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A Quantitative morphometric analysis of <t>BDNF-immunoreactivity</t> in the CA1 region. B Quantitative morphometric analysis of BDNF-immunoreactivity in the stratum lacunosum-moleculare (SLM) region. C Quantitative morphometric analysis of BDNF-immunoreactivity in the paraventricular nucleus (PVN). D Representative images of BDNF-immunoreactivity in the PVN across all experimental groups. BDNF-positive cells in red; scale bar: 200 µm. E Quantitative morphometric analysis <t>of</t> <t>NPY-immunoreactivity</t> in the CA1 region. F Quantitative morphometric analysis of NPY-immunoreactivity in the SLM region. G Quantitative morphometric analysis of NPY-immunoreactivity in the PVN. H Representative images of NPY-immunoreactivity in the PVN across all experimental groups. NPY-positive cells in green; scale bar: 200 µm. Data Presentation: ( A–C and E–G ) show individual data points with mean ± SEM.
Antibodies Against Bdnf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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A Quantitative morphometric analysis of <t>BDNF-immunoreactivity</t> in the CA1 region. B Quantitative morphometric analysis of BDNF-immunoreactivity in the stratum lacunosum-moleculare (SLM) region. C Quantitative morphometric analysis of BDNF-immunoreactivity in the paraventricular nucleus (PVN). D Representative images of BDNF-immunoreactivity in the PVN across all experimental groups. BDNF-positive cells in red; scale bar: 200 µm. E Quantitative morphometric analysis <t>of</t> <t>NPY-immunoreactivity</t> in the CA1 region. F Quantitative morphometric analysis of NPY-immunoreactivity in the SLM region. G Quantitative morphometric analysis of NPY-immunoreactivity in the PVN. H Representative images of NPY-immunoreactivity in the PVN across all experimental groups. NPY-positive cells in green; scale bar: 200 µm. Data Presentation: ( A–C and E–G ) show individual data points with mean ± SEM.
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Persistent hyperalgesia in the RPP model (A and B) Paw withdrawal latency (A) and 50% paw withdrawal threshold (B) of each rat ( n = 3–6). (C) Representative histological images of DRG from T10-S4 by H&E staining. Arrow, Schwann cell; ∗, nuclei; #, cytoplasm. Scale bars, 50 μm and 25 μm. (D and E) Representative IHC images (D) and quantification (E) of <t>BDNF</t> in the DRG from T10-S4. Brown DAB staining indicates BDNF immunopositivity. The staining intensity was semi-quantitatively scored as follows: (1) weak, (2) moderate, and (3) intense. Scale bars, 50 μm. ( n = 3 biological replicates per group). (F) Serum BDNF level on days 12 and 24 of RPP modeling ( n = 3). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, two-way ANOVA (A and B) or one-way ANOVA (E and F).
Rat Bdnf Elisa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fig. 2 Riluzole treatment restores <t>hippocampal</t> <t>BDNF</t> in the irradiated hippocampus. 10–12 weeks old WT male mice received cranial radiation therapy (RT) followed by riluzole (RZ) treatment (13 mg/kg) in drinking water for 6–7 weeks. An <t>ELISA-based</t> quantification of BDNF from the micro-dissected hippocampus showed RT-induced reductions in the RT + Vehicle group. Importantly, RZ treatment in the cranially irradiated mice showed significant restoration of BDNF levels. Data are presented as mean ± SEM (N = 6–10 mice per group). P values were derived from two-way ANOVA and Bonferroni’s multiple comparisons test
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Fig. 2 Riluzole treatment restores <t>hippocampal</t> <t>BDNF</t> in the irradiated hippocampus. 10–12 weeks old WT male mice received cranial radiation therapy (RT) followed by riluzole (RZ) treatment (13 mg/kg) in drinking water for 6–7 weeks. An <t>ELISA-based</t> quantification of BDNF from the micro-dissected hippocampus showed RT-induced reductions in the RT + Vehicle group. Importantly, RZ treatment in the cranially irradiated mice showed significant restoration of BDNF levels. Data are presented as mean ± SEM (N = 6–10 mice per group). P values were derived from two-way ANOVA and Bonferroni’s multiple comparisons test
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Fig. 2 Riluzole treatment restores <t>hippocampal</t> <t>BDNF</t> in the irradiated hippocampus. 10–12 weeks old WT male mice received cranial radiation therapy (RT) followed by riluzole (RZ) treatment (13 mg/kg) in drinking water for 6–7 weeks. An <t>ELISA-based</t> quantification of BDNF from the micro-dissected hippocampus showed RT-induced reductions in the RT + Vehicle group. Importantly, RZ treatment in the cranially irradiated mice showed significant restoration of BDNF levels. Data are presented as mean ± SEM (N = 6–10 mice per group). P values were derived from two-way ANOVA and Bonferroni’s multiple comparisons test
