bicuculline bic  (Alomone Labs)


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    Alomone Labs bicuculline bic
    Bicuculline Bic, 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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    bic 4ap  (Alomone Labs)


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    Alomone Labs bic 4ap
    a Nuclear DNMT3A1 immunofluorescence is prominent in MAP2-positive neurons but much less in GFAP-positive astrocytes at 15 DIV hippocampal cultures. Scale bars are 20 μm. b , c Downregulation of DNMT3A1 protein levels in 14–15 DIV hippocampal primary neurons following treatment with <t>Bic/4AP</t> for 1 h, 3 h or 6 h as evidenced by quantitative immunocytochemistry. Scale bar is 20 μm. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. d – f DNMT3a1 protein levels are decreased following the removal of tonic inhibition in DIV 21 cortical neurons. β-Actin was used as an internal control for normalization. Student’s t -test * p < 0.05. g , h Hippocampal neurons were treated with Bic/4AP for 10 min or 3 h. Media from 10 min-long treated neurons was washed out and cells were kept for 3 h before fixation. Both treatments were equally effective to reduce nuclear DNMT3A1 immunofluorescence. Application of 100 μM NMDA for 10 min had no effect. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.
    Bic 4ap, supplied by Alomone Labs, 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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    1) Product Images from "Synaptic control of DNA methylation involves activity-dependent degradation of DNMT3A1 in the nucleus"

    Article Title: Synaptic control of DNA methylation involves activity-dependent degradation of DNMT3A1 in the nucleus

    Journal: Neuropsychopharmacology

    doi: 10.1038/s41386-020-0780-2

    a Nuclear DNMT3A1 immunofluorescence is prominent in MAP2-positive neurons but much less in GFAP-positive astrocytes at 15 DIV hippocampal cultures. Scale bars are 20 μm. b , c Downregulation of DNMT3A1 protein levels in 14–15 DIV hippocampal primary neurons following treatment with Bic/4AP for 1 h, 3 h or 6 h as evidenced by quantitative immunocytochemistry. Scale bar is 20 μm. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. d – f DNMT3a1 protein levels are decreased following the removal of tonic inhibition in DIV 21 cortical neurons. β-Actin was used as an internal control for normalization. Student’s t -test * p < 0.05. g , h Hippocampal neurons were treated with Bic/4AP for 10 min or 3 h. Media from 10 min-long treated neurons was washed out and cells were kept for 3 h before fixation. Both treatments were equally effective to reduce nuclear DNMT3A1 immunofluorescence. Application of 100 μM NMDA for 10 min had no effect. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.
    Figure Legend Snippet: a Nuclear DNMT3A1 immunofluorescence is prominent in MAP2-positive neurons but much less in GFAP-positive astrocytes at 15 DIV hippocampal cultures. Scale bars are 20 μm. b , c Downregulation of DNMT3A1 protein levels in 14–15 DIV hippocampal primary neurons following treatment with Bic/4AP for 1 h, 3 h or 6 h as evidenced by quantitative immunocytochemistry. Scale bar is 20 μm. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. d – f DNMT3a1 protein levels are decreased following the removal of tonic inhibition in DIV 21 cortical neurons. β-Actin was used as an internal control for normalization. Student’s t -test * p < 0.05. g , h Hippocampal neurons were treated with Bic/4AP for 10 min or 3 h. Media from 10 min-long treated neurons was washed out and cells were kept for 3 h before fixation. Both treatments were equally effective to reduce nuclear DNMT3A1 immunofluorescence. Application of 100 μM NMDA for 10 min had no effect. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.

    Techniques Used: Immunofluorescence, Immunocytochemistry, Inhibition

    a , b Treatment with the NMDAR antagonist APV (20 μM) prevented the reduction in the nuclear levels of DNMT3A1 following synaptic stimulation by Bic/4AP for 6 h. c , d Treatment with the GluN2A inhibitor NVP-AAM077 (50 nM) prevented the reduction in the nuclear levels of DNMT3A1 following synaptic stimulation by Bic/4AP for 6 h. Two-way ANOVA followed by Bonferroni’s post hoc test. e Timeline view of hippocampal neuron treatment by Bic/4AP for 6 h with or without NVP-AAM077. f , g Quantitative immunoblotting revealed the inhibition of DNMT3A1 degradation by the use of NVP-AAM077. One-sample t-test is performed while the hypothetical value is set to 100. h , i shRNA-based knockdown of GluN2A in the presence of synaptic stimulation by Bic/4AP for 6 h prevented the DNMT3A1 degradation. j , k Treatment with the GluN2B subunit inhibitor ifenprodil (10 μM) in the presence of synaptic stimulation with Bic/4AP for 6 h did not prevent the reduction in the nuclear levels of Dnmt3A1. Scale bars, 20 μm. Two-way ANOVA followed by Bonferroni’s post hoc test. *** p < 0.001, n.s. not significant. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.
    Figure Legend Snippet: a , b Treatment with the NMDAR antagonist APV (20 μM) prevented the reduction in the nuclear levels of DNMT3A1 following synaptic stimulation by Bic/4AP for 6 h. c , d Treatment with the GluN2A inhibitor NVP-AAM077 (50 nM) prevented the reduction in the nuclear levels of DNMT3A1 following synaptic stimulation by Bic/4AP for 6 h. Two-way ANOVA followed by Bonferroni’s post hoc test. e Timeline view of hippocampal neuron treatment by Bic/4AP for 6 h with or without NVP-AAM077. f , g Quantitative immunoblotting revealed the inhibition of DNMT3A1 degradation by the use of NVP-AAM077. One-sample t-test is performed while the hypothetical value is set to 100. h , i shRNA-based knockdown of GluN2A in the presence of synaptic stimulation by Bic/4AP for 6 h prevented the DNMT3A1 degradation. j , k Treatment with the GluN2B subunit inhibitor ifenprodil (10 μM) in the presence of synaptic stimulation with Bic/4AP for 6 h did not prevent the reduction in the nuclear levels of Dnmt3A1. Scale bars, 20 μm. Two-way ANOVA followed by Bonferroni’s post hoc test. *** p < 0.001, n.s. not significant. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.

