article Snippet: Anti-mGluR5 Antibody (Alomone Labs, Cat# AGC-007, dilution 1:50), Anti-GRIK3 (GluK3) Antibody (Alomone Labs, Cat# AGC-040, dilution 1:100), Anti-GRIK4 (KA1) Antibody (Alomone Labs, Cat# AGC-041, dilution 1:50), Anti-GRIK5 (GluK5) Antibody (Alomone Labs, Cat# AGC-042, dilution 1:100), GRIA3 Antibody (LifeSpan Biosciences, Cat# LS-C331307, dilution 1:50), and Anti-GluR4 (GluA4) Antibody (Alomone Labs, Cat# AGC-019, dilution 1:50).

    Techniques: Reverse Transcription Polymerase Chain Reaction, Molecular Weight, Positive Control

    Glutamate effects are blocked with AMPA/kainate and GRM5 receptor antagonists. Cell numbers and proportions of dead cells in blastocysts pretreated with the mixture of AMPA, kainate, and GRM5 receptor antagonists (CNQX and MPEP) prior to L-glutamic acid exposure. GlAc 5 mM, blastocysts incubated with L-glutamic acid (at 5 mM final concentration) for 24 h; CNQX + MPEP, blastocysts incubated with CNQX and MPEP (at 300 μM and 10 μM final concentrations, respectively) for 24 h; GlAc 5 mM + (CNQX + MPEP), blastocysts incubated with CNQX + MPEP antagonists for 20 min prior to addition of L-glutamic acid (for the following 24 h incubation). TE, trophectoderm, ICM, inner cell mass. The number of blastocysts in the groups ( n ): Control, n = 32; GlAc 5 mM, n = 33; CNQX + MPEP, n = 28; GlAc 5 mM + (CNQX + MPEP), n = 34. The values are arithmetical mean + SEM. Statistical significance of differences: * P < 0.05, * * P < 0.01, * * * P < 0.001.

    Journal: Biology of Reproduction

    Article Title: Glutamate can act as a signaling molecule in mouse preimplantation embryos

    doi: 10.1093/biolre/ioac126

    Figure Lengend Snippet: Glutamate effects are blocked with AMPA/kainate and GRM5 receptor antagonists. Cell numbers and proportions of dead cells in blastocysts pretreated with the mixture of AMPA, kainate, and GRM5 receptor antagonists (CNQX and MPEP) prior to L-glutamic acid exposure. GlAc 5 mM, blastocysts incubated with L-glutamic acid (at 5 mM final concentration) for 24 h; CNQX + MPEP, blastocysts incubated with CNQX and MPEP (at 300 μM and 10 μM final concentrations, respectively) for 24 h; GlAc 5 mM + (CNQX + MPEP), blastocysts incubated with CNQX + MPEP antagonists for 20 min prior to addition of L-glutamic acid (for the following 24 h incubation). TE, trophectoderm, ICM, inner cell mass. The number of blastocysts in the groups ( n ): Control, n = 32; GlAc 5 mM, n = 33; CNQX + MPEP, n = 28; GlAc 5 mM + (CNQX + MPEP), n = 34. The values are arithmetical mean + SEM. Statistical significance of differences: * P < 0.05, * * P < 0.01, * * * P < 0.001.

    Article Snippet: Anti-mGluR5 Antibody (Alomone Labs, Cat# AGC-007, dilution 1:50), Anti-GRIK3 (GluK3) Antibody (Alomone Labs, Cat# AGC-040, dilution 1:100), Anti-GRIK4 (KA1) Antibody (Alomone Labs, Cat# AGC-041, dilution 1:50), Anti-GRIK5 (GluK5) Antibody (Alomone Labs, Cat# AGC-042, dilution 1:100), GRIA3 Antibody (LifeSpan Biosciences, Cat# LS-C331307, dilution 1:50), and Anti-GluR4 (GluA4) Antibody (Alomone Labs, Cat# AGC-019, dilution 1:50).

    Techniques: Incubation, Concentration Assay

    KEY RESOURCES TABLE

    Journal: Cell reports

    Article Title: Alzheimer’s vulnerable brain region relies on a distinct retromer core dedicated to endosomal recycling

    doi: 10.1016/j.celrep.2021.110182

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: Rabbit polyclonal anti-mGluR5 , Alomones lab , Cat#AGC-007; RRID: AB_2039991.