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Fig. 2 Riluzole treatment restores <t>hippocampal</t> <t>BDNF</t> in the irradiated hippocampus. 10–12 weeks old WT male mice received cranial radiation therapy (RT) followed by riluzole (RZ) treatment (13 mg/kg) in drinking water for 6–7 weeks. An <t>ELISA-based</t> quantification of BDNF from the micro-dissected hippocampus showed RT-induced reductions in the RT + Vehicle group. Importantly, RZ treatment in the cranially irradiated mice showed significant restoration of BDNF levels. Data are presented as mean ± SEM (N = 6–10 mice per group). P values were derived from two-way ANOVA and Bonferroni’s multiple comparisons test
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Fig. 2 Riluzole treatment restores <t>hippocampal</t> <t>BDNF</t> in the irradiated hippocampus. 10–12 weeks old WT male mice received cranial radiation therapy (RT) followed by riluzole (RZ) treatment (13 mg/kg) in drinking water for 6–7 weeks. An <t>ELISA-based</t> quantification of BDNF from the micro-dissected hippocampus showed RT-induced reductions in the RT + Vehicle group. Importantly, RZ treatment in the cranially irradiated mice showed significant restoration of BDNF levels. Data are presented as mean ± SEM (N = 6–10 mice per group). P values were derived from two-way ANOVA and Bonferroni’s multiple comparisons test
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Figure4. <t>BDNF-TrkBsignalinginducesCREBphosphorylationbutdoesnotinfluencetotalCREBproteinlevels.Primaryneurons</t> were treated at 7 DIV with 50 ng/ml BDNF for the indicated time periods. A, CREB1 mRNA levels, measured using qRT-PCR, are represented as fold induction relative to CREB1 mRNA levels in untreated cells. B, Western blot analysis determining CREB and phospho-Ser-133CREB(P-CREB)proteinlevelsandCoomassiestainingforloadingcontrol.C,QuantificationoftotalCREBprotein levels. CREB protein levels were normalized using Coomassie staining, and normalized CREB protein level in nontreated cells was setas1.D,QuantificationofCREBphosphorylationlevels.P-CREBproteinlevelswerenormalizedtototalCREBproteinlevels,and therelativelevelofP-CREBproteininnontreatedcellswassetas1.A,C,D,Averageofthreeindependentexperiments(n 3)is shown. Error bars indicate SEM. Statistical significance relative to respective mRNA (A) or protein (C, D) levels in untreated cells: ***p 0.001; *p 0.05 (paired two-tailed t test, corrected for multiple comparisons using Holm–Sidak method).
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Figure4. <t>BDNF-TrkBsignalinginducesCREBphosphorylationbutdoesnotinfluencetotalCREBproteinlevels.Primaryneurons</t> were treated at 7 DIV with 50 ng/ml BDNF for the indicated time periods. A, CREB1 mRNA levels, measured using qRT-PCR, are represented as fold induction relative to CREB1 mRNA levels in untreated cells. B, Western blot analysis determining CREB and phospho-Ser-133CREB(P-CREB)proteinlevelsandCoomassiestainingforloadingcontrol.C,QuantificationoftotalCREBprotein levels. CREB protein levels were normalized using Coomassie staining, and normalized CREB protein level in nontreated cells was setas1.D,QuantificationofCREBphosphorylationlevels.P-CREBproteinlevelswerenormalizedtototalCREBproteinlevels,and therelativelevelofP-CREBproteininnontreatedcellswassetas1.A,C,D,Averageofthreeindependentexperiments(n 3)is shown. Error bars indicate SEM. Statistical significance relative to respective mRNA (A) or protein (C, D) levels in untreated cells: ***p 0.001; *p 0.05 (paired two-tailed t test, corrected for multiple comparisons using Holm–Sidak method).
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Figure4. <t>BDNF-TrkBsignalinginducesCREBphosphorylationbutdoesnotinfluencetotalCREBproteinlevels.Primaryneurons</t> were treated at 7 DIV with 50 ng/ml BDNF for the indicated time periods. A, CREB1 mRNA levels, measured using qRT-PCR, are represented as fold induction relative to CREB1 mRNA levels in untreated cells. B, Western blot analysis determining CREB and phospho-Ser-133CREB(P-CREB)proteinlevelsandCoomassiestainingforloadingcontrol.C,QuantificationoftotalCREBprotein levels. CREB protein levels were normalized using Coomassie staining, and normalized CREB protein level in nontreated cells was setas1.D,QuantificationofCREBphosphorylationlevels.P-CREBproteinlevelswerenormalizedtototalCREBproteinlevels,and therelativelevelofP-CREBproteininnontreatedcellswassetas1.A,C,D,Averageofthreeindependentexperiments(n 3)is shown. Error bars indicate SEM. Statistical significance relative to respective mRNA (A) or protein (C, D) levels in untreated cells: ***p 0.001; *p 0.05 (paired two-tailed t test, corrected for multiple comparisons using Holm–Sidak method).
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Image Search Results


