Journal: Neurochemistry international

Article Title: Water treadmill training protects the integrity of the blood-spinal cord barrier following SCI via the BDNF/TrkB-CREB signalling pathway.

doi: 10.1016/j.neuint.2020.104945

Figure Lengend Snippet: Fig. 1. TT upregulated the BDNF/TrkB-CREB signalling pathway and prevented the loss of TJ and AJ proteins following SCI. (A–H) Representative western blots and quantification data for BDNF/β-Actin, PI3K/β-Actin, p-TrkB/TrkB, p-AKT/AKT and p-CREB/CREB in each group, columns represent the mean ± SD, n = 5. (I) Double staining for Claudin-5, Occludin, p120-Catenin, and β-Catenin/CD31/Hoechst. Red: Claudin-5/Occludin/p120-Catenin/β-Catenin; green: CD31; blue: Hoechst. Scale bar, 20 μm #p < 0.05 for the M group versus the S group, *p < 0.05 for the TM group versus the M group. (#p, *p < 0.05; ##p, **p < 0.01; ###p, ***p < 0.001).

Article Snippet: Anti-BDNF, anti-TrkB and anti-p-TrkB antibodies were purchased from Proteintech (Rosemont, IL, USA). β-Actin was purchased from Abcam (330 Cambridge Science Park, Cambridge, UK).

Techniques: Western Blot, Double Staining

Journal: Neurochemistry international

Article Title: Water treadmill training protects the integrity of the blood-spinal cord barrier following SCI via the BDNF/TrkB-CREB signalling pathway.

doi: 10.1016/j.neuint.2020.104945

Figure Lengend Snippet: Fig. 2. The inhibitor downregulated the BDNF/TrkB-CREB signalling pathway and increased the permeability of the spinal cord, accompanied by poor motor function recovery. (A–H) Representative western blots and quantification data of BDNF/β-Actin, PI3K/β-Actin, p-TrkB/TrkB, p-AKT/AKT and p-CREB/CREB in the M and IM groups. Columns represent the mean ± SD, n = 5. (I) BBB scores in M, IM groups. (J, L) Representative quantification data of spinal cord water content in the M and IM groups; columns represent the mean ± SD, n = 5. (K) Representative Evans blue dye permeabilized into the spinal cord after SCI and (M) quantification of the amount of Evans blue (μg/g), n = 5. $p < 0.05 for the IM group versus the M group ($p < 0.05; $$p < 0.01; $$$p < 0.001).

Article Snippet: Anti-BDNF, anti-TrkB and anti-p-TrkB antibodies were purchased from Proteintech (Rosemont, IL, USA). β-Actin was purchased from Abcam (330 Cambridge Science Park, Cambridge, UK).

Techniques: Permeability, Western Blot

Journal: Neurochemistry international

Article Title: Water treadmill training protects the integrity of the blood-spinal cord barrier following SCI via the BDNF/TrkB-CREB signalling pathway.

doi: 10.1016/j.neuint.2020.104945

Figure Lengend Snippet: Fig. 5. TT decreased endothelial permeability and improved functional recovery by upregulating the BDNF/TrkB-CREB signalling pathway. (A, C) Representative quantification data of spinal cord water content in the TM and ITM groups. Columns represent the mean ± SD, n = 5. &p < 0.05 for the ITM group versus the TM group (B, D) Representative Evans blue dye permeabilized into the spinal cord after SCI and quantification of the amount of Evans blue (μg/g), n = 5. (E) BBB scores in TM and ITM groups. (F) TEM shows the vascular EC-EC junctions in the TM and ITM. Arrows indicate an open tight junction and the scale bars are 0.5 μm. (G) Quantification of the TJ gap width between the TM and ITM; columns represent the mean ± SD. (H) Quantification of the TJ length between the TM and ITM; columns represent the mean ± SD. (&p < 0.05; &&p < 0.01; &&&p < 0.001).

Article Snippet: Anti-BDNF, anti-TrkB and anti-p-TrkB antibodies were purchased from Proteintech (Rosemont, IL, USA). β-Actin was purchased from Abcam (330 Cambridge Science Park, Cambridge, UK).