    Techniques: Recombinant, Bicinchoninic Acid Protein Assay, Enzyme-linked Immunosorbent Assay, Construct, Plasmid Preparation, Software

    List of TRPV1 antibodies tested on sheep DRGs

    Journal: eNeuro

    Article Title: Functional Characterization of Ovine Dorsal Root Ganglion Neurons Reveal Peripheral Sensitization after Osteochondral Defect

    doi: 10.1523/ENEURO.0237-21.2021

    Figure Lengend Snippet: List of TRPV1 antibodies tested on sheep DRGs

    Article Snippet: Anti-TRPV1, guinea pig polyclonal , Primary , Alomone , AGP-118.

    Techniques:

    A. Example responses of the CINs to a positive current pulse in the control and the Er81 cKO conditions. B. Average action potential rate during across all positive current pulses. The inset shows a time-expanded view of the early response (0-0.1 s; p = 0.280, n = 16 cells from 5 control mice and 18 cells from 2 Er81 cKO mice). C. Average action potential rate during positive current steps (sample size as in B). D. Adaptation index as a function of the current step amplitude (sample size as in B). E. Example trace of the putative I Kr following a depolarising voltage pulse. F. Mean traces of I Kr as a function of time at different holding potentials (-50 to −20 mV, 10 mV steps). G. Average I Kr as a function of the holding potential (control; n = 14, 3 mice and cKO; n = 16, 2 mice, -30 mV; p = 0.138, −20 mV; p = 0.272). H-J . Expression of KCNQ2 mRNA ( H , n = 6 control and n = 5 Er81 cKO), examples of CINs ( I , green) stained for KCNQ2 protein ( I , red) and the summary of the protein expression ( J , n = 5 control mice and n = 4 Er81 cKO mice, p = 0.302). K-M. Expression of mGluR5 mRNA ( K , n = 7 control and n = 6 Er81 cKO), examples of CINs ( L , green) stained for mGluR5 protein ( L , red) and the summary of the protein expression ( M , n = 5 control mice and n = 4 Er81 cKO mice). Data are presented as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: bioRxiv

    Article Title: Loss of the Er81 Transcription Factor in Cholinergic Cells Alters Striatal Activity and Habit Formation

    doi: 10.1101/2020.01.14.905497

    Figure Lengend Snippet: A. Example responses of the CINs to a positive current pulse in the control and the Er81 cKO conditions. B. Average action potential rate during across all positive current pulses. The inset shows a time-expanded view of the early response (0-0.1 s; p = 0.280, n = 16 cells from 5 control mice and 18 cells from 2 Er81 cKO mice). C. Average action potential rate during positive current steps (sample size as in B). D. Adaptation index as a function of the current step amplitude (sample size as in B). E. Example trace of the putative I Kr following a depolarising voltage pulse. F. Mean traces of I Kr as a function of time at different holding potentials (-50 to −20 mV, 10 mV steps). G. Average I Kr as a function of the holding potential (control; n = 14, 3 mice and cKO; n = 16, 2 mice, -30 mV; p = 0.138, −20 mV; p = 0.272). H-J . Expression of KCNQ2 mRNA ( H , n = 6 control and n = 5 Er81 cKO), examples of CINs ( I , green) stained for KCNQ2 protein ( I , red) and the summary of the protein expression ( J , n = 5 control mice and n = 4 Er81 cKO mice, p = 0.302). K-M. Expression of mGluR5 mRNA ( K , n = 7 control and n = 6 Er81 cKO), examples of CINs ( L , green) stained for mGluR5 protein ( L , red) and the summary of the protein expression ( M , n = 5 control mice and n = 4 Er81 cKO mice). Data are presented as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Tissues were then stained using the following primary antibodies overnight: mouse anti-β Galactosidase (1:1000; Promega), rabbit anti-Er81 (1:5000; generous gift from Prof Silvia Arber; KO-validated ( )), Chicken anti-GFP (1:3000; Aves Lab), mouse anti-parvalbumin (1:3000; Sigma), goat anti-ChAT (1:200; Merck), guinea pig anti-vGluT1 and -vGluT2 (1:2000; Chemicon) and anti-vGluT3 (1:2000; Merck), mouse anti-Lhx6 (1:X; Santa Cruz), rabbit anti-mgluR5 (1:50; Alomone), sheep anti-Neuropeptide Y (1:1000; Merck), rabbit anti-KCNQ2 and anti-HCN2 (1:200; Thermofisher), mouse anti-c-Fos (1:500; Santa Cruz) or rabbit anti-p-Ser240–244-S6rp (1:500; Cell Signalling).