    Techniques Used: Western Blot, Inhibition, shRNA

    a NEDD8 is abundantly expressed in the nucleus of 16 DIV hippocampal neurons whereas weaker staining was observed at synapses. Scale bar 20 μm (top panel), 5 μm (lower panel). b Immunoprecipitation of CUL4B protein from nuclear extracts of cortical primary neurons (top panel) results in co-precipitation of DNMT3A1 (lower panel, indicated with an arrow). c , d Hippocampal primary neurons were treated with Bic/4AP for 6 h in the presence or absence of MLN4924 (5 nM). Scale bars, 20 μm. Quantitative immunocytochemistry revealed that blocking neddylation prevents DNMT3A1 degradation. e Representative immunofluorescence images of nuclear NEDD8 and total cytosine methylation (5meC) at basal conditions or after treatment with Bic/4AP for 6 h. Scale bar is 20 μm. f , g Upon synaptic activation nuclear NEDD8 and 5meC levels remained unchanged. Unpaired Student’s t -test. n.s. not significant. h , i CUL4B was immunoprecipitated from nuclear extracts of primary cortical neurons and neddylated CUL4B was quantified. Following 10 min of synaptic stimulation, the amount of neddylated CUL4B was increased. Unpaired Student’s t -test ** p < 0.01. j , k shRNA knockdown of NEDD8 in hippocampal primary neurons reduced DNMT3A1 degradation following 10 min-long Bic/4AP treatment and fixation of cells 3 h after washout of the drug-containing-media. Two-way ANOVA followed by Bonferroni’s post-hoc test. *** p < 0.001, scale bar, 20 μm. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.
    Figure Legend Snippet: a NEDD8 is abundantly expressed in the nucleus of 16 DIV hippocampal neurons whereas weaker staining was observed at synapses. Scale bar 20 μm (top panel), 5 μm (lower panel). b Immunoprecipitation of CUL4B protein from nuclear extracts of cortical primary neurons (top panel) results in co-precipitation of DNMT3A1 (lower panel, indicated with an arrow). c , d Hippocampal primary neurons were treated with Bic/4AP for 6 h in the presence or absence of MLN4924 (5 nM). Scale bars, 20 μm. Quantitative immunocytochemistry revealed that blocking neddylation prevents DNMT3A1 degradation. e Representative immunofluorescence images of nuclear NEDD8 and total cytosine methylation (5meC) at basal conditions or after treatment with Bic/4AP for 6 h. Scale bar is 20 μm. f , g Upon synaptic activation nuclear NEDD8 and 5meC levels remained unchanged. Unpaired Student’s t -test. n.s. not significant. h , i CUL4B was immunoprecipitated from nuclear extracts of primary cortical neurons and neddylated CUL4B was quantified. Following 10 min of synaptic stimulation, the amount of neddylated CUL4B was increased. Unpaired Student’s t -test ** p < 0.01. j , k shRNA knockdown of NEDD8 in hippocampal primary neurons reduced DNMT3A1 degradation following 10 min-long Bic/4AP treatment and fixation of cells 3 h after washout of the drug-containing-media. Two-way ANOVA followed by Bonferroni’s post-hoc test. *** p < 0.001, scale bar, 20 μm. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.

    Techniques Used: Staining, Immunoprecipitation, Immunocytochemistry, Blocking Assay, Immunofluorescence, Methylation, Activation Assay, shRNA

    bic 4ap  (Alomone Labs)


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    Alomone Labs bic 4ap
    A Nuclear DNMT3a1 immunofluorescence is prominent in MAP2-positive neurons but much less in GFAP-positive astrocytes at 15 DIV hippocampal cultures. Scale bars are 20 µm. B and C Down-regulation of DNMT3a1 protein levels in 14-15 DIV hippocampal primary neurons following treatment with <t>bic/4AP</t> for 1h, 3h or 6h as evidenced by quantitative immunocytochemistry. Scale bar is 20 µm. Students t-test **p<0.01, ***p<0.001. D to F DNMT3a1 protein levels are decreased following removal of tonic inhibition in DIV 21 cortical neurons. β-Actin was used as an internal control for normalization. Student’s t-test *p<0.05. G and H Treatment of neurons with bic/4AP for 10 min or 3 h was equally effective to reduce nuclear DNMT3a1 immunofluoresence. Application of 100 µM NMDA for 10 min had no effect. Students t-test **p<0.01, ***p<0.001.
    Bic 4ap, supplied by Alomone Labs, 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/bic 4ap/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bic 4ap - by Bioz Stars, 2023-02
    86/100 stars

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    1) Product Images from "Synaptic control of DNA-methylation involves activity-dependent degradation of DNMT3a1 in the nucleus"

    Article Title: Synaptic control of DNA-methylation involves activity-dependent degradation of DNMT3a1 in the nucleus

    Journal: bioRxiv

    doi: 10.1101/602151

    A Nuclear DNMT3a1 immunofluorescence is prominent in MAP2-positive neurons but much less in GFAP-positive astrocytes at 15 DIV hippocampal cultures. Scale bars are 20 µm. B and C Down-regulation of DNMT3a1 protein levels in 14-15 DIV hippocampal primary neurons following treatment with bic/4AP for 1h, 3h or 6h as evidenced by quantitative immunocytochemistry. Scale bar is 20 µm. Students t-test **p<0.01, ***p<0.001. D to F DNMT3a1 protein levels are decreased following removal of tonic inhibition in DIV 21 cortical neurons. β-Actin was used as an internal control for normalization. Student’s t-test *p<0.05. G and H Treatment of neurons with bic/4AP for 10 min or 3 h was equally effective to reduce nuclear DNMT3a1 immunofluoresence. Application of 100 µM NMDA for 10 min had no effect. Students t-test **p<0.01, ***p<0.001.
    Figure Legend Snippet: A Nuclear DNMT3a1 immunofluorescence is prominent in MAP2-positive neurons but much less in GFAP-positive astrocytes at 15 DIV hippocampal cultures. Scale bars are 20 µm. B and C Down-regulation of DNMT3a1 protein levels in 14-15 DIV hippocampal primary neurons following treatment with bic/4AP for 1h, 3h or 6h as evidenced by quantitative immunocytochemistry. Scale bar is 20 µm. Students t-test **p<0.01, ***p<0.001. D to F DNMT3a1 protein levels are decreased following removal of tonic inhibition in DIV 21 cortical neurons. β-Actin was used as an internal control for normalization. Student’s t-test *p<0.05. G and H Treatment of neurons with bic/4AP for 10 min or 3 h was equally effective to reduce nuclear DNMT3a1 immunofluoresence. Application of 100 µM NMDA for 10 min had no effect. Students t-test **p<0.01, ***p<0.001.