Techniques: Permeability, Functional Assay

Journal: Neurochemistry international

Article Title: Water treadmill training protects the integrity of the blood-spinal cord barrier following SCI via the BDNF/TrkB-CREB signalling pathway.

doi: 10.1016/j.neuint.2020.104945

Figure Lengend Snippet: Fig. 6. TT inhibited BSCB disruption by upregulating the BDNF/TrkB-CREB signalling pathway. (A, B) Representative western blots and quantification data of TJ and AJ proteins in the TM and ITM groups. Columns represent the mean ± SD, n = 5. (C) Claudin- 5, Occludin, p120-Catenin, and β-Catenin/CD31/ Hoechst staining of sections from the spinal cord in the TM and ITM groups. Red: Claudin-5/Occludin/ p120-Catenin/β-Catenin; green: CD31; blue: Hoechst. Scale bar, 20 μm. (&p < 0.05; &&p < 0.01; &&&p < 0.001).

Article Snippet: Anti-BDNF, anti-TrkB and anti-p-TrkB antibodies were purchased from Proteintech (Rosemont, IL, USA). β-Actin was purchased from Abcam (330 Cambridge Science Park, Cambridge, UK).

Techniques: Disruption, Western Blot, Staining

Journal: Frontiers in Neurology

Article Title: A Thalamic-Fronto-Parietal Structural Covariance Network Emerging in the Course of Recovery from Hand Paresis after Ischemic Stroke

doi: 10.3389/fneur.2015.00211

Figure Lengend Snippet: Spatial topography of longitudinal structural covariance network correlating with hand function recovery . (A) shows the six largest clusters of supra-threshold voxels for the second principal component (PC2 TBM ) projected onto a standard three dimensional brain and onto a cytoarchitectonic atlas (cluster 3+) in MNI space. Clusters are labeled according to their (positive or negative) correlation with gray matter volume expansion in the medio-dorsal thalamus. The threshold for positive clusters corresponds to the first percentile of voxel values (absolute value 0.0064), the threshold for the negative cluster to the ninety-ninth percentile (absolute value 0.0095). (B) shows the spatial relationship between the covariance network clusters and lesion maps of patient subgroups. Color-coded contours define areas with ≥20% lesion probability in each subgroup. Size, localization, cytoarchitectonic assignment, and functional correlates of the individual clusters are summarized in Table .

Article Snippet: These clusters were localized using the Jülich cytoarchitectonic probabilistic atlas (SPM Anatomy toolbox, Version 1.8, made available through the Human Brain Mapping division at the Forschungszentrum Jülich at http://www.fz-juelich.de/inm/inm-1/DE/Forschung/_docs/SPMAnatomyToolbox/SPMAnatomyToolbox_node.html ).

Techniques: Labeling, Functional Assay

Journal: Frontiers in Neurology

Article Title: A Thalamic-Fronto-Parietal Structural Covariance Network Emerging in the Course of Recovery from Hand Paresis after Ischemic Stroke

doi: 10.3389/fneur.2015.00211

Figure Lengend Snippet: Clusters of the longitudinal structural covariance network (PC2 TBM ) related to hand function recovery: size, localization, cytoarchitectonic assignment, and functional correlates .

Article Snippet: These clusters were localized using the Jülich cytoarchitectonic probabilistic atlas (SPM Anatomy toolbox, Version 1.8, made available through the Human Brain Mapping division at the Forschungszentrum Jülich at http://www.fz-juelich.de/inm/inm-1/DE/Forschung/_docs/SPMAnatomyToolbox/SPMAnatomyToolbox_node.html ).

Techniques: Functional Assay, Transformation Assay

Journal: Endocrinology

Article Title: Loss of Action via Neurotensin-Leptin Receptor Neurons Disrupts Leptin and Ghrelin-Mediated Control of Energy Balance

doi: 10.1210/en.2017-00122

Figure Lengend Snippet: Antibodies Used

Article Snippet: Briefly, brain sections were exposed to primary antibodies for either cFos [Santa Cruz, goat, 1:500; research resource identifier (RRID): AB_2629503] or pSTAT3 (Cell Signaling, rabbit, 1:500; RRID: AB_331269), followed by species-specific biotinylated antibodies (Jackson ImmunoResearch, 1:100; RRIDs: AB_2340397 and AB_2340593), avidin-biotinylation reaction (Vectastain; Vector Laboratories), and diaminobenzidine detection (Sigma).

