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polyclonal igg anti trkb  (R&D Systems)


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    Structured Review

    R&D Systems polyclonal igg anti trkb
    Polyclonal Igg Anti Trkb, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 153 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/polyclonal+igg+anti+trkb/pmc12867223-161-52-56?v=R%26D+Systems
    Average 94 stars, based on 153 article reviews
    polyclonal igg anti trkb - by Bioz Stars, 2026-07
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    GR agonist Dex regulated brain-derived neurotrophic factor (BDNF), <t>TrkB</t> and N-methyl-D-aspartate (NMDA) receptor NR2B subunit expression in the spinal dorsal horn of rats with depression and neuropathic pain. Intrathecal administration of Dex (4 μg per rat, daily for 1 week) exacerbated the enhancement of spinal BDNF (A) , TrkB (B) and NR2B (C) expressions in the Dex-NOB-SNL group compared to the Veh-NOB-SNL group and induced significant up-regulation of these proteins in the Dex-OB-SNL group compared to those in the Veh-OB-SNL group. The protein expression levels of NOB-Sham rats and OB-Sham rats were not affected by Dex. * p < 0.05, *** p < 0.001 vs. corresponding NOB-Sham groups; # p < 0.05, ### p < 0.001 vs. corresponding OB-Sham groups; $ p < 0.05, $$ p < 0.01, $$$ p < 0.001 vs. corresponding NOB-SNL groups; && p < 0.01, &&& p < 0.001 vs. corresponding vehicle groups; n = 5–6 per group.
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    GR agonist Dex regulated brain-derived neurotrophic factor (BDNF), <t>TrkB</t> and N-methyl-D-aspartate (NMDA) receptor NR2B subunit expression in the spinal dorsal horn of rats with depression and neuropathic pain. Intrathecal administration of Dex (4 μg per rat, daily for 1 week) exacerbated the enhancement of spinal BDNF (A) , TrkB (B) and NR2B (C) expressions in the Dex-NOB-SNL group compared to the Veh-NOB-SNL group and induced significant up-regulation of these proteins in the Dex-OB-SNL group compared to those in the Veh-OB-SNL group. The protein expression levels of NOB-Sham rats and OB-Sham rats were not affected by Dex. * p < 0.05, *** p < 0.001 vs. corresponding NOB-Sham groups; # p < 0.05, ### p < 0.001 vs. corresponding OB-Sham groups; $ p < 0.05, $$ p < 0.01, $$$ p < 0.001 vs. corresponding NOB-SNL groups; && p < 0.01, &&& p < 0.001 vs. corresponding vehicle groups; n = 5–6 per group.
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    GR agonist Dex regulated brain-derived neurotrophic factor (BDNF), <t>TrkB</t> and N-methyl-D-aspartate (NMDA) receptor NR2B subunit expression in the spinal dorsal horn of rats with depression and neuropathic pain. Intrathecal administration of Dex (4 μg per rat, daily for 1 week) exacerbated the enhancement of spinal BDNF (A) , TrkB (B) and NR2B (C) expressions in the Dex-NOB-SNL group compared to the Veh-NOB-SNL group and induced significant up-regulation of these proteins in the Dex-OB-SNL group compared to those in the Veh-OB-SNL group. The protein expression levels of NOB-Sham rats and OB-Sham rats were not affected by Dex. * p < 0.05, *** p < 0.001 vs. corresponding NOB-Sham groups; # p < 0.05, ### p < 0.001 vs. corresponding OB-Sham groups; $ p < 0.05, $$ p < 0.01, $$$ p < 0.001 vs. corresponding NOB-SNL groups; && p < 0.01, &&& p < 0.001 vs. corresponding vehicle groups; n = 5–6 per group.
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    GR agonist Dex regulated brain-derived neurotrophic factor (BDNF), <t>TrkB</t> and N-methyl-D-aspartate (NMDA) receptor NR2B subunit expression in the spinal dorsal horn of rats with depression and neuropathic pain. Intrathecal administration of Dex (4 μg per rat, daily for 1 week) exacerbated the enhancement of spinal BDNF (A) , TrkB (B) and NR2B (C) expressions in the Dex-NOB-SNL group compared to the Veh-NOB-SNL group and induced significant up-regulation of these proteins in the Dex-OB-SNL group compared to those in the Veh-OB-SNL group. The protein expression levels of NOB-Sham rats and OB-Sham rats were not affected by Dex. * p < 0.05, *** p < 0.001 vs. corresponding NOB-Sham groups; # p < 0.05, ### p < 0.001 vs. corresponding OB-Sham groups; $ p < 0.05, $$ p < 0.01, $$$ p < 0.001 vs. corresponding NOB-SNL groups; && p < 0.01, &&& p < 0.001 vs. corresponding vehicle groups; n = 5–6 per group.
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    GR agonist Dex regulated brain-derived neurotrophic factor (BDNF), <t>TrkB</t> and N-methyl-D-aspartate (NMDA) receptor NR2B subunit expression in the spinal dorsal horn of rats with depression and neuropathic pain. Intrathecal administration of Dex (4 μg per rat, daily for 1 week) exacerbated the enhancement of spinal BDNF (A) , TrkB (B) and NR2B (C) expressions in the Dex-NOB-SNL group compared to the Veh-NOB-SNL group and induced significant up-regulation of these proteins in the Dex-OB-SNL group compared to those in the Veh-OB-SNL group. The protein expression levels of NOB-Sham rats and OB-Sham rats were not affected by Dex. * p < 0.05, *** p < 0.001 vs. corresponding NOB-Sham groups; # p < 0.05, ### p < 0.001 vs. corresponding OB-Sham groups; $ p < 0.05, $$ p < 0.01, $$$ p < 0.001 vs. corresponding NOB-SNL groups; && p < 0.01, &&& p < 0.001 vs. corresponding vehicle groups; n = 5–6 per group.
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    GR agonist Dex regulated brain-derived neurotrophic factor (BDNF), TrkB and N-methyl-D-aspartate (NMDA) receptor NR2B subunit expression in the spinal dorsal horn of rats with depression and neuropathic pain. Intrathecal administration of Dex (4 μg per rat, daily for 1 week) exacerbated the enhancement of spinal BDNF (A) , TrkB (B) and NR2B (C) expressions in the Dex-NOB-SNL group compared to the Veh-NOB-SNL group and induced significant up-regulation of these proteins in the Dex-OB-SNL group compared to those in the Veh-OB-SNL group. The protein expression levels of NOB-Sham rats and OB-Sham rats were not affected by Dex. * p < 0.05, *** p < 0.001 vs. corresponding NOB-Sham groups; # p < 0.05, ### p < 0.001 vs. corresponding OB-Sham groups; $ p < 0.05, $$ p < 0.01, $$$ p < 0.001 vs. corresponding NOB-SNL groups; && p < 0.01, &&& p < 0.001 vs. corresponding vehicle groups; n = 5–6 per group.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Impaired Spinal Glucocorticoid Receptor Signaling Contributes to the Attenuating Effect of Depression on Mechanical Allodynia and Thermal Hyperalgesia in Rats with Neuropathic Pain