A Quantitative morphometric analysis of BDNF-immunoreactivity in the CA1 region. B Quantitative morphometric analysis of BDNF-immunoreactivity in the stratum lacunosum-moleculare (SLM) region. C Quantitative morphometric analysis of BDNF-immunoreactivity in the paraventricular nucleus (PVN). D Representative images of BDNF-immunoreactivity in the PVN across all experimental groups. BDNF-positive cells in red; scale bar: 200 µm. E Quantitative morphometric analysis of NPY-immunoreactivity in the CA1 region. F Quantitative morphometric analysis of NPY-immunoreactivity in the SLM region. G Quantitative morphometric analysis of NPY-immunoreactivity in the PVN. H Representative images of NPY-immunoreactivity in the PVN across all experimental groups. NPY-positive cells in green; scale bar: 200 µm. Data Presentation: ( A–C and E–G ) show individual data points with mean ± SEM.

Journal: Translational Psychiatry

Article Title: Impact of subanesthetic ketamine delivered via AmyloLipid nanovesicle (ALN)-based intranasal system on biobehavioral responses in an animal model of PTSD

doi: 10.1038/s41398-026-03979-7

Figure Lengend Snippet: A Quantitative morphometric analysis of BDNF-immunoreactivity in the CA1 region. B Quantitative morphometric analysis of BDNF-immunoreactivity in the stratum lacunosum-moleculare (SLM) region. C Quantitative morphometric analysis of BDNF-immunoreactivity in the paraventricular nucleus (PVN). D Representative images of BDNF-immunoreactivity in the PVN across all experimental groups. BDNF-positive cells in red; scale bar: 200 µm. E Quantitative morphometric analysis of NPY-immunoreactivity in the CA1 region. F Quantitative morphometric analysis of NPY-immunoreactivity in the SLM region. G Quantitative morphometric analysis of NPY-immunoreactivity in the PVN. H Representative images of NPY-immunoreactivity in the PVN across all experimental groups. NPY-positive cells in green; scale bar: 200 µm. Data Presentation: ( A–C and E–G ) show individual data points with mean ± SEM.

