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elisa kits  (R&D Systems)


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    R&D Systems elisa kits
    FIGURE 4 Elevation <t>of</t> <t>CNTF</t> production in hippocampal astrocytes via activation of the BDNF/TrkB/mTORC1 signalling pathway. (a) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of CON, AAV1‐GFP‐ injected, and AAV1‐Rheb(S16H)‐injected rats (black arrows). Scale bars, 500 μm (inset 20 μm). (b) Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of CON and AAV1‐Rheb (S16H)‐injected rats. Scale bars, 100 μm (inset 10 μm). (c, d) Western blot analysis of the levels of CNTF expression in the hippocampus of AAV1‐ GFP‐injected or AAV1‐Rheb(S16H)‐injected rats, with or without BDNF neutralizing antibody (B.NA) or TrkB neutralizing antibody (T.NA). Differences among groups were evaluated by Kruskal–Wallis test (c) or one‐way ANOVA (d) and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus Rheb(S16H) alone (n = 5 for each group). (e) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of recombinant BDNF‐injected rats (black arrows). Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of recombinant BDNF‐injected rats. Scale bar, 50 μm. (f) Western blot analysis of CNTF. Differences between groups were evaluated by Student's unpaired t test. *P < .05 versus CON (n = 5 for each group). (g–i) Measurement of CNTF concentration in the conditioned medium (CM) of recombinant BDNF‐treated astrocyte cultures using <t>ELISA</t> kits. (g) Schematic of the experimental design for measuring the levels of CNTF in hippocampal astrocyte cultures. (h) Histogram showing the dose‐dependent effects of recombinant BDNF on CNTF release in astrocyte cultures. Differences among groups were evaluated by Kruskal–Wallis test and Tukey's post hoc analysis. *P < .05 versus CON (n = 5 for each group). (i) Quantitative results showing the CNTF concentration after the treatment of astrocyte cultures with recombinant BDNF (80 ng·ml−1), with or without GNF‐5837 (10 μM) or rapamycin (80 nM). Differences among groups were evaluated by one‐way ANOVA and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus recombinant BDNF alone (n = 5 for each group)
    Elisa Kits, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rat+cntf+elisa+kit/Rat+CNTF+DuoSet+ELISA/pm31658360-109-15-25
    Average 94 stars, based on 8 article reviews
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    Images

    1) Product Images from "Neurotrophic interactions between neurons and astrocytes following AAV1-Rheb(S16H) transduction in the hippocampus in vivo."

    Article Title: Neurotrophic interactions between neurons and astrocytes following AAV1-Rheb(S16H) transduction in the hippocampus in vivo.

