probdnf protein  (Alomone Labs)


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    Structured Review

    Alomone Labs probdnf protein
    Schematic diagram showing how <t>proBDNF</t> dampens CD4 + T cell activity and contributes to the pathogenesis of SAE. In sepsis, proBDNF expression is increased in peripheral blood and meningeal immune cells, which then decreases the infiltration of CD4 + T cells in the meninges. As a result, meningeal pro-inflammatory cytokines such as IL-6 and IL-1β are upregulated, but anti-inflammatory cytokines including IL-4 and IL-13 are downregulated, finally leading to SAE. SAE, sepsis-associated encephalopathy
    Probdnf Protein, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/probdnf protein/product/Alomone Labs
    Average 94 stars, based on 14 article reviews
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    probdnf protein - by Bioz Stars, 2022-08
    94/100 stars

    Images

    1) Product Images from "ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells"

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    Journal: Journal of Neuroinflammation

    doi: 10.1186/s12974-020-01850-0

    Schematic diagram showing how proBDNF dampens CD4 + T cell activity and contributes to the pathogenesis of SAE. In sepsis, proBDNF expression is increased in peripheral blood and meningeal immune cells, which then decreases the infiltration of CD4 + T cells in the meninges. As a result, meningeal pro-inflammatory cytokines such as IL-6 and IL-1β are upregulated, but anti-inflammatory cytokines including IL-4 and IL-13 are downregulated, finally leading to SAE. SAE, sepsis-associated encephalopathy
    Figure Legend Snippet: Schematic diagram showing how proBDNF dampens CD4 + T cell activity and contributes to the pathogenesis of SAE. In sepsis, proBDNF expression is increased in peripheral blood and meningeal immune cells, which then decreases the infiltration of CD4 + T cells in the meninges. As a result, meningeal pro-inflammatory cytokines such as IL-6 and IL-1β are upregulated, but anti-inflammatory cytokines including IL-4 and IL-13 are downregulated, finally leading to SAE. SAE, sepsis-associated encephalopathy

    Techniques Used: Activity Assay, Expressing

    Exogenous proBDNF protein reduced CD4 + T cells but increased CD8 + T cells of septic mice in vitro. Mice injected with saline or LPS (5 mg kg −1 ) for 5 days and the splenocytes were isolated and cultured for 3 days in vitro. Exogenous proBDNF did not alter the percentage of a CD3 + T cells in CD45 + cells or the percentage of b CD4 + T cells or c CD8 + T cells in CD3 + T cells in splenocytes from mice treated with saline. d Exogenous proBDNF did not alter the percentage of CD3 + T cells in CD45 + cells in splenocytes in septic mice. e–f ProBDNF treatment significantly decreased the percentage of e CD4 + T cells but increased the percentage of f CD8 + T cells in CD3 + T cells in splenocytes in LPS-treated mice. n = 4 in each group. Data were analyzed by one-way ANOVA and followed by Tukey post hoc test, * P
    Figure Legend Snippet: Exogenous proBDNF protein reduced CD4 + T cells but increased CD8 + T cells of septic mice in vitro. Mice injected with saline or LPS (5 mg kg −1 ) for 5 days and the splenocytes were isolated and cultured for 3 days in vitro. Exogenous proBDNF did not alter the percentage of a CD3 + T cells in CD45 + cells or the percentage of b CD4 + T cells or c CD8 + T cells in CD3 + T cells in splenocytes from mice treated with saline. d Exogenous proBDNF did not alter the percentage of CD3 + T cells in CD45 + cells in splenocytes in septic mice. e–f ProBDNF treatment significantly decreased the percentage of e CD4 + T cells but increased the percentage of f CD8 + T cells in CD3 + T cells in splenocytes in LPS-treated mice. n = 4 in each group. Data were analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Techniques Used: Mouse Assay, In Vitro, Injection, Isolation, Cell Culture

    Increased proBDNF expression in meningeal and peripheral blood immune cells in septic mice. Mice were i.p. injected with LPS (5 mg kg −1 ) and meninges and peripheral blood were harvested for immunofluorescence staining or flow cytometry. a Representative whole mount meningeal immunofluorescence images showed markedly increased proBDNF-positive staining cells in the meninges in mice at 1 day after LPS injection compared to saline injected mice. The high magnification images around the arrows are displayed in a white square as insets. Bar = 100 μm. b – f Representative meningeal single cell flow cytometry images ( upper panel ) and its statistical analysis ( lower panel ) indicated that proBDNF MFI was increased in meningeal b CD3 + T cells, c CD4 + T cells, d CD8 + T cells, and f CD11b + monocytes/macrophages at 1 day after LPS injection. proBDNF in meningeal e CD19 + B cells upregulated until 5 days after LPS injection. n = 10 in the Con group, n = 6 in LPS groups. g – k Upregulation of proBDNF in g CD3 + T cells, h CD4 + T cells, i CD8 + T cells, j CD19 + B cells, and k CD11b + monocytes/macrophages in peripheral blood in LPS-injected mice were detected. n = 9 in Con group, n = 8 in the LPS1d group, n = 4 in the LPS 5d group. Data b – k were analyzed by one-way ANOVA and followed by Tukey post hoc test, * P
    Figure Legend Snippet: Increased proBDNF expression in meningeal and peripheral blood immune cells in septic mice. Mice were i.p. injected with LPS (5 mg kg −1 ) and meninges and peripheral blood were harvested for immunofluorescence staining or flow cytometry. a Representative whole mount meningeal immunofluorescence images showed markedly increased proBDNF-positive staining cells in the meninges in mice at 1 day after LPS injection compared to saline injected mice. The high magnification images around the arrows are displayed in a white square as insets. Bar = 100 μm. b – f Representative meningeal single cell flow cytometry images ( upper panel ) and its statistical analysis ( lower panel ) indicated that proBDNF MFI was increased in meningeal b CD3 + T cells, c CD4 + T cells, d CD8 + T cells, and f CD11b + monocytes/macrophages at 1 day after LPS injection. proBDNF in meningeal e CD19 + B cells upregulated until 5 days after LPS injection. n = 10 in the Con group, n = 6 in LPS groups. g – k Upregulation of proBDNF in g CD3 + T cells, h CD4 + T cells, i CD8 + T cells, j CD19 + B cells, and k CD11b + monocytes/macrophages in peripheral blood in LPS-injected mice were detected. n = 9 in Con group, n = 8 in the LPS1d group, n = 4 in the LPS 5d group. Data b – k were analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Techniques Used: Expressing, Mouse Assay, Injection, Immunofluorescence, Staining, Flow Cytometry