Article Snippet: Sections were fixed with ethanol, rinsed in phosphate-buffered saline (PBS), blocked with normal goat serum in PBS for 2 h, incubated overnight at 4 °C with primary antibodies against BDNF (1:300, ANT-010, Alomone Labs, Israel), NPY (1:100, AB-221145, Abcam, UK), or HCN1 (1:750, APC-056, Alomone Labs, Israel).

Techniques:

Persistent hyperalgesia in the RPP model (A and B) Paw withdrawal latency (A) and 50% paw withdrawal threshold (B) of each rat ( n = 3–6). (C) Representative histological images of DRG from T10-S4 by H&E staining. Arrow, Schwann cell; ∗, nuclei; #, cytoplasm. Scale bars, 50 μm and 25 μm. (D and E) Representative IHC images (D) and quantification (E) of BDNF in the DRG from T10-S4. Brown DAB staining indicates BDNF immunopositivity. The staining intensity was semi-quantitatively scored as follows: (1) weak, (2) moderate, and (3) intense. Scale bars, 50 μm. ( n = 3 biological replicates per group). (F) Serum BDNF level on days 12 and 24 of RPP modeling ( n = 3). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, two-way ANOVA (A and B) or one-way ANOVA (E and F).

Journal: iScience

Article Title: A pharmacological rat model of recurrent pelvic pain exhibiting hyperalgesia and depression-like behaviors

doi: 10.1016/j.isci.2026.115059

Figure Lengend Snippet: Persistent hyperalgesia in the RPP model (A and B) Paw withdrawal latency (A) and 50% paw withdrawal threshold (B) of each rat ( n = 3–6). (C) Representative histological images of DRG from T10-S4 by H&E staining. Arrow, Schwann cell; ∗, nuclei; #, cytoplasm. Scale bars, 50 μm and 25 μm. (D and E) Representative IHC images (D) and quantification (E) of BDNF in the DRG from T10-S4. Brown DAB staining indicates BDNF immunopositivity. The staining intensity was semi-quantitatively scored as follows: (1) weak, (2) moderate, and (3) intense. Scale bars, 50 μm. ( n = 3 biological replicates per group). (F) Serum BDNF level on days 12 and 24 of RPP modeling ( n = 3). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, two-way ANOVA (A and B) or one-way ANOVA (E and F).

Article Snippet: Rat BDNF ELISA Kit , Elabscience , Cat# E-EL-R1235.

Techniques: Staining

Comorbid depression-like behavior in the RPP model (A and B) Serum BDNF (A) and 5-HT (B) levels in the RPP model ( n = 6). (C and D) Sucrose preference ratio (C) and immobility time (D) in the RPP model ( n = 8). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, paired t test (A and B) or two-way ANOVA (C and D).

Journal: iScience

Article Title: A pharmacological rat model of recurrent pelvic pain exhibiting hyperalgesia and depression-like behaviors

doi: 10.1016/j.isci.2026.115059

Figure Lengend Snippet: Comorbid depression-like behavior in the RPP model (A and B) Serum BDNF (A) and 5-HT (B) levels in the RPP model ( n = 6). (C and D) Sucrose preference ratio (C) and immobility time (D) in the RPP model ( n = 8). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, paired t test (A and B) or two-way ANOVA (C and D).

Article Snippet: Rat BDNF ELISA Kit , Elabscience , Cat# E-EL-R1235.

Techniques:

Fig. 2 Riluzole treatment restores hippocampal BDNF in the irradiated hippocampus. 10–12 weeks old WT male mice received cranial radiation therapy (RT) followed by riluzole (RZ) treatment (13 mg/kg) in drinking water for 6–7 weeks. An ELISA-based quantification of BDNF from the micro-dissected hippocampus showed RT-induced reductions in the RT + Vehicle group. Importantly, RZ treatment in the cranially irradiated mice showed significant restoration of BDNF levels. Data are presented as mean ± SEM (N = 6–10 mice per group). P values were derived from two-way ANOVA and Bonferroni’s multiple comparisons test

Journal: Acta neuropathologica communications

Article Title: BDNF augmentation reverses cranial radiation therapy-induced cognitive decline and neurodegenerative consequences.