    doi: 10.3389/fncel.2017.00145

    Figure Lengend Snippet: GR agonist Dex regulated brain-derived neurotrophic factor (BDNF), TrkB and N-methyl-D-aspartate (NMDA) receptor NR2B subunit expression in the spinal dorsal horn of rats with depression and neuropathic pain. Intrathecal administration of Dex (4 μg per rat, daily for 1 week) exacerbated the enhancement of spinal BDNF (A) , TrkB (B) and NR2B (C) expressions in the Dex-NOB-SNL group compared to the Veh-NOB-SNL group and induced significant up-regulation of these proteins in the Dex-OB-SNL group compared to those in the Veh-OB-SNL group. The protein expression levels of NOB-Sham rats and OB-Sham rats were not affected by Dex. * p < 0.05, *** p < 0.001 vs. corresponding NOB-Sham groups; # p < 0.05, ### p < 0.001 vs. corresponding OB-Sham groups; $ p < 0.05, $$ p < 0.01, $$$ p < 0.001 vs. corresponding NOB-SNL groups; && p < 0.01, &&& p < 0.001 vs. corresponding vehicle groups; n = 5–6 per group.

    Article Snippet: The membrane was blocked with 5% w/v nonfat dry milk or bovine serum albumin (BSA) in TBST (20 mM Tris-base, pH 7.6, 137 mM NaCl and 0.1% Tween 20) for 1 h at room temperature and then incubated with the primary antibodies polyclonal GR, polyclonal BDNF, polyclonal TrkB (1:200, Santa Cruz Biotechnology, sc-1004, sc-20981, sc-8316, Santa Cruz, CA, USA), polyclonal NR2B (1:1000, Cell Signaling Technology, # 4207, Beverly, MA, USA), monoclonal GAPDH, polyclonal histone H3 (1:200; Santa Cruz Biotechnology, sc-137179, sc-10809, Santa Cruz, CA, USA) overnight at 4°C with gentle shaking.

    Techniques: Derivative Assay, Expressing