Techniques:

Journal: Endocrinology

Article Title: Loss of Action via Neurotensin-Leptin Receptor Neurons Disrupts Leptin and Ghrelin-Mediated Control of Energy Balance

doi: 10.1210/en.2017-00122

Figure Lengend Snippet: Nts and OX neurons respond to distinct hormonal cues. (A) Male NtsEGFP mice were treated with vehicle or leptin (5 mg/kg, IP, 2 hours) and brains were immunostained for Nts-EGFP (green), OX (red), and pSTAT3, a marker of leptin-activated LepRb neurons (blue). (A, top) Filled arrows identify pSTAT3-labeled nuclei within Nts-EGFP neurons, which are leptin-activated NtsLepRb neurons. (A, bottom) Unfilled arrows identify the same pSTAT3-labeled nuclei, none of which are found within OX neurons. (C) Quantification of the percentage of Nts and OX neurons that contain pSTAT3 (e.g., are activated by leptin) in response to vehicle or leptin treatment (vehicle n = 4, leptin n = 5). (C) Male NtsEGFP mice were treated with ghrelin (100 μg/treatment, IP, 4 hours) and brains were immunostained for Nts-EGFP (green), OX (red), and cFos, a marker of neuronal depolarization (blue). (D, top) Unfilled arrows identify cFos-labeled nuclei that are not found within Nts neurons. (C, bottom) Filled arrows identify the same cFos-labeled nuclei from the top panels, which are found within OX neurons. (D) Quantification of the percentage of Nts and OX neurons that contain cFos (e.g., are activated by ghrelin) in response to vehicle or ghrelin treatment (vehicle n = 4, leptin n = 4). Graphed data represent average values ± SEM. Statistical differences were determined via one-way ANOVA. **P ≤ 0.01, ***P ≤ 0.001, ****P ≤ 0.0001.

Article Snippet: Briefly, brain sections were exposed to primary antibodies for either cFos [Santa Cruz, goat, 1:500; research resource identifier (RRID): AB_2629503] or pSTAT3 (Cell Signaling, rabbit, 1:500; RRID: AB_331269), followed by species-specific biotinylated antibodies (Jackson ImmunoResearch, 1:100; RRIDs: AB_2340397 and AB_2340593), avidin-biotinylation reaction (Vectastain; Vector Laboratories), and diaminobenzidine detection (Sigma).

Techniques: Marker, Labeling

Journal: Endocrinology

Article Title: Loss of Action via Neurotensin-Leptin Receptor Neurons Disrupts Leptin and Ghrelin-Mediated Control of Energy Balance

doi: 10.1210/en.2017-00122

Figure Lengend Snippet: Loss of leptin action via NtsLepRb neurons blunts the ghrelin-mediated activation of OX neurons. (A) Generation of LRKO mice, which lack functional LepRb only in Nts neurons. (B) Backcrossed control (Nts++;Leprflfl) and LRKO (NtsCre+;Leprflfl) mice were treated with vehicle or leptin (5 mg/kg, IP, 2 hours) and brains were immunostained for pSTAT3 to identify leptin-activated LepRb neurons. LRKO mice have fewer pSTAT3-positive neurons in the LHA compared with controls, confirming loss of functional LepRb from LHA NtsLepRb neurons. (C) Male control and LRKO mice were treated with saline or ghrelin (3 µg, ICV, 4 hours) and brains were analyzed via immunohistochemistry and immunofluorescence for OX (red) and cFos (green). Arrows identify OX neurons that contain cFos-labeled nuclei (e.g., OX:cFos cells), which are activated OX neurons. (D) Quantitation of the percentage of OX neurons that contain cFos (OX:cFos) in treated control and LRKO mice. (Control + saline, n = 6; control + ghrelin, n = 6; LRKO + vehicle, n = 3; LRKO + ghrelin, n = 3.) (E) Quantitation of the total number of LHA OX neurons from three representative LHA sections of control mice (n = 12) and LRKO mice (n = 6). Graphed data represent average values ± SEM. *P ≤ 0.05 by ANOVA.

Article Snippet: Briefly, brain sections were exposed to primary antibodies for either cFos [Santa Cruz, goat, 1:500; research resource identifier (RRID): AB_2629503] or pSTAT3 (Cell Signaling, rabbit, 1:500; RRID: AB_331269), followed by species-specific biotinylated antibodies (Jackson ImmunoResearch, 1:100; RRIDs: AB_2340397 and AB_2340593), avidin-biotinylation reaction (Vectastain; Vector Laboratories), and diaminobenzidine detection (Sigma).

Techniques: Activation Assay, Functional Assay, Immunohistochemistry, Immunofluorescence, Labeling, Quantitation Assay