    Effect of i.c.v. injection of anti-proBDNF antibody on fear memory and meningeal immune activity in the septic mice. Mice were bilateral i.c.v. injected with 1 μg McAb-proB 3 days before LPS injection. Behavior tests were performed 1 day after LPS injection. a Representative images showed the broad and thorough diffusion of drugs in cerebroventricular lumen following i.c.v. injection with methylene blue. b McAb-proB i.c.v. injection did not influence weight of mice. c–e There was no difference of c fear conditioning acquiring performance in each group, nor McAb-proB increased the freezing time of d contextual or e cued fear conditioning test as compared to IgG control after LPS injection. n = 6 in each group. Data b , c , and e were analyzed by repeated measures ANOVA and followed by Bonferroni post hoc test and data d was analyzed by one-way ANOVA and followed by Tukey post hoc test, * P
    Figure Legend Snippet: Effect of i.c.v. injection of anti-proBDNF antibody on fear memory and meningeal immune activity in the septic mice. Mice were bilateral i.c.v. injected with 1 μg McAb-proB 3 days before LPS injection. Behavior tests were performed 1 day after LPS injection. a Representative images showed the broad and thorough diffusion of drugs in cerebroventricular lumen following i.c.v. injection with methylene blue. b McAb-proB i.c.v. injection did not influence weight of mice. c–e There was no difference of c fear conditioning acquiring performance in each group, nor McAb-proB increased the freezing time of d contextual or e cued fear conditioning test as compared to IgG control after LPS injection. n = 6 in each group. Data b , c , and e were analyzed by repeated measures ANOVA and followed by Bonferroni post hoc test and data d was analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Techniques Used: Injection, Activity Assay, Mouse Assay, Diffusion-based Assay

    Systemic blockade of proBDNF ameliorated cognitive dysfunction and restored meningeal and peripheral CD4 + T cell ratio in septic mice. Mice were i.p. injected with proBDNF 30 min before LPS (5 mg kg −1 ) injection. Fear conditioning testing was performed 1 day after LPS injection. Meninges and peripheral blood were harvested 5 days after LPS injection for flow cytometry. a McAb-proB did not influence the weight of mice or b fear conditioning acquiring. c , d McAb-proB greatly alleviated memory deficit induced by LPS injection in mice as indicated by the increased freezing time in ( c ) contextual and ( d ) cued fear conditioning tests in the McAb-proB group relative to the IgG control. n = 8 in each group. Data a , b , and d were analyzed by repeated measures ANOVA and followed by Bonferroni post hoc tests. Data c was analyzed by one-way ANOVA and followed by Tukey post hoc test, * P
    Figure Legend Snippet: Systemic blockade of proBDNF ameliorated cognitive dysfunction and restored meningeal and peripheral CD4 + T cell ratio in septic mice. Mice were i.p. injected with proBDNF 30 min before LPS (5 mg kg −1 ) injection. Fear conditioning testing was performed 1 day after LPS injection. Meninges and peripheral blood were harvested 5 days after LPS injection for flow cytometry. a McAb-proB did not influence the weight of mice or b fear conditioning acquiring. c , d McAb-proB greatly alleviated memory deficit induced by LPS injection in mice as indicated by the increased freezing time in ( c ) contextual and ( d ) cued fear conditioning tests in the McAb-proB group relative to the IgG control. n = 8 in each group. Data a , b , and d were analyzed by repeated measures ANOVA and followed by Bonferroni post hoc tests. Data c was analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Techniques Used: Mouse Assay, Injection, Flow Cytometry

    Systemic blockade of proBDNF restored meningeal pro-inflammatory microenvironment in septic mice. Mice were i.p. injected with proBDNF 30 min before LPS (5 mg kg −1 ) injection. Meninges were harvested 5 days after LPS injection for qPCR. a The level of CD4 gene expression was higher in the meninges of the McAb-proB group than in IgG controls in septic mice. b–f Gene levels were significantly lower in b IL-1β and c IL-6 but higher in d IL-4, e IFN-γ, and f IL-13 in the meninges after LPS injection in the McAb-proB group as compared to IgG control. n = 5 in each group. All experiments were performed at least in triplicate. Data were analyzed by unpaired T test, * P
    Figure Legend Snippet: Systemic blockade of proBDNF restored meningeal pro-inflammatory microenvironment in septic mice. Mice were i.p. injected with proBDNF 30 min before LPS (5 mg kg −1 ) injection. Meninges were harvested 5 days after LPS injection for qPCR. a The level of CD4 gene expression was higher in the meninges of the McAb-proB group than in IgG controls in septic mice. b–f Gene levels were significantly lower in b IL-1β and c IL-6 but higher in d IL-4, e IFN-γ, and f IL-13 in the meninges after LPS injection in the McAb-proB group as compared to IgG control. n = 5 in each group. All experiments were performed at least in triplicate. Data were analyzed by unpaired T test, * P

    Techniques Used: Mouse Assay, Injection, Real-time Polymerase Chain Reaction, Expressing

    2) Product Images from "Prelimbic proBDNF facilitates memory destabilization by regulation of neuronal function in juveniles"

    Article Title: Prelimbic proBDNF facilitates memory destabilization by regulation of neuronal function in juveniles

    Journal: bioRxiv

    doi: 10.1101/2021.12.30.474526

    The increase proBDNF alters synaptic currents, promotes LFS-induced synaptic depression and strengthens the theta phase-gamma amplitude coupling during the PR-LTM test. (A) Schematic describing the timeline for morphological analysis (Top-left). Illustration of the region of interest in prelimbic images (Top-middle), and dendritic segment analysis for spine quantification (Top-right). Red circles indicated the mushroom type spine, yellow circles indicated thin type spine and blue circles indicated stubby type spine. Sample images were projected at minimal intensity and inverted, background was then subtracted, followed by brightness/contrast adjustment. Scale bars, 5 μm. Quantification of spine density (Bottom-left) and the proportion of spine (Bottom-right). No statistical difference in spine density was found between juvenile and adult groups. However, a significant higher proportion of thin type spine but a lower mushroom type spine was observed in juveniles compared with adults. (B) Schematic describing the timeline for EPSCs recordings (Top-left). Representative continuous traces (Top-middle) and average waveform (Top-right) of the pharmacologically isolated NMDA EPSCs in the prelimbic neurons of adult, juvenile and juvenile+anti groups. No change in the amplitude of EPSCs (Bottom-left) was found but the frequency (Bottom-middle) and decay time (Bottom-right) were significantly increased in juvenile group. The enhanced frequency and decay time of NMDA currents in juvenile group were inhibited after infusions of anti-proBDNF antibody. (* P
    Figure Legend Snippet: The increase proBDNF alters synaptic currents, promotes LFS-induced synaptic depression and strengthens the theta phase-gamma amplitude coupling during the PR-LTM test. (A) Schematic describing the timeline for morphological analysis (Top-left). Illustration of the region of interest in prelimbic images (Top-middle), and dendritic segment analysis for spine quantification (Top-right). Red circles indicated the mushroom type spine, yellow circles indicated thin type spine and blue circles indicated stubby type spine. Sample images were projected at minimal intensity and inverted, background was then subtracted, followed by brightness/contrast adjustment. Scale bars, 5 μm. Quantification of spine density (Bottom-left) and the proportion of spine (Bottom-right). No statistical difference in spine density was found between juvenile and adult groups. However, a significant higher proportion of thin type spine but a lower mushroom type spine was observed in juveniles compared with adults. (B) Schematic describing the timeline for EPSCs recordings (Top-left). Representative continuous traces (Top-middle) and average waveform (Top-right) of the pharmacologically isolated NMDA EPSCs in the prelimbic neurons of adult, juvenile and juvenile+anti groups. No change in the amplitude of EPSCs (Bottom-left) was found but the frequency (Bottom-middle) and decay time (Bottom-right) were significantly increased in juvenile group. The enhanced frequency and decay time of NMDA currents in juvenile group were inhibited after infusions of anti-proBDNF antibody. (* P