    Techniques Used: Immunofluorescence, Immunocytochemistry, Inhibition

    A and B Treatment with the NMDAR antagonist APV (20 µM) prevented the reduction in the nuclear levels of DNMT3a1 following synaptic stimulation by bic/4AP for 6 h. C and D Treatment with the GluN2A inhibitor NVP-AAM077 (50 nM) prevented the reduction in the nuclear levels of DNMT3a1 following synaptic stimulation by bic/4AP for 6 h. E and F shRNA-based knockdown of GluN2A in the presence of synaptic stimulation with bic/4AP for 6 h prevented the DNMT3a1 degradation following synaptic stimulation by bic/4AP for 6 h. G and H Treatment with the GluN2B subunit inhibitor ifenprodil (10 µM) in the presence of synaptic stimulation with bic/4AP for 6 h did not prevent the reduction in the nuclear levels of Dnmt3a1. Scale bars, 20 µm. Two-way ANOVA followed by Bonferroni’s post hoc test. ***P<0.001, n.s. not significant.
    Figure Legend Snippet: A and B Treatment with the NMDAR antagonist APV (20 µM) prevented the reduction in the nuclear levels of DNMT3a1 following synaptic stimulation by bic/4AP for 6 h. C and D Treatment with the GluN2A inhibitor NVP-AAM077 (50 nM) prevented the reduction in the nuclear levels of DNMT3a1 following synaptic stimulation by bic/4AP for 6 h. E and F shRNA-based knockdown of GluN2A in the presence of synaptic stimulation with bic/4AP for 6 h prevented the DNMT3a1 degradation following synaptic stimulation by bic/4AP for 6 h. G and H Treatment with the GluN2B subunit inhibitor ifenprodil (10 µM) in the presence of synaptic stimulation with bic/4AP for 6 h did not prevent the reduction in the nuclear levels of Dnmt3a1. Scale bars, 20 µm. Two-way ANOVA followed by Bonferroni’s post hoc test. ***P<0.001, n.s. not significant.

    Techniques Used: shRNA

    A and B Representative immunofluorescence images of 11 DIV hippocampal primary neurons transfected with either shScrambled or GluN2A shRNA, fixed after 4 days after transfection at 15 DIV. shRNA knockdown confirms the significant less surface expression of GluN2A. Scale bar is 10 µm. Unpaired two-tailed Student’s t-test. C and D The L-type calcium channel blocker Nifedipine (10 µM) attenuated the degradation of DNMT3A1 when 14-15 DIV hippocampal primary neurons were stimulated by bic/4AP for 6h. Two-way ANOVA followed by Bonferroni’s post hoc test. Scale bar is 20 µm. E and F The CamKII inhibitor KN93 (5 µM) abolished the degradation of DNMT3A1 when 14-15 DIV hippocampal primary neurons were stimulated by bic/4AP for 6h. Scale bar is 20 µm. Two-way ANOVA followed by Bonferroni’s post hoc test. ***P<0.001, n.s. not significant.
    Figure Legend Snippet: A and B Representative immunofluorescence images of 11 DIV hippocampal primary neurons transfected with either shScrambled or GluN2A shRNA, fixed after 4 days after transfection at 15 DIV. shRNA knockdown confirms the significant less surface expression of GluN2A. Scale bar is 10 µm. Unpaired two-tailed Student’s t-test. C and D The L-type calcium channel blocker Nifedipine (10 µM) attenuated the degradation of DNMT3A1 when 14-15 DIV hippocampal primary neurons were stimulated by bic/4AP for 6h. Two-way ANOVA followed by Bonferroni’s post hoc test. Scale bar is 20 µm. E and F The CamKII inhibitor KN93 (5 µM) abolished the degradation of DNMT3A1 when 14-15 DIV hippocampal primary neurons were stimulated by bic/4AP for 6h. Scale bar is 20 µm. Two-way ANOVA followed by Bonferroni’s post hoc test. ***P<0.001, n.s. not significant.

    Techniques Used: Immunofluorescence, Transfection, shRNA, Expressing, Two Tailed Test