    Journal: British journal of pharmacology

    doi: 10.1111/bph.14882

    FIGURE 4 Elevation of CNTF production in hippocampal astrocytes via activation of the BDNF/TrkB/mTORC1 signalling pathway. (a) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of CON, AAV1‐GFP‐ injected, and AAV1‐Rheb(S16H)‐injected rats (black arrows). Scale bars, 500 μm (inset 20 μm). (b) Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of CON and AAV1‐Rheb (S16H)‐injected rats. Scale bars, 100 μm (inset 10 μm). (c, d) Western blot analysis of the levels of CNTF expression in the hippocampus of AAV1‐ GFP‐injected or AAV1‐Rheb(S16H)‐injected rats, with or without BDNF neutralizing antibody (B.NA) or TrkB neutralizing antibody (T.NA). Differences among groups were evaluated by Kruskal–Wallis test (c) or one‐way ANOVA (d) and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus Rheb(S16H) alone (n = 5 for each group). (e) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of recombinant BDNF‐injected rats (black arrows). Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of recombinant BDNF‐injected rats. Scale bar, 50 μm. (f) Western blot analysis of CNTF. Differences between groups were evaluated by Student's unpaired t test. *P < .05 versus CON (n = 5 for each group). (g–i) Measurement of CNTF concentration in the conditioned medium (CM) of recombinant BDNF‐treated astrocyte cultures using ELISA kits. (g) Schematic of the experimental design for measuring the levels of CNTF in hippocampal astrocyte cultures. (h) Histogram showing the dose‐dependent effects of recombinant BDNF on CNTF release in astrocyte cultures. Differences among groups were evaluated by Kruskal–Wallis test and Tukey's post hoc analysis. *P < .05 versus CON (n = 5 for each group). (i) Quantitative results showing the CNTF concentration after the treatment of astrocyte cultures with recombinant BDNF (80 ng·ml−1), with or without GNF‐5837 (10 μM) or rapamycin (80 nM). Differences among groups were evaluated by one‐way ANOVA and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus recombinant BDNF alone (n = 5 for each group)
    Figure Legend Snippet: FIGURE 4 Elevation of CNTF production in hippocampal astrocytes via activation of the BDNF/TrkB/mTORC1 signalling pathway. (a) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of CON, AAV1‐GFP‐ injected, and AAV1‐Rheb(S16H)‐injected rats (black arrows). Scale bars, 500 μm (inset 20 μm). (b) Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of CON and AAV1‐Rheb (S16H)‐injected rats. Scale bars, 100 μm (inset 10 μm). (c, d) Western blot analysis of the levels of CNTF expression in the hippocampus of AAV1‐ GFP‐injected or AAV1‐Rheb(S16H)‐injected rats, with or without BDNF neutralizing antibody (B.NA) or TrkB neutralizing antibody (T.NA). Differences among groups were evaluated by Kruskal–Wallis test (c) or one‐way ANOVA (d) and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus Rheb(S16H) alone (n = 5 for each group). (e) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of recombinant BDNF‐injected rats (black arrows). Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of recombinant BDNF‐injected rats. Scale bar, 50 μm. (f) Western blot analysis of CNTF. Differences between groups were evaluated by Student's unpaired t test. *P < .05 versus CON (n = 5 for each group). (g–i) Measurement of CNTF concentration in the conditioned medium (CM) of recombinant BDNF‐treated astrocyte cultures using ELISA kits. (g) Schematic of the experimental design for measuring the levels of CNTF in hippocampal astrocyte cultures. (h) Histogram showing the dose‐dependent effects of recombinant BDNF on CNTF release in astrocyte cultures. Differences among groups were evaluated by Kruskal–Wallis test and Tukey's post hoc analysis. *P < .05 versus CON (n = 5 for each group). (i) Quantitative results showing the CNTF concentration after the treatment of astrocyte cultures with recombinant BDNF (80 ng·ml−1), with or without GNF‐5837 (10 μM) or rapamycin (80 nM). Differences among groups were evaluated by one‐way ANOVA and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus recombinant BDNF alone (n = 5 for each group)

    Techniques Used: Activation Assay, Immunohistochemical staining, Staining, Expressing, Injection, Double Immunofluorescence Staining, Western Blot, Recombinant, Concentration Assay, Enzyme-linked Immunosorbent Assay

    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: Denervated hippocampus provides a favorable microenvironment for neuronal differentiation of endogenous neural stem cells
    Article Snippet: .. Supernatants were harvested and the amount of CNTF was determined using a rat CNTF ELISA kit (R&D, Minneapolis, MN, USA), according to the manufacturer's instruction. ..

    Article Title: Combined suppression of CASP2 and CASP6 protects retinal ganglion cells from apoptosis and promotes axon regeneration through CNTF-mediated JAK/STAT signalling
    Article Snippet: .. A commercially available rat CNTF ELISA kit (R&D Systems) was used to detect CNTF in cultured retinal cell lysates, following the manufacturer’s instructions. ..

    Cell Culture:

    Article Title: Combined suppression of CASP2 and CASP6 protects retinal ganglion cells from apoptosis and promotes axon regeneration through CNTF-mediated JAK/STAT signalling
    Article Snippet: .. A commercially available rat CNTF ELISA kit (R&D Systems) was used to detect CNTF in cultured retinal cell lysates, following the manufacturer’s instructions. ..