    Techniques Used: Isolation

    The higher prelimbic proBDNF expression during the juvenile period facilitates retrieval-dependent memory destabilization. Quantification of the proBDNF (A) and its receptor p75 NTR (B) levels in prelimbic cortex of juvenile and adult rats. Representative immunoblots the expression of proBDNF and p75 NTR (Top). A significant increase in the proBDNF levels was detected in juvenile group, as well the p75 NTR levels (Bottom). (* P
    Figure Legend Snippet: The higher prelimbic proBDNF expression during the juvenile period facilitates retrieval-dependent memory destabilization. Quantification of the proBDNF (A) and its receptor p75 NTR (B) levels in prelimbic cortex of juvenile and adult rats. Representative immunoblots the expression of proBDNF and p75 NTR (Top). A significant increase in the proBDNF levels was detected in juvenile group, as well the p75 NTR levels (Bottom). (* P

    Techniques Used: Expressing, Western Blot

    Up-regulation of proBDNF-p75NTR signaling mediated by NMDA-GluN2B contributes to enhance the modulation of existing fear memory traces in juvenile rats. (A) Schematic describing the behavioral timeline for the retrieval-dependent memory destabilization experiment using rats conditioned with four tones (Top). Immediately following the memory retrieval, the rats infused with TAT-Pep5, K252a or vehicle into the prelimbic cortex 15 min prior to the mBDNF, proBDNF or vehicle infusion. Two days later, PR-LTM was assessed by exposed the rats to the novel context. Similar, no significant difference in the percentage freezing during the memory retrieval but the percentage freezing level during the PR-LTM test was significant lower in juvenile group than adult group (Bottom). No obvious effect of mBDNF on freeze behavior was found. Infusions of p75 NTR blocker TAT-Pep5 could significantly enhance the percentage of freeze behavior. Meanwhile, infusions of TAT-Pep5, but not K252a, markedly blocked the effects of proBDNF treatment. (* P
    Figure Legend Snippet: Up-regulation of proBDNF-p75NTR signaling mediated by NMDA-GluN2B contributes to enhance the modulation of existing fear memory traces in juvenile rats. (A) Schematic describing the behavioral timeline for the retrieval-dependent memory destabilization experiment using rats conditioned with four tones (Top). Immediately following the memory retrieval, the rats infused with TAT-Pep5, K252a or vehicle into the prelimbic cortex 15 min prior to the mBDNF, proBDNF or vehicle infusion. Two days later, PR-LTM was assessed by exposed the rats to the novel context. Similar, no significant difference in the percentage freezing during the memory retrieval but the percentage freezing level during the PR-LTM test was significant lower in juvenile group than adult group (Bottom). No obvious effect of mBDNF on freeze behavior was found. Infusions of p75 NTR blocker TAT-Pep5 could significantly enhance the percentage of freeze behavior. Meanwhile, infusions of TAT-Pep5, but not K252a, markedly blocked the effects of proBDNF treatment. (* P

    Techniques Used:

    3) Product Images from "p75 Neurotrophin Receptor Activation Regulates the Timing of the Maturation of Cortical Parvalbumin Interneuron Connectivity and Promotes Juvenile-like Plasticity in Adult Visual Cortex"

    Article Title: p75 Neurotrophin Receptor Activation Regulates the Timing of the Maturation of Cortical Parvalbumin Interneuron Connectivity and Promotes Juvenile-like Plasticity in Adult Visual Cortex

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.2881-18.2019

    proBNDF-mediated p75NTR activation in cortical PV cells reduces their perisomatic boutons. A , Experimental approach. B , The intensity of perisomatic PV immunostaining (green) is reduced in the binocular visual cortex ipsilateral to the minipump-releasing mut-proBDNF (Ipsi) compared with the contralateral cortex (Contra) in the same animal. On the other hand, perisomatic PV intensity in the ipsilateral cortex of PV_Cre;p75 flx/flx mice is similar to that observed in the contralateral, untreated cortex. C , Low ( C1 ) and high ( C2 ) magnification of PNN (red, WFA staining) enwrapping PV cells (green) shows a dramatic reduction in both PNN density and intensity in the visual cortex infused with mut-proBFNF. This effect is abolished in PV_Cre;p75 flx/flx mice. Scale bars: C1 , 100 μm; B , C2 , 10 μm. D , Quantification of the mean intensity of perisomatic PV-positive puncta in ipsilateral compared with contralateral cortex. I/C ratio is obtained for each animal and then averaged between different animals. Mean I/C ratio is significantly reduced in Mut-proBDNF-infused p75 Ctrl mice compared with Mut-proBDNF-infused PV_Cre;p75 flx/flx mice (unpaired t test, df = 8, t = 6.077, p = 0.0003). E , The ratio of mean PNN intensity around PV cells in ipsilateral versus contralateral cortex is significantly lower in p75 Ctrl than PV_Cre;p75 flx/flx mice infused with mut-proBDNF (unpaired t test, df = 8, t = 15.33, p
    Figure Legend Snippet: proBNDF-mediated p75NTR activation in cortical PV cells reduces their perisomatic boutons. A , Experimental approach. B , The intensity of perisomatic PV immunostaining (green) is reduced in the binocular visual cortex ipsilateral to the minipump-releasing mut-proBDNF (Ipsi) compared with the contralateral cortex (Contra) in the same animal. On the other hand, perisomatic PV intensity in the ipsilateral cortex of PV_Cre;p75 flx/flx mice is similar to that observed in the contralateral, untreated cortex. C , Low ( C1 ) and high ( C2 ) magnification of PNN (red, WFA staining) enwrapping PV cells (green) shows a dramatic reduction in both PNN density and intensity in the visual cortex infused with mut-proBFNF. This effect is abolished in PV_Cre;p75 flx/flx mice. Scale bars: C1 , 100 μm; B , C2 , 10 μm. D , Quantification of the mean intensity of perisomatic PV-positive puncta in ipsilateral compared with contralateral cortex. I/C ratio is obtained for each animal and then averaged between different animals. Mean I/C ratio is significantly reduced in Mut-proBDNF-infused p75 Ctrl mice compared with Mut-proBDNF-infused PV_Cre;p75 flx/flx mice (unpaired t test, df = 8, t = 6.077, p = 0.0003). E , The ratio of mean PNN intensity around PV cells in ipsilateral versus contralateral cortex is significantly lower in p75 Ctrl than PV_Cre;p75 flx/flx mice infused with mut-proBDNF (unpaired t test, df = 8, t = 15.33, p