    Techniques: Expressing, Staining

    a, Upper: schematic of the injection process for mGluR5–CRISPR into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b, RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., ***P < 0.001, ****p < 0.0001, one-way ANOVA. c, Left: immunostaining of mGluR5 (cyan) 5 weeks after stereotaxic injection of saline (control) or mGluR5–CRISPR into the striatum of WT or Fmr1 KO mice. Scale bar, 100 μm. Right: the number of mGluR5+ cells in WT control, WT mGluR5–CRISPR, Fmr1 KO control and Fmr1 KO mGluR5–CRISPR groups were counted and normalized to the number of DAPI+ cells. n = 8–10, mean ± s.e.m., ****P < 0.0001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.

    Journal: Nature biomedical engineering

    Article Title: Nanoparticle delivery of CRISPR into the brain rescues a mouse model of fragile X syndrome from exaggerated repetitive behaviours

    doi: 10.1038/s41551-018-0252-8

    Figure Lengend Snippet: a, Upper: schematic of the injection process for mGluR5–CRISPR into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b, RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., ***P < 0.001, ****p < 0.0001, one-way ANOVA. c, Left: immunostaining of mGluR5 (cyan) 5 weeks after stereotaxic injection of saline (control) or mGluR5–CRISPR into the striatum of WT or Fmr1 KO mice. Scale bar, 100 μm. Right: the number of mGluR5+ cells in WT control, WT mGluR5–CRISPR, Fmr1 KO control and Fmr1 KO mGluR5–CRISPR groups were counted and normalized to the number of DAPI+ cells. n = 8–10, mean ± s.e.m., ****P < 0.0001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.

    Article Snippet: Antibodies The mouse monoclonal RFP antibody (6G6) was purchased from ChromoTek, the chicken polyclonal GFP antibody (GFP-1020) from Aves Labs (Tigard), the rabbit polyclonal GFAP antibody (AB5804) and the mouse monoclonal NeuN antibody (MAB377) from Millipore, the rabbit polyclonal IBA1 antibody (019–19741) from Wako Chemicals, and the rabbit polyclonal mGluR5 antibody (AGC-007) was from Alomone Labs.

    Techniques: Injection, CRISPR, Knock-Out, Amplification, Quantitative RT-PCR, Immunostaining

    a–c, Three weeks after stereotaxic injection of either saline (control) or mGluR5–CRISPR into the striatum of WT and Fmr1 KO mice, the marble-burying assay (a) or the empty cage observation test (b,c) was performed. a, Left: percentage of marbles buried after 30 min of the marble-burying test. Right: representative images after marble-burying assay for 30 min. Jumping (b) and line crossing behaviours (c) were scored during 10 min of an empty cage observation test. n = 10–12 for each group, mean ± s.e.m., *P < 0.05, **P < 0.01, ***P < 0.001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.

    Journal: Nature biomedical engineering

    Article Title: Nanoparticle delivery of CRISPR into the brain rescues a mouse model of fragile X syndrome from exaggerated repetitive behaviours

    doi: 10.1038/s41551-018-0252-8

    Figure Lengend Snippet: a–c, Three weeks after stereotaxic injection of either saline (control) or mGluR5–CRISPR into the striatum of WT and Fmr1 KO mice, the marble-burying assay (a) or the empty cage observation test (b,c) was performed. a, Left: percentage of marbles buried after 30 min of the marble-burying test. Right: representative images after marble-burying assay for 30 min. Jumping (b) and line crossing behaviours (c) were scored during 10 min of an empty cage observation test. n = 10–12 for each group, mean ± s.e.m., *P < 0.05, **P < 0.01, ***P < 0.001 by one-way ANOVA. P values were calculated between WT control and Fmr1 KO control, WT control and WT mGluR5–CRISPR, or Fmr1 KO control and Fmr1 KO mGluR5–CRISPR.

    Article Snippet: Antibodies The mouse monoclonal RFP antibody (6G6) was purchased from ChromoTek, the chicken polyclonal GFP antibody (GFP-1020) from Aves Labs (Tigard), the rabbit polyclonal GFAP antibody (AB5804) and the mouse monoclonal NeuN antibody (MAB377) from Millipore, the rabbit polyclonal IBA1 antibody (019–19741) from Wako Chemicals, and the rabbit polyclonal mGluR5 antibody (AGC-007) was from Alomone Labs.

    Techniques: Injection, CRISPR