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    FIGURE 4 Elevation <t>of</t> <t>CNTF</t> production in hippocampal astrocytes via activation of the BDNF/TrkB/mTORC1 signalling pathway. (a) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of CON, AAV1‐GFP‐ injected, and AAV1‐Rheb(S16H)‐injected rats (black arrows). Scale bars, 500 μm (inset 20 μm). (b) Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of CON and AAV1‐Rheb (S16H)‐injected rats. Scale bars, 100 μm (inset 10 μm). (c, d) Western blot analysis of the levels of CNTF expression in the hippocampus of AAV1‐ GFP‐injected or AAV1‐Rheb(S16H)‐injected rats, with or without BDNF neutralizing antibody (B.NA) or TrkB neutralizing antibody (T.NA). Differences among groups were evaluated by Kruskal–Wallis test (c) or one‐way ANOVA (d) and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus Rheb(S16H) alone (n = 5 for each group). (e) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of recombinant BDNF‐injected rats (black arrows). Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of recombinant BDNF‐injected rats. Scale bar, 50 μm. (f) Western blot analysis of CNTF. Differences between groups were evaluated by Student's unpaired t test. *P < .05 versus CON (n = 5 for each group). (g–i) Measurement of CNTF concentration in the conditioned medium (CM) of recombinant BDNF‐treated astrocyte cultures using <t>ELISA</t> kits. (g) Schematic of the experimental design for measuring the levels of CNTF in hippocampal astrocyte cultures. (h) Histogram showing the dose‐dependent effects of recombinant BDNF on CNTF release in astrocyte cultures. Differences among groups were evaluated by Kruskal–Wallis test and Tukey's post hoc analysis. *P < .05 versus CON (n = 5 for each group). (i) Quantitative results showing the CNTF concentration after the treatment of astrocyte cultures with recombinant BDNF (80 ng·ml−1), with or without GNF‐5837 (10 μM) or rapamycin (80 nM). Differences among groups were evaluated by one‐way ANOVA and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus recombinant BDNF alone (n = 5 for each group)
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    FIGURE 4 Elevation <t>of</t> <t>CNTF</t> production in hippocampal astrocytes via activation of the BDNF/TrkB/mTORC1 signalling pathway. (a) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of CON, AAV1‐GFP‐ injected, and AAV1‐Rheb(S16H)‐injected rats (black arrows). Scale bars, 500 μm (inset 20 μm). (b) Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of CON and AAV1‐Rheb (S16H)‐injected rats. Scale bars, 100 μm (inset 10 μm). (c, d) Western blot analysis of the levels of CNTF expression in the hippocampus of AAV1‐ GFP‐injected or AAV1‐Rheb(S16H)‐injected rats, with or without BDNF neutralizing antibody (B.NA) or TrkB neutralizing antibody (T.NA). Differences among groups were evaluated by Kruskal–Wallis test (c) or one‐way ANOVA (d) and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus Rheb(S16H) alone (n = 5 for each group). (e) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of recombinant BDNF‐injected rats (black arrows). Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of recombinant BDNF‐injected rats. Scale bar, 50 μm. (f) Western blot analysis of CNTF. Differences between groups were evaluated by Student's unpaired t test. *P < .05 versus CON (n = 5 for each group). (g–i) Measurement of CNTF concentration in the conditioned medium (CM) of recombinant BDNF‐treated astrocyte cultures using <t>ELISA</t> kits. (g) Schematic of the experimental design for measuring the levels of CNTF in hippocampal astrocyte cultures. (h) Histogram showing the dose‐dependent effects of recombinant BDNF on CNTF release in astrocyte cultures. Differences among groups were evaluated by Kruskal–Wallis test and Tukey's post hoc analysis. *P < .05 versus CON (n = 5 for each group). (i) Quantitative results showing the CNTF concentration after the treatment of astrocyte cultures with recombinant BDNF (80 ng·ml−1), with or without GNF‐5837 (10 μM) or rapamycin (80 nM). Differences among groups were evaluated by one‐way ANOVA and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus recombinant BDNF alone (n = 5 for each group)
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    FIGURE 4 Elevation <t>of</t> <t>CNTF</t> production in hippocampal astrocytes via activation of the BDNF/TrkB/mTORC1 signalling pathway. (a) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of CON, AAV1‐GFP‐ injected, and AAV1‐Rheb(S16H)‐injected rats (black arrows). Scale bars, 500 μm (inset 20 μm). (b) Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of CON and AAV1‐Rheb (S16H)‐injected rats. Scale bars, 100 μm (inset 10 μm). (c, d) Western blot analysis of the levels of CNTF expression in the hippocampus of AAV1‐ GFP‐injected or AAV1‐Rheb(S16H)‐injected rats, with or without BDNF neutralizing antibody (B.NA) or TrkB neutralizing antibody (T.NA). Differences among groups were evaluated by Kruskal–Wallis test (c) or one‐way ANOVA (d) and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus Rheb(S16H) alone (n = 5 for each group). (e) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of recombinant BDNF‐injected rats (black arrows). Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of recombinant BDNF‐injected rats. Scale bar, 50 μm. (f) Western blot analysis of CNTF. Differences between groups were evaluated by Student's unpaired t test. *P < .05 versus CON (n = 5 for each group). (g–i) Measurement of CNTF concentration in the conditioned medium (CM) of recombinant BDNF‐treated astrocyte cultures using <t>ELISA</t> kits. (g) Schematic of the experimental design for measuring the levels of CNTF in hippocampal astrocyte cultures. (h) Histogram showing the dose‐dependent effects of recombinant BDNF on CNTF release in astrocyte cultures. Differences among groups were evaluated by Kruskal–Wallis test and Tukey's post hoc analysis. *P < .05 versus CON (n = 5 for each group). (i) Quantitative results showing the CNTF concentration after the treatment of astrocyte cultures with recombinant BDNF (80 ng·ml−1), with or without GNF‐5837 (10 μM) or rapamycin (80 nM). Differences among groups were evaluated by one‐way ANOVA and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus recombinant BDNF alone (n = 5 for each group)
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    FIGURE 4 Elevation <t>of</t> <t>CNTF</t> production in hippocampal astrocytes via activation of the BDNF/TrkB/mTORC1 signalling pathway. (a) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of CON, AAV1‐GFP‐ injected, and AAV1‐Rheb(S16H)‐injected rats (black arrows). Scale bars, 500 μm (inset 20 μm). (b) Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of CON and AAV1‐Rheb (S16H)‐injected rats. Scale bars, 100 μm (inset 10 μm). (c, d) Western blot analysis of the levels of CNTF expression in the hippocampus of AAV1‐ GFP‐injected or AAV1‐Rheb(S16H)‐injected rats, with or without BDNF neutralizing antibody (B.NA) or TrkB neutralizing antibody (T.NA). Differences among groups were evaluated by Kruskal–Wallis test (c) or one‐way ANOVA (d) and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus Rheb(S16H) alone (n = 5 for each group). (e) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of recombinant BDNF‐injected rats (black arrows). Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of recombinant BDNF‐injected rats. Scale bar, 50 μm. (f) Western blot analysis of CNTF. Differences between groups were evaluated by Student's unpaired t test. *P < .05 versus CON (n = 5 for each group). (g–i) Measurement of CNTF concentration in the conditioned medium (CM) of recombinant BDNF‐treated astrocyte cultures using <t>ELISA</t> kits. (g) Schematic of the experimental design for measuring the levels of CNTF in hippocampal astrocyte cultures. (h) Histogram showing the dose‐dependent effects of recombinant BDNF on CNTF release in astrocyte cultures. Differences among groups were evaluated by Kruskal–Wallis test and Tukey's post hoc analysis. *P < .05 versus CON (n = 5 for each group). (i) Quantitative results showing the CNTF concentration after the treatment of astrocyte cultures with recombinant BDNF (80 ng·ml−1), with or without GNF‐5837 (10 μM) or rapamycin (80 nM). Differences among groups were evaluated by one‐way ANOVA and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus recombinant BDNF alone (n = 5 for each group)
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    Image Search Results