    A NEDD8 is abundantly expressed in the nucleus of 16 DIV hippocampal neurons whereas weaker staining was observed at synapses. Scale bar 20 µm (top panel), 5 µm (lower panel). B Immunoprecipitation of CUL4B protein from nuclear extracts of cortical primary neurons (top panel) results in co-precipitation of Dnmt3a1 (lower panel, indicated with an arrow). C and D Hippocampal primary neurons were treated with bic/4AP for 6 h in the presence or absence of MLN4924 (5 nM). Scale bars, 20 µm. Quantitative immunocytochemistry revealed that blocking neddylation prevents Dnmt3a1 degradation. E Representative immunofluorescence images of nuclear NEDD8 and total cytosine methylation (5mC) at basal conditions or after treatment with bic/4AP for 6 h. Scale bar is 20 µm. F and G Upon synaptic activation nuclear NEDD8 and 5mC levels remained unchanged. Student’s t-test. n.s. not significant. H and I CUL4B was immunoprecipitated from nuclear extracts of primary cortical neurons and neddylated CUL4B was quantified. Following 10 min of synaptic stimulation the amount of neddylated CUL4B was increased. Student’s t-test **p<0.01. J and K shRNA-based knockdown of NEDD8 in hippocampal primary neurons occluded the DNMT3A1 degradation following 10 min-long bic/4AP treatment and fixation of cells 3 h after washout of the drug-containing-media. Two-way ANOVA followed by Bonferroni’s post-hoc test. ***p<0.001, scale bar, 20 µm.
    Figure Legend Snippet: A NEDD8 is abundantly expressed in the nucleus of 16 DIV hippocampal neurons whereas weaker staining was observed at synapses. Scale bar 20 µm (top panel), 5 µm (lower panel). B Immunoprecipitation of CUL4B protein from nuclear extracts of cortical primary neurons (top panel) results in co-precipitation of Dnmt3a1 (lower panel, indicated with an arrow). C and D Hippocampal primary neurons were treated with bic/4AP for 6 h in the presence or absence of MLN4924 (5 nM). Scale bars, 20 µm. Quantitative immunocytochemistry revealed that blocking neddylation prevents Dnmt3a1 degradation. E Representative immunofluorescence images of nuclear NEDD8 and total cytosine methylation (5mC) at basal conditions or after treatment with bic/4AP for 6 h. Scale bar is 20 µm. F and G Upon synaptic activation nuclear NEDD8 and 5mC levels remained unchanged. Student’s t-test. n.s. not significant. H and I CUL4B was immunoprecipitated from nuclear extracts of primary cortical neurons and neddylated CUL4B was quantified. Following 10 min of synaptic stimulation the amount of neddylated CUL4B was increased. Student’s t-test **p<0.01. J and K shRNA-based knockdown of NEDD8 in hippocampal primary neurons occluded the DNMT3A1 degradation following 10 min-long bic/4AP treatment and fixation of cells 3 h after washout of the drug-containing-media. Two-way ANOVA followed by Bonferroni’s post-hoc test. ***p<0.001, scale bar, 20 µm.

    Techniques Used: Staining, Immunoprecipitation, Immunocytochemistry, Blocking Assay, Immunofluorescence, Methylation, Activation Assay, shRNA

    A and B DIV 14 hippocampal neurons were transfected with RFP expressed under control of an actin promoter and cells were fixed two days after transfection. Homer1 positive dendritic spine numbers were counted. There is not any significant alteration in the total spine number following MLN4924 treatments following the synaptic stimulation with bic/4AP for 6 h. Scale bars are 5 µm. C and D Representative images and quantification display the endogenous rat-Nedd8 knockdown generated in 16 DIV primary hippocampal neurons. Unpaired two-tailed Student’s t-test, *** p<0.0001. Scale bar in C is 20 µm. E Heterologous expression of human-NEDD8 and shRNA mRNA knockdown and shScrambled control in HEK-T cells was detected with either the anti-myc antibody (upper panel) or the anti-NEDD8 antibody (lower panel). The knockdown of Nedd8 was detected by anti-myc and as well as anti-NEDD8 antibodies.
    Figure Legend Snippet: A and B DIV 14 hippocampal neurons were transfected with RFP expressed under control of an actin promoter and cells were fixed two days after transfection. Homer1 positive dendritic spine numbers were counted. There is not any significant alteration in the total spine number following MLN4924 treatments following the synaptic stimulation with bic/4AP for 6 h. Scale bars are 5 µm. C and D Representative images and quantification display the endogenous rat-Nedd8 knockdown generated in 16 DIV primary hippocampal neurons. Unpaired two-tailed Student’s t-test, *** p<0.0001. Scale bar in C is 20 µm. E Heterologous expression of human-NEDD8 and shRNA mRNA knockdown and shScrambled control in HEK-T cells was detected with either the anti-myc antibody (upper panel) or the anti-NEDD8 antibody (lower panel). The knockdown of Nedd8 was detected by anti-myc and as well as anti-NEDD8 antibodies.

    Techniques Used: Transfection, Generated, Two Tailed Test, Expressing, shRNA

    A Bdnf exon IV expression was induced in cultured hippocampal primary neurons following bic/4AP treatment for 6h and this induction was lowered by 5 nM MLN4924. Two-way ANOVA followed by Bonferroni’s post hoc test, **P<0.01 ***P<0.001. B Bdnf exon IV expression was induced following LTP induction for 6h in CA1 region of Hippocampus and this induction was lowered by 50 nM MLN4924. Two-way ANOVA followed by Bonferroni’s post hoc test, *p<0.05 **P<0.01 ***P<0.001. C Methylation analysis based on the restriction of the methylation-sensitive sites showed demethylation of Bdnf promoter IV following LTP induction in CA1 (one-tailed Student’s t-test, t15=1.939, p=0.0358) and promoter methylation was increased when treated with MLN4924 irrespective of LTP induction or basal conditions. Two-way ANOVA followed by Bonferroni’s post hoc test, *p<0.05 **P<0.01. D MeDIP-qPCR analysis revealed demethylation of Bdnf promoter IV following LTP induction in CA1 (one-tailed Student’s t-test, t17=2,198 p=0.0421) and promoter methylation was increased when treated with MLN4924 irrespective of LTP induction or basal conditions. Two-way ANOVA followed by Bonferroni’s post hoc test, *p<0.05 **P<0.01. E MeDIP-qPCR analysis did not show any alteration in Bdnf promoter I methylation. Two-way ANOVA followed by Bonferroni’s post hoc test.
    Figure Legend Snippet: A Bdnf exon IV expression was induced in cultured hippocampal primary neurons following bic/4AP treatment for 6h and this induction was lowered by 5 nM MLN4924. Two-way ANOVA followed by Bonferroni’s post hoc test, **P<0.01 ***P<0.001. B Bdnf exon IV expression was induced following LTP induction for 6h in CA1 region of Hippocampus and this induction was lowered by 50 nM MLN4924. Two-way ANOVA followed by Bonferroni’s post hoc test, *p<0.05 **P<0.01 ***P<0.001. C Methylation analysis based on the restriction of the methylation-sensitive sites showed demethylation of Bdnf promoter IV following LTP induction in CA1 (one-tailed Student’s t-test, t15=1.939, p=0.0358) and promoter methylation was increased when treated with MLN4924 irrespective of LTP induction or basal conditions. Two-way ANOVA followed by Bonferroni’s post hoc test, *p<0.05 **P<0.01. D MeDIP-qPCR analysis revealed demethylation of Bdnf promoter IV following LTP induction in CA1 (one-tailed Student’s t-test, t17=2,198 p=0.0421) and promoter methylation was increased when treated with MLN4924 irrespective of LTP induction or basal conditions. Two-way ANOVA followed by Bonferroni’s post hoc test, *p<0.05 **P<0.01. E MeDIP-qPCR analysis did not show any alteration in Bdnf promoter I methylation. Two-way ANOVA followed by Bonferroni’s post hoc test.