doi: 10.1186/s40478-024-01906-9

Figure Lengend Snippet: Fig. 2 Riluzole treatment restores hippocampal BDNF in the irradiated hippocampus. 10–12 weeks old WT male mice received cranial radiation therapy (RT) followed by riluzole (RZ) treatment (13 mg/kg) in drinking water for 6–7 weeks. An ELISA-based quantification of BDNF from the micro-dissected hippocampus showed RT-induced reductions in the RT + Vehicle group. Importantly, RZ treatment in the cranially irradiated mice showed significant restoration of BDNF levels. Data are presented as mean ± SEM (N = 6–10 mice per group). P values were derived from two-way ANOVA and Bonferroni’s multiple comparisons test

Article Snippet: BDNF levels were quantified using a commercially available ELISA kit (E-EL-M0203, Elabscience Biotechnology) and uncoated ELISA plates (Nunc MaxiSorp, Biolegend).

Techniques: Irradiation, Enzyme-linked Immunosorbent Assay, Derivative Assay

Figure4. BDNF-TrkBsignalinginducesCREBphosphorylationbutdoesnotinfluencetotalCREBproteinlevels.Primaryneurons were treated at 7 DIV with 50 ng/ml BDNF for the indicated time periods. A, CREB1 mRNA levels, measured using qRT-PCR, are represented as fold induction relative to CREB1 mRNA levels in untreated cells. B, Western blot analysis determining CREB and phospho-Ser-133CREB(P-CREB)proteinlevelsandCoomassiestainingforloadingcontrol.C,QuantificationoftotalCREBprotein levels. CREB protein levels were normalized using Coomassie staining, and normalized CREB protein level in nontreated cells was setas1.D,QuantificationofCREBphosphorylationlevels.P-CREBproteinlevelswerenormalizedtototalCREBproteinlevels,and therelativelevelofP-CREBproteininnontreatedcellswassetas1.A,C,D,Averageofthreeindependentexperiments(n 3)is shown. Error bars indicate SEM. Statistical significance relative to respective mRNA (A) or protein (C, D) levels in untreated cells: ***p 0.001; *p 0.05 (paired two-tailed t test, corrected for multiple comparisons using Holm–Sidak method).

Journal: The Journal of Neuroscience

Article Title: CREB Family Transcription Factors Are Major Mediators of BDNF Transcriptional Autoregulation in Cortical Neurons

doi: 10.1523/jneurosci.0367-19.2019

Figure Lengend Snippet: Figure4. BDNF-TrkBsignalinginducesCREBphosphorylationbutdoesnotinfluencetotalCREBproteinlevels.Primaryneurons were treated at 7 DIV with 50 ng/ml BDNF for the indicated time periods. A, CREB1 mRNA levels, measured using qRT-PCR, are represented as fold induction relative to CREB1 mRNA levels in untreated cells. B, Western blot analysis determining CREB and phospho-Ser-133CREB(P-CREB)proteinlevelsandCoomassiestainingforloadingcontrol.C,QuantificationoftotalCREBprotein levels. CREB protein levels were normalized using Coomassie staining, and normalized CREB protein level in nontreated cells was setas1.D,QuantificationofCREBphosphorylationlevels.P-CREBproteinlevelswerenormalizedtototalCREBproteinlevels,and therelativelevelofP-CREBproteininnontreatedcellswassetas1.A,C,D,Averageofthreeindependentexperiments(n 3)is shown. Error bars indicate SEM. Statistical significance relative to respective mRNA (A) or protein (C, D) levels in untreated cells: ***p 0.001; *p 0.05 (paired two-tailed t test, corrected for multiple comparisons using Holm–Sidak method).

Article Snippet: After baseline recording for 20 min, the infusion of 2 l of 1 g/ l BDNF (Alomone Labs) over 25 min at a rate of 0.08 l/min followed. cytochrome C (CytC; Sigma Millipore) was used as a control for BDNF infusion.