    FIGURE 4 Elevation of CNTF production in hippocampal astrocytes via activation of the BDNF/TrkB/mTORC1 signalling pathway. (a) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of CON, AAV1‐GFP‐ injected, and AAV1‐Rheb(S16H)‐injected rats (black arrows). Scale bars, 500 μm (inset 20 μm). (b) Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of CON and AAV1‐Rheb (S16H)‐injected rats. Scale bars, 100 μm (inset 10 μm). (c, d) Western blot analysis of the levels of CNTF expression in the hippocampus of AAV1‐ GFP‐injected or AAV1‐Rheb(S16H)‐injected rats, with or without BDNF neutralizing antibody (B.NA) or TrkB neutralizing antibody (T.NA). Differences among groups were evaluated by Kruskal–Wallis test (c) or one‐way ANOVA (d) and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus Rheb(S16H) alone (n = 5 for each group). (e) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of recombinant BDNF‐injected rats (black arrows). Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of recombinant BDNF‐injected rats. Scale bar, 50 μm. (f) Western blot analysis of CNTF. Differences between groups were evaluated by Student's unpaired t test. *P < .05 versus CON (n = 5 for each group). (g–i) Measurement of CNTF concentration in the conditioned medium (CM) of recombinant BDNF‐treated astrocyte cultures using ELISA kits. (g) Schematic of the experimental design for measuring the levels of CNTF in hippocampal astrocyte cultures. (h) Histogram showing the dose‐dependent effects of recombinant BDNF on CNTF release in astrocyte cultures. Differences among groups were evaluated by Kruskal–Wallis test and Tukey's post hoc analysis. *P < .05 versus CON (n = 5 for each group). (i) Quantitative results showing the CNTF concentration after the treatment of astrocyte cultures with recombinant BDNF (80 ng·ml−1), with or without GNF‐5837 (10 μM) or rapamycin (80 nM). Differences among groups were evaluated by one‐way ANOVA and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus recombinant BDNF alone (n = 5 for each group)