    Techniques Used: Activation Assay, Immunostaining, Mouse Assay, Staining

    Modulation of tPA activity affects the formation of PV cell innervations during early postnatal development. A , Control EP18 PV cell ( A1 , green represents Ctrl). B , PV cell treated with the tPA inhibitor PPACK from EP10–EP18 shows simpler axonal arborization, contacting less potential targets ( B2 , blue represents NeuN-positive somata). C , PV cell treated with tPA in the same time window shows a very complex axonal arbor ( C2 ) and an increase in both terminal branching and perisomatic boutons ( C3 , arrowheads) compared with control cells ( A2 , A3 ). D , PV cell treated simultaneously with tPA and mut-proBDNF shows axonal branching and perisomatic innervation more similar to those formed by PV cell treated with mut-proBDNF alone, suggesting that the effects of tPA application may be mediated by a decrease in endogenous proBDNF/mBDNF ratio. Stars indicate NeuN-positive somata that are not innervated. Scale bars: A1–D1 , 50 μm; A2–D2 , 10 μm; A3–D3 , 5 μm. E , Perisomatic boutons density (one-way ANOVA, F (3,20) = 121.2, p
    Figure Legend Snippet: Modulation of tPA activity affects the formation of PV cell innervations during early postnatal development. A , Control EP18 PV cell ( A1 , green represents Ctrl). B , PV cell treated with the tPA inhibitor PPACK from EP10–EP18 shows simpler axonal arborization, contacting less potential targets ( B2 , blue represents NeuN-positive somata). C , PV cell treated with tPA in the same time window shows a very complex axonal arbor ( C2 ) and an increase in both terminal branching and perisomatic boutons ( C3 , arrowheads) compared with control cells ( A2 , A3 ). D , PV cell treated simultaneously with tPA and mut-proBDNF shows axonal branching and perisomatic innervation more similar to those formed by PV cell treated with mut-proBDNF alone, suggesting that the effects of tPA application may be mediated by a decrease in endogenous proBDNF/mBDNF ratio. Stars indicate NeuN-positive somata that are not innervated. Scale bars: A1–D1 , 50 μm; A2–D2 , 10 μm; A3–D3 , 5 μm. E , Perisomatic boutons density (one-way ANOVA, F (3,20) = 121.2, p

    Techniques Used: Activity Assay

    proBNDF-mediated p75NTR activation in cortical PV cells restores ocular dominance plasticity in adult visual cortex in vivo . A , Typical VEP responses to the stimulation of either contralateral (blue) or ipsilateral (red) eye to the cortex in which the recording is performed in p75NTR Ctrl mice infused with either vehicle or mut-proBDNF, and PV_Cre;p75NTR flx/flx mice infused with mut-proBDNF. Calibration bars: 50 μV, 100 ms. B , C/I VEP ratio mean values. Three days of monocular deprivation do not affect the C/I VEP ratio in adult mice, although it leads to a significant decrease in the C/I VEP ratio in animals treated with mut-proBDNF. Mut-proBDNF effects are, however, abolished in PV_Cre;p75 flx/flx mice (one-way ANOVA, F (2,18) = 8.903, p = 0.0021). p75NTR Ctrl + vehicle: n = 9 mice; p75NTR Ctrl + mut-proBDNF: n = 5 mice; PV_Cre;p75 flx/flx +mut-proBDNF: n = 7 mice. C , ODI of p75NTR Ctrl mice infused with vehicle solution and PV_Cre;p75 flx/flx mice infused with mut-proBDNF are not significantly different from those of undeprived animals, whereas ODIs in p75 Ctrl mice treated with mut-proBDNF are significantly shifted toward the open eye (one-way ANOVA, F (2,443) = 5.203, p = 0.0058). D , Mean spontaneous discharge is significantly increased only in p75 Ctrl mice treated with mut-proBDNF (one-way ANOVA, F (2,443) = 4.580, p = 0.0107). p75NTR Ctrl + vehicle: n = 9 mice, 174 cells; p75NTR Ctrl + mut-proBDNF: n = 5 mice, 147 cells; PV_Cre;p75 flx/flx +mut-proBDNF: n = 6 mice, 125 cells. Gray area represents the C/I VEP ratio ( B ) or the ODI range ( C ) (mean ± SEM) in adult nondeprived animals ( n = 5 mice, 99 cells). * indicate p
    Figure Legend Snippet: proBNDF-mediated p75NTR activation in cortical PV cells restores ocular dominance plasticity in adult visual cortex in vivo . A , Typical VEP responses to the stimulation of either contralateral (blue) or ipsilateral (red) eye to the cortex in which the recording is performed in p75NTR Ctrl mice infused with either vehicle or mut-proBDNF, and PV_Cre;p75NTR flx/flx mice infused with mut-proBDNF. Calibration bars: 50 μV, 100 ms. B , C/I VEP ratio mean values. Three days of monocular deprivation do not affect the C/I VEP ratio in adult mice, although it leads to a significant decrease in the C/I VEP ratio in animals treated with mut-proBDNF. Mut-proBDNF effects are, however, abolished in PV_Cre;p75 flx/flx mice (one-way ANOVA, F (2,18) = 8.903, p = 0.0021). p75NTR Ctrl + vehicle: n = 9 mice; p75NTR Ctrl + mut-proBDNF: n = 5 mice; PV_Cre;p75 flx/flx +mut-proBDNF: n = 7 mice. C , ODI of p75NTR Ctrl mice infused with vehicle solution and PV_Cre;p75 flx/flx mice infused with mut-proBDNF are not significantly different from those of undeprived animals, whereas ODIs in p75 Ctrl mice treated with mut-proBDNF are significantly shifted toward the open eye (one-way ANOVA, F (2,443) = 5.203, p = 0.0058). D , Mean spontaneous discharge is significantly increased only in p75 Ctrl mice treated with mut-proBDNF (one-way ANOVA, F (2,443) = 4.580, p = 0.0107). p75NTR Ctrl + vehicle: n = 9 mice, 174 cells; p75NTR Ctrl + mut-proBDNF: n = 5 mice, 147 cells; PV_Cre;p75 flx/flx +mut-proBDNF: n = 6 mice, 125 cells. Gray area represents the C/I VEP ratio ( B ) or the ODI range ( C ) (mean ± SEM) in adult nondeprived animals ( n = 5 mice, 99 cells). * indicate p

