Neuromics/BDNF/PR29001-100/100 ug
Type: Protein
Species Reactivity: H; M
B=Bovine; Ca=Cat; Ch=Chicken; D=Dog; EQ=Equine; GP=Guinea Pig; H=Human; M=Mouse; P=Porcine; Pr=Primate; R=Rat; Rb=Rabbit; Y=Yeast; Xe=Xenopus; Ze=Zebrafish; ; ; ; NA-Not Applicable; STP=Step-Tactin Proteins; All![\"Bioactive](\"https://www.ebiomall.com/images/neuromics/2017/A8xad63x66x1.gif\")
Brain Derived Growth Factor (BDNF) promotes the survival of neuronal populations that are all located either in the central nervous system or directly connected to it. Major regulator of synaptic transmission and plasticity at adult synapses in many regions of the cns. the versatility of BDNF is emphasized by its contribution to a range of adaptive neuronal responses including long-term potentiation (ltp), long-term depression (ltd), certain forms of short-term synaptic plasticity, as well as homeostatic regulation of intrinsic neuronal excitability.
A–H, Photomicrographs showing BDNF expression in the L5–L6 spinal cord segment of spinal-intact and SCI animals. Scale bar, 20 μm. A, The specificity of the antibody was tested by incubating spinal cord sections in the absence of the primary antibody. No staining was observed in these conditions. B–D, In the spinal cord, BDNF expression was found in the dorsal horns of the spinal cord, particularly in the superficial layers of the cord. It significantly increased in a time-dependent manner after SCI (C, D, H; *p < 0.05 vs spinal intact, ***p < 0.01 vs spinal intact). E, Intrathecal sequestration of BDNF with TrkB-Ig2 for 1 week caused a marked decrease in BDNF expression in the dorsal horn compared with nontreated 1 week SCI rats (H; #p < 0.05 vs nontreated SCI rats at the same time point). F, G, BDNF intrathecal administration significantly increased BDNF expression in the superficial layers of the spinal cord in both experimental groups (H; &p < 0.05 vs nontreated SCI rats at the same time point). H, Bar graph depicting the mean intensity of BDNF expression in the L5/L6 spinal cord segment from all experimental groups. BDNF levels were upregulated at 1 and 4 weeks after SCI when compared with spinal-intact animals. Whereas BDNF sequestration with TrkB-Ig2 caused a decrease in its expression, chronic treatment with recombinant BDNF resulted in an increase of immunoreactivity.The Journal of Neuroscience, 4 February 2015, 35(5): 2146-2160; doi: 10.1523/JNEUROSCI.0373-14.2015.
Note: hBDNF is fully biologically active when compared to a standard. The ED50 is calculated by the dose-dependent induction of ACHE (acetylcholine esterase) in rat basal forebrain septal culture and is within a range of 20 - 40 ng/ml.
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