    Journal: British journal of pharmacology

    Article Title: Neurotrophic interactions between neurons and astrocytes following AAV1-Rheb(S16H) transduction in the hippocampus in vivo.

    doi: 10.1111/bph.14882

    Figure Lengend Snippet: FIGURE 4 Elevation of CNTF production in hippocampal astrocytes via activation of the BDNF/TrkB/mTORC1 signalling pathway. (a) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of CON, AAV1‐GFP‐ injected, and AAV1‐Rheb(S16H)‐injected rats (black arrows). Scale bars, 500 μm (inset 20 μm). (b) Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of CON and AAV1‐Rheb (S16H)‐injected rats. Scale bars, 100 μm (inset 10 μm). (c, d) Western blot analysis of the levels of CNTF expression in the hippocampus of AAV1‐ GFP‐injected or AAV1‐Rheb(S16H)‐injected rats, with or without BDNF neutralizing antibody (B.NA) or TrkB neutralizing antibody (T.NA). Differences among groups were evaluated by Kruskal–Wallis test (c) or one‐way ANOVA (d) and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus Rheb(S16H) alone (n = 5 for each group). (e) Immunohistochemical staining showing increased CNTF expression in glia‐like cells of the hippocampal CA1 region of recombinant BDNF‐injected rats (black arrows). Double immunofluorescence staining against GFAP (green) and CNTF (red) showing the co‐localization of these two markers in the CA1 region of the hippocampus of recombinant BDNF‐injected rats. Scale bar, 50 μm. (f) Western blot analysis of CNTF. Differences between groups were evaluated by Student's unpaired t test. *P < .05 versus CON (n = 5 for each group). (g–i) Measurement of CNTF concentration in the conditioned medium (CM) of recombinant BDNF‐treated astrocyte cultures using ELISA kits. (g) Schematic of the experimental design for measuring the levels of CNTF in hippocampal astrocyte cultures. (h) Histogram showing the dose‐dependent effects of recombinant BDNF on CNTF release in astrocyte cultures. Differences among groups were evaluated by Kruskal–Wallis test and Tukey's post hoc analysis. *P < .05 versus CON (n = 5 for each group). (i) Quantitative results showing the CNTF concentration after the treatment of astrocyte cultures with recombinant BDNF (80 ng·ml−1), with or without GNF‐5837 (10 μM) or rapamycin (80 nM). Differences among groups were evaluated by one‐way ANOVA and Tukey's post hoc analysis. *P < .05 versus CON and #P < .05 versus recombinant BDNF alone (n = 5 for each group)

    Article Snippet: To quantify the CNTF released in the BDNF‐treated astrocyte culture medium, we used commercially available ELISA kits according to the manufacturer's protocol (Cat No. DY557; R&D Systems).

    Techniques: Activation Assay, Immunohistochemical staining, Staining, Expressing, Injection, Double Immunofluorescence Staining, Western Blot, Recombinant, Concentration Assay, Enzyme-linked Immunosorbent Assay