    Techniques Used: Activation Assay, In Vivo, Mouse Assay

    mut-proBDNF destabilizes PV cell innervation, even after it has reached maturity. A , Control PV cell ( A1 , Ctrl, green) at EP32 with exuberant innervation field characterized by extensive branching contacting the majority of potential targets, dense boutons along axons ( A2 ), and terminal branches with prominent and clustered boutons ( A3 ; arrowheads) around NeuN-positive somata (blue). B , PV cell treated with wt-proBDNF from EP26-EP32 shows overall similar axon size ( B1 ), percentage of potentially targeted neurons ( B2 ), and perisomatic innervations ( B3 ) as control, untreated PV cells. C , PV cell treated with mut-proBDNF from EP26-EP32 shows a drastic reduction both in percentage of innervated cells ( C2 ) and perisomatic innervation ( C3 ). Stars indicate NeuN-positive somata that are not innervated. Scale bars: A1–C1 , 50 μm; A2–C2 , 10 μm; A3–C3 , 5 μm. D , Perisomatic bouton density (one-way ANOVA, F (2,18) = 93.34, p
    Figure Legend Snippet: mut-proBDNF destabilizes PV cell innervation, even after it has reached maturity. A , Control PV cell ( A1 , Ctrl, green) at EP32 with exuberant innervation field characterized by extensive branching contacting the majority of potential targets, dense boutons along axons ( A2 ), and terminal branches with prominent and clustered boutons ( A3 ; arrowheads) around NeuN-positive somata (blue). B , PV cell treated with wt-proBDNF from EP26-EP32 shows overall similar axon size ( B1 ), percentage of potentially targeted neurons ( B2 ), and perisomatic innervations ( B3 ) as control, untreated PV cells. C , PV cell treated with mut-proBDNF from EP26-EP32 shows a drastic reduction both in percentage of innervated cells ( C2 ) and perisomatic innervation ( C3 ). Stars indicate NeuN-positive somata that are not innervated. Scale bars: A1–C1 , 50 μm; A2–C2 , 10 μm; A3–C3 , 5 μm. D , Perisomatic bouton density (one-way ANOVA, F (2,18) = 93.34, p

    Techniques Used:

    4) Product Images from "NMDA-Dependent Switch of proBDNF Actions on Developing GABAergic Synapses"

    Article Title: NMDA-Dependent Switch of proBDNF Actions on Developing GABAergic Synapses

    Journal: Cerebral Cortex (New York, NY)

    doi: 10.1093/cercor/bhs071

    Paracrine actions of proBDNF on GABAergic synaptic activity. Schematic representation of the steps leading to the p75 NTR -dependent LLP GABA-A and LLD GABA-A . CA3 pyramidal cells release proBDNF in response to the activation of L-type Ca 2+ channel during
    Figure Legend Snippet: Paracrine actions of proBDNF on GABAergic synaptic activity. Schematic representation of the steps leading to the p75 NTR -dependent LLP GABA-A and LLD GABA-A . CA3 pyramidal cells release proBDNF in response to the activation of L-type Ca 2+ channel during

    Techniques Used: Activity Assay, Activation Assay

    Endogenous activation of p75 NTR is required for LLD GABA-A induction. ( A ) Immunofluorescence detection of proBDNF and p75 NTR in a 4-days-old rat hippocampi (red signal, upper images), superimposed on neuro-tracer immunofluorescence (Nt, green signal, lower
    Figure Legend Snippet: Endogenous activation of p75 NTR is required for LLD GABA-A induction. ( A ) Immunofluorescence detection of proBDNF and p75 NTR in a 4-days-old rat hippocampi (red signal, upper images), superimposed on neuro-tracer immunofluorescence (Nt, green signal, lower

    Techniques Used: Activation Assay, Immunofluorescence

    Regulated secretion of proBDNF is required for LLD GABA-A induction. ( A ) Average time course of sGABA A -PSCs frequency before and after activity recovery with aprotinin and nifedipine (10 μM) in the absence (control, open symbol, n = 6) or the presence
    Figure Legend Snippet: Regulated secretion of proBDNF is required for LLD GABA-A induction. ( A ) Average time course of sGABA A -PSCs frequency before and after activity recovery with aprotinin and nifedipine (10 μM) in the absence (control, open symbol, n = 6) or the presence

    Techniques Used: Activity Assay

    5) Product Images from "ProNGF promotes neurite growth from a subset of NGF-dependent neurons by a p75NTR-dependent mechanism"

    Article Title: ProNGF promotes neurite growth from a subset of NGF-dependent neurons by a p75NTR-dependent mechanism

    Journal: Development (Cambridge, England)