    Techniques Used: Expressing, Cell Culture, Methylation, One-tailed Test, Methylated DNA Immunoprecipitation

    bicuculline bic  (Alomone Labs)


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    Alomone Labs bicuculline bic
    Bicuculline Bic, 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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    bicuculline bic  (Alomone Labs)


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    Alomone Labs bicuculline bic
    Bicuculline Bic, 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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    bicuculline methiodide bic  (Alomone Labs)


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    Alomone Labs bicuculline methiodide bic
    Bicuculline Methiodide Bic, 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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    bicuculline methiodide bic  (Alomone Labs)


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    Alomone Labs bicuculline methiodide bic
    Morphine inhibits hypocretin neurons. A, Morphine (10 μm) reduced spike frequency and hyperpolarized the membrane potential. B, Morphine (10 μm) hyperpolarized the membrane potential in TTX (0.5 <t>μm),</t> <t>AP5</t> (50 μm), CNQX (10 μm), and <t>BIC</t> (30 μm). C, Morphine (10 μm) inhibited the Ba2+ (Ca2+) current evoked by a step depolarization. D, mENK (50 μm) hyperpolarized the membrane potential in TTX (0.5 μm), AP5 (50 μm), CNQX (10 μm), and BIC (30 μm). E, mENK-mediated current is G-protein-coupled inwardly rectifying potassium current. E1, Control and mENK-induced inward current generated by a ramp pulse from −160 to +10 mV under voltage clamp. The cells were in TTX (0.5 μm), AP5 (50 μm), CNQX (10 μm), and bicuculline (30 μm). Holding potential = −90 mV. E2, The resultant currents after subtraction of the control from mENK current. mENK-mediated current is potassium and GTP dependent. E3, Current responses to 20 mV voltage steps from −140 to −60 mV in the presence or absence of mENK. E4, The reversal potential of mENK-induced current was near EK. F, Morphine (10 μm) reduced mEPSC frequency.
    Bicuculline Methiodide Bic, 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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    1) Product Images from "μ-Opioid Receptor-Mediated Depression of the Hypothalamic Hypocretin/Orexin Arousal System"

    Article Title: μ-Opioid Receptor-Mediated Depression of the Hypothalamic Hypocretin/Orexin Arousal System

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.5447-07.2008

    Morphine inhibits hypocretin neurons. A, Morphine (10 μm) reduced spike frequency and hyperpolarized the membrane potential. B, Morphine (10 μm) hyperpolarized the membrane potential in TTX (0.5 μm), AP5 (50 μm), CNQX (10 μm), and BIC (30 μm). C, Morphine (10 μm) inhibited the Ba2+ (Ca2+) current evoked by a step depolarization. D, mENK (50 μm) hyperpolarized the membrane potential in TTX (0.5 μm), AP5 (50 μm), CNQX (10 μm), and BIC (30 μm). E, mENK-mediated current is G-protein-coupled inwardly rectifying potassium current. E1, Control and mENK-induced inward current generated by a ramp pulse from −160 to +10 mV under voltage clamp. The cells were in TTX (0.5 μm), AP5 (50 μm), CNQX (10 μm), and bicuculline (30 μm). Holding potential = −90 mV. E2, The resultant currents after subtraction of the control from mENK current. mENK-mediated current is potassium and GTP dependent. E3, Current responses to 20 mV voltage steps from −140 to −60 mV in the presence or absence of mENK. E4, The reversal potential of mENK-induced current was near EK. F, Morphine (10 μm) reduced mEPSC frequency.
    Figure Legend Snippet: Morphine inhibits hypocretin neurons. A, Morphine (10 μm) reduced spike frequency and hyperpolarized the membrane potential. B, Morphine (10 μm) hyperpolarized the membrane potential in TTX (0.5 μm), AP5 (50 μm), CNQX (10 μm), and BIC (30 μm). C, Morphine (10 μm) inhibited the Ba2+ (Ca2+) current evoked by a step depolarization. D, mENK (50 μm) hyperpolarized the membrane potential in TTX (0.5 μm), AP5 (50 μm), CNQX (10 μm), and BIC (30 μm). E, mENK-mediated current is G-protein-coupled inwardly rectifying potassium current. E1, Control and mENK-induced inward current generated by a ramp pulse from −160 to +10 mV under voltage clamp. The cells were in TTX (0.5 μm), AP5 (50 μm), CNQX (10 μm), and bicuculline (30 μm). Holding potential = −90 mV. E2, The resultant currents after subtraction of the control from mENK current. mENK-mediated current is potassium and GTP dependent. E3, Current responses to 20 mV voltage steps from −140 to −60 mV in the presence or absence of mENK. E4, The reversal potential of mENK-induced current was near EK. F, Morphine (10 μm) reduced mEPSC frequency.

    Techniques Used: Generated

    bicuculline methiodide bic  (Alomone Labs)