Techniques: Quantitative RT-PCR, Western Blot, Staining, Two Tailed Test

Figure 7. CRTC1 localizes to the nucleus after BDNF treatment. At 8 DIV, neurons were treated with 25 mM KCl, as a positive control, or 50 ng/ml BDNF. Immunocytochemistry was performed using anti-CRTC1 antibody (green). Hoechst 33324 was used to visualize nuclei (blue).

Journal: The Journal of Neuroscience

Article Title: CREB Family Transcription Factors Are Major Mediators of BDNF Transcriptional Autoregulation in Cortical Neurons

doi: 10.1523/jneurosci.0367-19.2019

Figure Lengend Snippet: Figure 7. CRTC1 localizes to the nucleus after BDNF treatment. At 8 DIV, neurons were treated with 25 mM KCl, as a positive control, or 50 ng/ml BDNF. Immunocytochemistry was performed using anti-CRTC1 antibody (green). Hoechst 33324 was used to visualize nuclei (blue).

Article Snippet: After baseline recording for 20 min, the infusion of 2 l of 1 g/ l BDNF (Alomone Labs) over 25 min at a rate of 0.08 l/min followed. cytochrome C (CytC; Sigma Millipore) was used as a control for BDNF infusion.

Techniques: Positive Control, Immunocytochemistry

Figure 14. CREB binds to BDNF promoter IV, is phosphorylated after BDNF-TrkB signaling, and recruits CBP. Primary neurons were treated at 7 DIV with 50 ng/ml BDNF for 1 h or left untreated (CTRL)andthensubjectedtoChIPassayusingCREB(A),phospho-Ser-133CREB(P-CREB)(B),orCBP(C)antibodies(ab).DNAenrichmentofc-Fospromoter,differentratBDNF(rBDNF)promoter(p) regions, and rat BDNF 3 untranslated region (rBDNF 3 UTR) was measured using qPCR. DNA enrichment is represented as percentage of input. Average of three or four (A, C, n 4; B, n 3) independentexperimentsisshown.ErrorbarsindicateSEM.NoantibodycontrolsdepictthesamedatasetinAandB.StatisticalsignificanceisrelativetotheenrichmentofrBDNF3UTRregionin respectively treated cells. Statistical analysis was not performed on no antibody controls. **p 0.01; *p 0.05 (paired two-tailed t test, corrected for multiple comparisons using Holm–Sidak method).

Journal: The Journal of Neuroscience

Article Title: CREB Family Transcription Factors Are Major Mediators of BDNF Transcriptional Autoregulation in Cortical Neurons

doi: 10.1523/jneurosci.0367-19.2019

Figure Lengend Snippet: Figure 14. CREB binds to BDNF promoter IV, is phosphorylated after BDNF-TrkB signaling, and recruits CBP. Primary neurons were treated at 7 DIV with 50 ng/ml BDNF for 1 h or left untreated (CTRL)andthensubjectedtoChIPassayusingCREB(A),phospho-Ser-133CREB(P-CREB)(B),orCBP(C)antibodies(ab).DNAenrichmentofc-Fospromoter,differentratBDNF(rBDNF)promoter(p) regions, and rat BDNF 3 untranslated region (rBDNF 3 UTR) was measured using qPCR. DNA enrichment is represented as percentage of input. Average of three or four (A, C, n 4; B, n 3) independentexperimentsisshown.ErrorbarsindicateSEM.NoantibodycontrolsdepictthesamedatasetinAandB.StatisticalsignificanceisrelativetotheenrichmentofrBDNF3UTRregionin respectively treated cells. Statistical analysis was not performed on no antibody controls. **p 0.01; *p 0.05 (paired two-tailed t test, corrected for multiple comparisons using Holm–Sidak method).

Article Snippet: After baseline recording for 20 min, the infusion of 2 l of 1 g/ l BDNF (Alomone Labs) over 25 min at a rate of 0.08 l/min followed. cytochrome C (CytC; Sigma Millipore) was used as a control for BDNF infusion.

Techniques: Two Tailed Test