    doi: 10.1242/dev.085266

    Specificity of neurite growth-promoting effects of proNGF, proBDNF and proNT3. ( A , B ) Neurite length and branching of E17 to P5 trigeminal neurons cultured for 24 hours without factors or with 10 ng/ml cleavage-resistant murine proNGF or 10 ng/ml mNGF. ( C , D ) Neurite length and branching of P5 trigeminal neurons cultured with a range of concentrations of mNGF and cleavage-resistant murine proNGF. ( E-G ) YFP-transfected SCG neurons (green) and pDsRed-transfected trigeminal neurons (red) co-cultured for 24 hours either without factors (E), or with 10 ng/ml cleavage-resistant murine proNGF (F) or 10 ng/ml mNGF (G). Scale bars: 100 μm. ( H ) Sholl plot of P3 trigeminal neurons incubated with mNGF, cleavage-resistant murine proNGF or cleavage-resistant human proNGF. ( I , J ) Neurite length and branching of P3 SCG, trigeminal and nodose neurons cultured for 24 hours with 10 ng/ml cleavage-resistant murine proNGF, 10 ng/ml cleavage-resistant murine proBDNF or 10 ng/ml native human proNT3. All cultures were supplemented with 25 μM Boc-D-FMK and the cultures with native proNT3 additionally received 1 μM batimastat. The mean±s.e.m. for at least three individual datasets are shown.
    Figure Legend Snippet: Specificity of neurite growth-promoting effects of proNGF, proBDNF and proNT3. ( A , B ) Neurite length and branching of E17 to P5 trigeminal neurons cultured for 24 hours without factors or with 10 ng/ml cleavage-resistant murine proNGF or 10 ng/ml mNGF. ( C , D ) Neurite length and branching of P5 trigeminal neurons cultured with a range of concentrations of mNGF and cleavage-resistant murine proNGF. ( E-G ) YFP-transfected SCG neurons (green) and pDsRed-transfected trigeminal neurons (red) co-cultured for 24 hours either without factors (E), or with 10 ng/ml cleavage-resistant murine proNGF (F) or 10 ng/ml mNGF (G). Scale bars: 100 μm. ( H ) Sholl plot of P3 trigeminal neurons incubated with mNGF, cleavage-resistant murine proNGF or cleavage-resistant human proNGF. ( I , J ) Neurite length and branching of P3 SCG, trigeminal and nodose neurons cultured for 24 hours with 10 ng/ml cleavage-resistant murine proNGF, 10 ng/ml cleavage-resistant murine proBDNF or 10 ng/ml native human proNT3. All cultures were supplemented with 25 μM Boc-D-FMK and the cultures with native proNT3 additionally received 1 μM batimastat. The mean±s.e.m. for at least three individual datasets are shown.

    Techniques Used: Cell Culture, Transfection, Incubation

    6) Product Images from "p75 Neurotrophin Receptor Activation Regulates the Timing of the Maturation of Cortical Parvalbumin Interneuron Connectivity and Promotes Juvenile-like Plasticity in Adult Visual Cortex"

    Article Title: p75 Neurotrophin Receptor Activation Regulates the Timing of the Maturation of Cortical Parvalbumin Interneuron Connectivity and Promotes Juvenile-like Plasticity in Adult Visual Cortex

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.2881-18.2019

    proBNDF-mediated p75NTR activation in cortical PV cells reduces their perisomatic boutons. A , Experimental approach. B , The intensity of perisomatic PV immunostaining (green) is reduced in the binocular visual cortex ipsilateral to the minipump-releasing mut-proBDNF (Ipsi) compared with the contralateral cortex (Contra) in the same animal. On the other hand, perisomatic PV intensity in the ipsilateral cortex of PV_Cre;p75 flx/flx mice is similar to that observed in the contralateral, untreated cortex. C , Low ( C1 ) and high ( C2 ) magnification of PNN (red, WFA staining) enwrapping PV cells (green) shows a dramatic reduction in both PNN density and intensity in the visual cortex infused with mut-proBFNF. This effect is abolished in PV_Cre;p75 flx/flx mice. Scale bars: C1 , 100 μm; B , C2 , 10 μm. D , Quantification of the mean intensity of perisomatic PV-positive puncta in ipsilateral compared with contralateral cortex. I/C ratio is obtained for each animal and then averaged between different animals. Mean I/C ratio is significantly reduced in Mut-proBDNF-infused p75 Ctrl mice compared with Mut-proBDNF-infused PV_Cre;p75 flx/flx mice (unpaired t test, df = 8, t = 6.077, p = 0.0003). E , The ratio of mean PNN intensity around PV cells in ipsilateral versus contralateral cortex is significantly lower in p75 Ctrl than PV_Cre;p75 flx/flx mice infused with mut-proBDNF (unpaired t test, df = 8, t = 15.33, p
    Figure Legend Snippet: proBNDF-mediated p75NTR activation in cortical PV cells reduces their perisomatic boutons. A , Experimental approach. B , The intensity of perisomatic PV immunostaining (green) is reduced in the binocular visual cortex ipsilateral to the minipump-releasing mut-proBDNF (Ipsi) compared with the contralateral cortex (Contra) in the same animal. On the other hand, perisomatic PV intensity in the ipsilateral cortex of PV_Cre;p75 flx/flx mice is similar to that observed in the contralateral, untreated cortex. C , Low ( C1 ) and high ( C2 ) magnification of PNN (red, WFA staining) enwrapping PV cells (green) shows a dramatic reduction in both PNN density and intensity in the visual cortex infused with mut-proBFNF. This effect is abolished in PV_Cre;p75 flx/flx mice. Scale bars: C1 , 100 μm; B , C2 , 10 μm. D , Quantification of the mean intensity of perisomatic PV-positive puncta in ipsilateral compared with contralateral cortex. I/C ratio is obtained for each animal and then averaged between different animals. Mean I/C ratio is significantly reduced in Mut-proBDNF-infused p75 Ctrl mice compared with Mut-proBDNF-infused PV_Cre;p75 flx/flx mice (unpaired t test, df = 8, t = 6.077, p = 0.0003). E , The ratio of mean PNN intensity around PV cells in ipsilateral versus contralateral cortex is significantly lower in p75 Ctrl than PV_Cre;p75 flx/flx mice infused with mut-proBDNF (unpaired t test, df = 8, t = 15.33, p

    Techniques Used: Activation Assay, Immunostaining, Mouse Assay, Staining

    Modulation of tPA activity affects the formation of PV cell innervations during early postnatal development. A , Control EP18 PV cell ( A1 , green represents Ctrl). B , PV cell treated with the tPA inhibitor PPACK from EP10–EP18 shows simpler axonal arborization, contacting less potential targets ( B2 , blue represents NeuN-positive somata). C , PV cell treated with tPA in the same time window shows a very complex axonal arbor ( C2 ) and an increase in both terminal branching and perisomatic boutons ( C3 , arrowheads) compared with control cells ( A2 , A3 ). D , PV cell treated simultaneously with tPA and mut-proBDNF shows axonal branching and perisomatic innervation more similar to those formed by PV cell treated with mut-proBDNF alone, suggesting that the effects of tPA application may be mediated by a decrease in endogenous proBDNF/mBDNF ratio. Stars indicate NeuN-positive somata that are not innervated. Scale bars: A1–D1 , 50 μm; A2–D2 , 10 μm; A3–D3 , 5 μm. E , Perisomatic boutons density (one-way ANOVA, F (3,20) = 121.2, p
    Figure Legend Snippet: Modulation of tPA activity affects the formation of PV cell innervations during early postnatal development. A , Control EP18 PV cell ( A1 , green represents Ctrl). B , PV cell treated with the tPA inhibitor PPACK from EP10–EP18 shows simpler axonal arborization, contacting less potential targets ( B2 , blue represents NeuN-positive somata). C , PV cell treated with tPA in the same time window shows a very complex axonal arbor ( C2 ) and an increase in both terminal branching and perisomatic boutons ( C3 , arrowheads) compared with control cells ( A2 , A3 ). D , PV cell treated simultaneously with tPA and mut-proBDNF shows axonal branching and perisomatic innervation more similar to those formed by PV cell treated with mut-proBDNF alone, suggesting that the effects of tPA application may be mediated by a decrease in endogenous proBDNF/mBDNF ratio. Stars indicate NeuN-positive somata that are not innervated. Scale bars: A1–D1 , 50 μm; A2–D2 , 10 μm; A3–D3 , 5 μm. E , Perisomatic boutons density (one-way ANOVA, F (3,20) = 121.2, p