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    Alomone Labs bicuculline methiodide bic
    Bicuculline Methiodide Bic, 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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    Alomone Labs bicuculline methiodide bic
    GIRK current activated by an α2 receptor. The α2 antagonist idazoxan (10 μm) blocked an NE-induced GIRK-type current. AP-5 (50 μm), CNQX (10 μm), <t>BIC</t> (30 μm), <t>and</t> <t>TTX</t> (0.5 μm) were used to block synaptic activity in this experiment. A1, Current was measured in the absence and in the presence of NE (50 μm) with and without idazoxan at voltages from -170 to -30 mV, varied by a voltage ramp lasting 100 msec. Current traces are signal averaged from four traces for control, NE, idazoxan, and NE plus idazoxan, respectively. A2, NE-induced current (B-A) was obtained by subtraction of the trace A from trace B; trace D-C was obtained by subtraction of the trace C from trace D. B, Ba2+ blocked NE-induced GIRK-type current. B1, Current was measured in the absence and the presence of NE (50 μm) with and without Ba2+. Current traces are signal averaged from four traces for control, NE, Ba2+, and NE plus Ba2+, respectively. B2, NE-induced current (B-A) was obtained by subtraction of the trace A from trace B; trace D-C was obtained by subtraction of the trace C from trace D. C1, Dependence on external K+. Current-voltage relationships for the NE-induced current with 6 and 16 mm external K+ are shown. Each trace is the difference between current in NE (50 μm) and control current (signal-averaged 1 NE and 1 control trace from each of 6 neurons). C2, Reversal potential as a function of external K+. Reversal potentials for NE-induced current are -81 mV with 6 mm K+ and -56 mV with 16 mm K+. The solid line is the Nernst potassium equilibrium potential (RT/F)*In([K+]o/[K+]i), with [K+]i = 145 mm and T = 30°C. Bath solution had an equimolar substitution of KCl for NaCl to obtain the desired KCl concentration. D, NE induced outward current at +20 mV and inward current at -130 mV under voltage clamp. When external [K+] was 6 mm, the membrane potential was held at -80 mV; when external [K+] was 16 mm, the membrane potential was held at -60 mV. E, NE initially induced an inwardly rectified K+ current with GTP-γ-S loaded in the pipette. E1, A typical neuron showing that the NE-induced inward current did not recover when the cell was loaded with GTP-γ-S. NE failed to induce the inward current when applied several minutes after cell dialysis. E2, A bar graph illustrates that the response to a second application of NE is significantly reduced (p < 0.05). Asterisks indicate significant statistical differences by ANOVA (p < 0.05).
    Bicuculline Methiodide Bic, 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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    1) Product Images from "Direct and Indirect Inhibition by Catecholamines of Hypocretin/Orexin Neurons"

    Article Title: Direct and Indirect Inhibition by Catecholamines of Hypocretin/Orexin Neurons

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.4015-04.2005

    GIRK current activated by an α2 receptor. The α2 antagonist idazoxan (10 μm) blocked an NE-induced GIRK-type current. AP-5 (50 μm), CNQX (10 μm), BIC (30 μm), and TTX (0.5 μm) were used to block synaptic activity in this experiment. A1, Current was measured in the absence and in the presence of NE (50 μm) with and without idazoxan at voltages from -170 to -30 mV, varied by a voltage ramp lasting 100 msec. Current traces are signal averaged from four traces for control, NE, idazoxan, and NE plus idazoxan, respectively. A2, NE-induced current (B-A) was obtained by subtraction of the trace A from trace B; trace D-C was obtained by subtraction of the trace C from trace D. B, Ba2+ blocked NE-induced GIRK-type current. B1, Current was measured in the absence and the presence of NE (50 μm) with and without Ba2+. Current traces are signal averaged from four traces for control, NE, Ba2+, and NE plus Ba2+, respectively. B2, NE-induced current (B-A) was obtained by subtraction of the trace A from trace B; trace D-C was obtained by subtraction of the trace C from trace D. C1, Dependence on external K+. Current-voltage relationships for the NE-induced current with 6 and 16 mm external K+ are shown. Each trace is the difference between current in NE (50 μm) and control current (signal-averaged 1 NE and 1 control trace from each of 6 neurons). C2, Reversal potential as a function of external K+. Reversal potentials for NE-induced current are -81 mV with 6 mm K+ and -56 mV with 16 mm K+. The solid line is the Nernst potassium equilibrium potential (RT/F)*In([K+]o/[K+]i), with [K+]i = 145 mm and T = 30°C. Bath solution had an equimolar substitution of KCl for NaCl to obtain the desired KCl concentration. D, NE induced outward current at +20 mV and inward current at -130 mV under voltage clamp. When external [K+] was 6 mm, the membrane potential was held at -80 mV; when external [K+] was 16 mm, the membrane potential was held at -60 mV. E, NE initially induced an inwardly rectified K+ current with GTP-γ-S loaded in the pipette. E1, A typical neuron showing that the NE-induced inward current did not recover when the cell was loaded with GTP-γ-S. NE failed to induce the inward current when applied several minutes after cell dialysis. E2, A bar graph illustrates that the response to a second application of NE is significantly reduced (p < 0.05). Asterisks indicate significant statistical differences by ANOVA (p < 0.05).
    Figure Legend Snippet: GIRK current activated by an α2 receptor. The α2 antagonist idazoxan (10 μm) blocked an NE-induced GIRK-type current. AP-5 (50 μm), CNQX (10 μm), BIC (30 μm), and TTX (0.5 μm) were used to block synaptic activity in this experiment. A1, Current was measured in the absence and in the presence of NE (50 μm) with and without idazoxan at voltages from -170 to -30 mV, varied by a voltage ramp lasting 100 msec. Current traces are signal averaged from four traces for control, NE, idazoxan, and NE plus idazoxan, respectively. A2, NE-induced current (B-A) was obtained by subtraction of the trace A from trace B; trace D-C was obtained by subtraction of the trace C from trace D. B, Ba2+ blocked NE-induced GIRK-type current. B1, Current was measured in the absence and the presence of NE (50 μm) with and without Ba2+. Current traces are signal averaged from four traces for control, NE, Ba2+, and NE plus Ba2+, respectively. B2, NE-induced current (B-A) was obtained by subtraction of the trace A from trace B; trace D-C was obtained by subtraction of the trace C from trace D. C1, Dependence on external K+. Current-voltage relationships for the NE-induced current with 6 and 16 mm external K+ are shown. Each trace is the difference between current in NE (50 μm) and control current (signal-averaged 1 NE and 1 control trace from each of 6 neurons). C2, Reversal potential as a function of external K+. Reversal potentials for NE-induced current are -81 mV with 6 mm K+ and -56 mV with 16 mm K+. The solid line is the Nernst potassium equilibrium potential (RT/F)*In([K+]o/[K+]i), with [K+]i = 145 mm and T = 30°C. Bath solution had an equimolar substitution of KCl for NaCl to obtain the desired KCl concentration. D, NE induced outward current at +20 mV and inward current at -130 mV under voltage clamp. When external [K+] was 6 mm, the membrane potential was held at -80 mV; when external [K+] was 16 mm, the membrane potential was held at -60 mV. E, NE initially induced an inwardly rectified K+ current with GTP-γ-S loaded in the pipette. E1, A typical neuron showing that the NE-induced inward current did not recover when the cell was loaded with GTP-γ-S. NE failed to induce the inward current when applied several minutes after cell dialysis. E2, A bar graph illustrates that the response to a second application of NE is significantly reduced (p < 0.05). Asterisks indicate significant statistical differences by ANOVA (p < 0.05).

    Techniques Used: Blocking Assay, Activity Assay, Concentration Assay, Transferring

    bicuculline methiodide bic  (Alomone Labs)


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    Alomone Labs bicuculline bic
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    Alomone Labs bic 4ap
    a Nuclear DNMT3A1 immunofluorescence is prominent in MAP2-positive neurons but much less in GFAP-positive astrocytes at 15 DIV hippocampal cultures. Scale bars are 20 μm. b , c Downregulation of DNMT3A1 protein levels in 14–15 DIV hippocampal primary neurons following treatment with <t>Bic/4AP</t> for 1 h, 3 h or 6 h as evidenced by quantitative immunocytochemistry. Scale bar is 20 μm. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. d – f DNMT3a1 protein levels are decreased following the removal of tonic inhibition in DIV 21 cortical neurons. β-Actin was used as an internal control for normalization. Student’s t -test * p < 0.05. g , h Hippocampal neurons were treated with Bic/4AP for 10 min or 3 h. Media from 10 min-long treated neurons was washed out and cells were kept for 3 h before fixation. Both treatments were equally effective to reduce nuclear DNMT3A1 immunofluorescence. Application of 100 μM NMDA for 10 min had no effect. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.
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    Alomone Labs bicuculline methiodide bic
    a Nuclear DNMT3A1 immunofluorescence is prominent in MAP2-positive neurons but much less in GFAP-positive astrocytes at 15 DIV hippocampal cultures. Scale bars are 20 μm. b , c Downregulation of DNMT3A1 protein levels in 14–15 DIV hippocampal primary neurons following treatment with <t>Bic/4AP</t> for 1 h, 3 h or 6 h as evidenced by quantitative immunocytochemistry. Scale bar is 20 μm. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. d – f DNMT3a1 protein levels are decreased following the removal of tonic inhibition in DIV 21 cortical neurons. β-Actin was used as an internal control for normalization. Student’s t -test * p < 0.05. g , h Hippocampal neurons were treated with Bic/4AP for 10 min or 3 h. Media from 10 min-long treated neurons was washed out and cells were kept for 3 h before fixation. Both treatments were equally effective to reduce nuclear DNMT3A1 immunofluorescence. Application of 100 μM NMDA for 10 min had no effect. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.
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    a Nuclear DNMT3A1 immunofluorescence is prominent in MAP2-positive neurons but much less in GFAP-positive astrocytes at 15 DIV hippocampal cultures. Scale bars are 20 μm. b , c Downregulation of DNMT3A1 protein levels in 14–15 DIV hippocampal primary neurons following treatment with Bic/4AP for 1 h, 3 h or 6 h as evidenced by quantitative immunocytochemistry. Scale bar is 20 μm. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. d – f DNMT3a1 protein levels are decreased following the removal of tonic inhibition in DIV 21 cortical neurons. β-Actin was used as an internal control for normalization. Student’s t -test * p < 0.05. g , h Hippocampal neurons were treated with Bic/4AP for 10 min or 3 h. Media from 10 min-long treated neurons was washed out and cells were kept for 3 h before fixation. Both treatments were equally effective to reduce nuclear DNMT3A1 immunofluorescence. Application of 100 μM NMDA for 10 min had no effect. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.

    Journal: Neuropsychopharmacology

    Article Title: Synaptic control of DNA methylation involves activity-dependent degradation of DNMT3A1 in the nucleus

    doi: 10.1038/s41386-020-0780-2

    Figure Lengend Snippet: a Nuclear DNMT3A1 immunofluorescence is prominent in MAP2-positive neurons but much less in GFAP-positive astrocytes at 15 DIV hippocampal cultures. Scale bars are 20 μm. b , c Downregulation of DNMT3A1 protein levels in 14–15 DIV hippocampal primary neurons following treatment with Bic/4AP for 1 h, 3 h or 6 h as evidenced by quantitative immunocytochemistry. Scale bar is 20 μm. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. d – f DNMT3a1 protein levels are decreased following the removal of tonic inhibition in DIV 21 cortical neurons. β-Actin was used as an internal control for normalization. Student’s t -test * p < 0.05. g , h Hippocampal neurons were treated with Bic/4AP for 10 min or 3 h. Media from 10 min-long treated neurons was washed out and cells were kept for 3 h before fixation. Both treatments were equally effective to reduce nuclear DNMT3A1 immunofluorescence. Application of 100 μM NMDA for 10 min had no effect. Unpaired Student’s t -test ** p < 0.01, *** p < 0.001. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.

    Article Snippet: Cortical neurons were treated with 1 μM tetrodotoxin (TTX, Alomone Labs, Jerusalem, Israel) for 12 h, media was washed-out and Bic/4AP were applied for 6 h at 21 DIV.

    Techniques: Immunofluorescence, Immunocytochemistry, Inhibition

    a , b Treatment with the NMDAR antagonist APV (20 μM) prevented the reduction in the nuclear levels of DNMT3A1 following synaptic stimulation by Bic/4AP for 6 h. c , d Treatment with the GluN2A inhibitor NVP-AAM077 (50 nM) prevented the reduction in the nuclear levels of DNMT3A1 following synaptic stimulation by Bic/4AP for 6 h. Two-way ANOVA followed by Bonferroni’s post hoc test. e Timeline view of hippocampal neuron treatment by Bic/4AP for 6 h with or without NVP-AAM077. f , g Quantitative immunoblotting revealed the inhibition of DNMT3A1 degradation by the use of NVP-AAM077. One-sample t-test is performed while the hypothetical value is set to 100. h , i shRNA-based knockdown of GluN2A in the presence of synaptic stimulation by Bic/4AP for 6 h prevented the DNMT3A1 degradation. j , k Treatment with the GluN2B subunit inhibitor ifenprodil (10 μM) in the presence of synaptic stimulation with Bic/4AP for 6 h did not prevent the reduction in the nuclear levels of Dnmt3A1. Scale bars, 20 μm. Two-way ANOVA followed by Bonferroni’s post hoc test. *** p < 0.001, n.s. not significant. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.