    Techniques Used: Activity Assay

    proBNDF-mediated p75NTR activation in cortical PV cells restores ocular dominance plasticity in adult visual cortex in vivo . A , Typical VEP responses to the stimulation of either contralateral (blue) or ipsilateral (red) eye to the cortex in which the recording is performed in p75NTR Ctrl mice infused with either vehicle or mut-proBDNF, and PV_Cre;p75NTR flx/flx mice infused with mut-proBDNF. Calibration bars: 50 μV, 100 ms. B , C/I VEP ratio mean values. Three days of monocular deprivation do not affect the C/I VEP ratio in adult mice, although it leads to a significant decrease in the C/I VEP ratio in animals treated with mut-proBDNF. Mut-proBDNF effects are, however, abolished in PV_Cre;p75 flx/flx mice (one-way ANOVA, F (2,18) = 8.903, p = 0.0021). p75NTR Ctrl + vehicle: n = 9 mice; p75NTR Ctrl + mut-proBDNF: n = 5 mice; PV_Cre;p75 flx/flx +mut-proBDNF: n = 7 mice. C , ODI of p75NTR Ctrl mice infused with vehicle solution and PV_Cre;p75 flx/flx mice infused with mut-proBDNF are not significantly different from those of undeprived animals, whereas ODIs in p75 Ctrl mice treated with mut-proBDNF are significantly shifted toward the open eye (one-way ANOVA, F (2,443) = 5.203, p = 0.0058). D , Mean spontaneous discharge is significantly increased only in p75 Ctrl mice treated with mut-proBDNF (one-way ANOVA, F (2,443) = 4.580, p = 0.0107). p75NTR Ctrl + vehicle: n = 9 mice, 174 cells; p75NTR Ctrl + mut-proBDNF: n = 5 mice, 147 cells; PV_Cre;p75 flx/flx +mut-proBDNF: n = 6 mice, 125 cells. Gray area represents the C/I VEP ratio ( B ) or the ODI range ( C ) (mean ± SEM) in adult nondeprived animals ( n = 5 mice, 99 cells). * indicate p
    Figure Legend Snippet: proBNDF-mediated p75NTR activation in cortical PV cells restores ocular dominance plasticity in adult visual cortex in vivo . A , Typical VEP responses to the stimulation of either contralateral (blue) or ipsilateral (red) eye to the cortex in which the recording is performed in p75NTR Ctrl mice infused with either vehicle or mut-proBDNF, and PV_Cre;p75NTR flx/flx mice infused with mut-proBDNF. Calibration bars: 50 μV, 100 ms. B , C/I VEP ratio mean values. Three days of monocular deprivation do not affect the C/I VEP ratio in adult mice, although it leads to a significant decrease in the C/I VEP ratio in animals treated with mut-proBDNF. Mut-proBDNF effects are, however, abolished in PV_Cre;p75 flx/flx mice (one-way ANOVA, F (2,18) = 8.903, p = 0.0021). p75NTR Ctrl + vehicle: n = 9 mice; p75NTR Ctrl + mut-proBDNF: n = 5 mice; PV_Cre;p75 flx/flx +mut-proBDNF: n = 7 mice. C , ODI of p75NTR Ctrl mice infused with vehicle solution and PV_Cre;p75 flx/flx mice infused with mut-proBDNF are not significantly different from those of undeprived animals, whereas ODIs in p75 Ctrl mice treated with mut-proBDNF are significantly shifted toward the open eye (one-way ANOVA, F (2,443) = 5.203, p = 0.0058). D , Mean spontaneous discharge is significantly increased only in p75 Ctrl mice treated with mut-proBDNF (one-way ANOVA, F (2,443) = 4.580, p = 0.0107). p75NTR Ctrl + vehicle: n = 9 mice, 174 cells; p75NTR Ctrl + mut-proBDNF: n = 5 mice, 147 cells; PV_Cre;p75 flx/flx +mut-proBDNF: n = 6 mice, 125 cells. Gray area represents the C/I VEP ratio ( B ) or the ODI range ( C ) (mean ± SEM) in adult nondeprived animals ( n = 5 mice, 99 cells). * indicate p

    Techniques Used: Activation Assay, In Vivo, Mouse Assay, Mass Spectrometry

    mut-proBDNF destabilizes PV cell innervation, even after it has reached maturity. A , Control PV cell ( A1 , Ctrl, green) at EP32 with exuberant innervation field characterized by extensive branching contacting the majority of potential targets, dense boutons along axons ( A2 ), and terminal branches with prominent and clustered boutons ( A3 ; arrowheads) around NeuN-positive somata (blue). B , PV cell treated with wt-proBDNF from EP26-EP32 shows overall similar axon size ( B1 ), percentage of potentially targeted neurons ( B2 ), and perisomatic innervations ( B3 ) as control, untreated PV cells. C , PV cell treated with mut-proBDNF from EP26-EP32 shows a drastic reduction both in percentage of innervated cells ( C2 ) and perisomatic innervation ( C3 ). Stars indicate NeuN-positive somata that are not innervated. Scale bars: A1–C1 , 50 μm; A2–C2 , 10 μm; A3–C3 , 5 μm. D , Perisomatic bouton density (one-way ANOVA, F (2,18) = 93.34, p
    Figure Legend Snippet: mut-proBDNF destabilizes PV cell innervation, even after it has reached maturity. A , Control PV cell ( A1 , Ctrl, green) at EP32 with exuberant innervation field characterized by extensive branching contacting the majority of potential targets, dense boutons along axons ( A2 ), and terminal branches with prominent and clustered boutons ( A3 ; arrowheads) around NeuN-positive somata (blue). B , PV cell treated with wt-proBDNF from EP26-EP32 shows overall similar axon size ( B1 ), percentage of potentially targeted neurons ( B2 ), and perisomatic innervations ( B3 ) as control, untreated PV cells. C , PV cell treated with mut-proBDNF from EP26-EP32 shows a drastic reduction both in percentage of innervated cells ( C2 ) and perisomatic innervation ( C3 ). Stars indicate NeuN-positive somata that are not innervated. Scale bars: A1–C1 , 50 μm; A2–C2 , 10 μm; A3–C3 , 5 μm. D , Perisomatic bouton density (one-way ANOVA, F (2,18) = 93.34, p