    Journal: Neuropsychopharmacology

    Article Title: Synaptic control of DNA methylation involves activity-dependent degradation of DNMT3A1 in the nucleus

    doi: 10.1038/s41386-020-0780-2

    Figure Lengend Snippet: a , b Treatment with the NMDAR antagonist APV (20 μM) prevented the reduction in the nuclear levels of DNMT3A1 following synaptic stimulation by Bic/4AP for 6 h. c , d Treatment with the GluN2A inhibitor NVP-AAM077 (50 nM) prevented the reduction in the nuclear levels of DNMT3A1 following synaptic stimulation by Bic/4AP for 6 h. Two-way ANOVA followed by Bonferroni’s post hoc test. e Timeline view of hippocampal neuron treatment by Bic/4AP for 6 h with or without NVP-AAM077. f , g Quantitative immunoblotting revealed the inhibition of DNMT3A1 degradation by the use of NVP-AAM077. One-sample t-test is performed while the hypothetical value is set to 100. h , i shRNA-based knockdown of GluN2A in the presence of synaptic stimulation by Bic/4AP for 6 h prevented the DNMT3A1 degradation. j , k Treatment with the GluN2B subunit inhibitor ifenprodil (10 μM) in the presence of synaptic stimulation with Bic/4AP for 6 h did not prevent the reduction in the nuclear levels of Dnmt3A1. Scale bars, 20 μm. Two-way ANOVA followed by Bonferroni’s post hoc test. *** p < 0.001, n.s. not significant. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.

    Article Snippet: Cortical neurons were treated with 1 μM tetrodotoxin (TTX, Alomone Labs, Jerusalem, Israel) for 12 h, media was washed-out and Bic/4AP were applied for 6 h at 21 DIV.

    Techniques: Western Blot, Inhibition, shRNA

    a NEDD8 is abundantly expressed in the nucleus of 16 DIV hippocampal neurons whereas weaker staining was observed at synapses. Scale bar 20 μm (top panel), 5 μm (lower panel). b Immunoprecipitation of CUL4B protein from nuclear extracts of cortical primary neurons (top panel) results in co-precipitation of DNMT3A1 (lower panel, indicated with an arrow). c , d Hippocampal primary neurons were treated with Bic/4AP for 6 h in the presence or absence of MLN4924 (5 nM). Scale bars, 20 μm. Quantitative immunocytochemistry revealed that blocking neddylation prevents DNMT3A1 degradation. e Representative immunofluorescence images of nuclear NEDD8 and total cytosine methylation (5meC) at basal conditions or after treatment with Bic/4AP for 6 h. Scale bar is 20 μm. f , g Upon synaptic activation nuclear NEDD8 and 5meC levels remained unchanged. Unpaired Student’s t -test. n.s. not significant. h , i CUL4B was immunoprecipitated from nuclear extracts of primary cortical neurons and neddylated CUL4B was quantified. Following 10 min of synaptic stimulation, the amount of neddylated CUL4B was increased. Unpaired Student’s t -test ** p < 0.01. j , k shRNA knockdown of NEDD8 in hippocampal primary neurons reduced DNMT3A1 degradation following 10 min-long Bic/4AP treatment and fixation of cells 3 h after washout of the drug-containing-media. Two-way ANOVA followed by Bonferroni’s post-hoc test. *** p < 0.001, scale bar, 20 μm. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.

    Journal: Neuropsychopharmacology

    Article Title: Synaptic control of DNA methylation involves activity-dependent degradation of DNMT3A1 in the nucleus

    doi: 10.1038/s41386-020-0780-2

    Figure Lengend Snippet: a NEDD8 is abundantly expressed in the nucleus of 16 DIV hippocampal neurons whereas weaker staining was observed at synapses. Scale bar 20 μm (top panel), 5 μm (lower panel). b Immunoprecipitation of CUL4B protein from nuclear extracts of cortical primary neurons (top panel) results in co-precipitation of DNMT3A1 (lower panel, indicated with an arrow). c , d Hippocampal primary neurons were treated with Bic/4AP for 6 h in the presence or absence of MLN4924 (5 nM). Scale bars, 20 μm. Quantitative immunocytochemistry revealed that blocking neddylation prevents DNMT3A1 degradation. e Representative immunofluorescence images of nuclear NEDD8 and total cytosine methylation (5meC) at basal conditions or after treatment with Bic/4AP for 6 h. Scale bar is 20 μm. f , g Upon synaptic activation nuclear NEDD8 and 5meC levels remained unchanged. Unpaired Student’s t -test. n.s. not significant. h , i CUL4B was immunoprecipitated from nuclear extracts of primary cortical neurons and neddylated CUL4B was quantified. Following 10 min of synaptic stimulation, the amount of neddylated CUL4B was increased. Unpaired Student’s t -test ** p < 0.01. j , k shRNA knockdown of NEDD8 in hippocampal primary neurons reduced DNMT3A1 degradation following 10 min-long Bic/4AP treatment and fixation of cells 3 h after washout of the drug-containing-media. Two-way ANOVA followed by Bonferroni’s post-hoc test. *** p < 0.001, scale bar, 20 μm. Error bars present S.E.M. Sample numbers for each experimental group indicate neurons from three different culture preparations.

    Article Snippet: Cortical neurons were treated with 1 μM tetrodotoxin (TTX, Alomone Labs, Jerusalem, Israel) for 12 h, media was washed-out and Bic/4AP were applied for 6 h at 21 DIV.

    Techniques: Staining, Immunoprecipitation, Immunocytochemistry, Blocking Assay, Immunofluorescence, Methylation, Activation Assay, shRNA