    Techniques Used:

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    Alomone Labs probdnf protein
    Schematic diagram showing how <t>proBDNF</t> dampens CD4 + T cell activity and contributes to the pathogenesis of SAE. In sepsis, proBDNF expression is increased in peripheral blood and meningeal immune cells, which then decreases the infiltration of CD4 + T cells in the meninges. As a result, meningeal pro-inflammatory cytokines such as IL-6 and IL-1β are upregulated, but anti-inflammatory cytokines including IL-4 and IL-13 are downregulated, finally leading to SAE. SAE, sepsis-associated encephalopathy
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    Schematic diagram showing how proBDNF dampens CD4 + T cell activity and contributes to the pathogenesis of SAE. In sepsis, proBDNF expression is increased in peripheral blood and meningeal immune cells, which then decreases the infiltration of CD4 + T cells in the meninges. As a result, meningeal pro-inflammatory cytokines such as IL-6 and IL-1β are upregulated, but anti-inflammatory cytokines including IL-4 and IL-13 are downregulated, finally leading to SAE. SAE, sepsis-associated encephalopathy

    Journal: Journal of Neuroinflammation

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    doi: 10.1186/s12974-020-01850-0

    Figure Lengend Snippet: Schematic diagram showing how proBDNF dampens CD4 + T cell activity and contributes to the pathogenesis of SAE. In sepsis, proBDNF expression is increased in peripheral blood and meningeal immune cells, which then decreases the infiltration of CD4 + T cells in the meninges. As a result, meningeal pro-inflammatory cytokines such as IL-6 and IL-1β are upregulated, but anti-inflammatory cytokines including IL-4 and IL-13 are downregulated, finally leading to SAE. SAE, sepsis-associated encephalopathy

    Article Snippet: 4 × 105 cells were put in each well of a 96-well flat-bottom plate and stimulated with 100, 200, or 500 ng ml−1 proBDNF protein (Alomone Labs, Israel, catalog: B243) as introduced by our previous studies [ ], respectively.

    Techniques: Activity Assay, Expressing

    Exogenous proBDNF protein reduced CD4 + T cells but increased CD8 + T cells of septic mice in vitro. Mice injected with saline or LPS (5 mg kg −1 ) for 5 days and the splenocytes were isolated and cultured for 3 days in vitro. Exogenous proBDNF did not alter the percentage of a CD3 + T cells in CD45 + cells or the percentage of b CD4 + T cells or c CD8 + T cells in CD3 + T cells in splenocytes from mice treated with saline. d Exogenous proBDNF did not alter the percentage of CD3 + T cells in CD45 + cells in splenocytes in septic mice. e–f ProBDNF treatment significantly decreased the percentage of e CD4 + T cells but increased the percentage of f CD8 + T cells in CD3 + T cells in splenocytes in LPS-treated mice. n = 4 in each group. Data were analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Journal: Journal of Neuroinflammation

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    doi: 10.1186/s12974-020-01850-0

    Figure Lengend Snippet: Exogenous proBDNF protein reduced CD4 + T cells but increased CD8 + T cells of septic mice in vitro. Mice injected with saline or LPS (5 mg kg −1 ) for 5 days and the splenocytes were isolated and cultured for 3 days in vitro. Exogenous proBDNF did not alter the percentage of a CD3 + T cells in CD45 + cells or the percentage of b CD4 + T cells or c CD8 + T cells in CD3 + T cells in splenocytes from mice treated with saline. d Exogenous proBDNF did not alter the percentage of CD3 + T cells in CD45 + cells in splenocytes in septic mice. e–f ProBDNF treatment significantly decreased the percentage of e CD4 + T cells but increased the percentage of f CD8 + T cells in CD3 + T cells in splenocytes in LPS-treated mice. n = 4 in each group. Data were analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Article Snippet: 4 × 105 cells were put in each well of a 96-well flat-bottom plate and stimulated with 100, 200, or 500 ng ml−1 proBDNF protein (Alomone Labs, Israel, catalog: B243) as introduced by our previous studies [ ], respectively.

    Techniques: Mouse Assay, In Vitro, Injection, Isolation, Cell Culture

    Increased proBDNF expression in meningeal and peripheral blood immune cells in septic mice. Mice were i.p. injected with LPS (5 mg kg −1 ) and meninges and peripheral blood were harvested for immunofluorescence staining or flow cytometry. a Representative whole mount meningeal immunofluorescence images showed markedly increased proBDNF-positive staining cells in the meninges in mice at 1 day after LPS injection compared to saline injected mice. The high magnification images around the arrows are displayed in a white square as insets. Bar = 100 μm. b – f Representative meningeal single cell flow cytometry images ( upper panel ) and its statistical analysis ( lower panel ) indicated that proBDNF MFI was increased in meningeal b CD3 + T cells, c CD4 + T cells, d CD8 + T cells, and f CD11b + monocytes/macrophages at 1 day after LPS injection. proBDNF in meningeal e CD19 + B cells upregulated until 5 days after LPS injection. n = 10 in the Con group, n = 6 in LPS groups. g – k Upregulation of proBDNF in g CD3 + T cells, h CD4 + T cells, i CD8 + T cells, j CD19 + B cells, and k CD11b + monocytes/macrophages in peripheral blood in LPS-injected mice were detected. n = 9 in Con group, n = 8 in the LPS1d group, n = 4 in the LPS 5d group. Data b – k were analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Journal: Journal of Neuroinflammation

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    doi: 10.1186/s12974-020-01850-0

    Figure Lengend Snippet: Increased proBDNF expression in meningeal and peripheral blood immune cells in septic mice. Mice were i.p. injected with LPS (5 mg kg −1 ) and meninges and peripheral blood were harvested for immunofluorescence staining or flow cytometry. a Representative whole mount meningeal immunofluorescence images showed markedly increased proBDNF-positive staining cells in the meninges in mice at 1 day after LPS injection compared to saline injected mice. The high magnification images around the arrows are displayed in a white square as insets. Bar = 100 μm. b – f Representative meningeal single cell flow cytometry images ( upper panel ) and its statistical analysis ( lower panel ) indicated that proBDNF MFI was increased in meningeal b CD3 + T cells, c CD4 + T cells, d CD8 + T cells, and f CD11b + monocytes/macrophages at 1 day after LPS injection. proBDNF in meningeal e CD19 + B cells upregulated until 5 days after LPS injection. n = 10 in the Con group, n = 6 in LPS groups. g – k Upregulation of proBDNF in g CD3 + T cells, h CD4 + T cells, i CD8 + T cells, j CD19 + B cells, and k CD11b + monocytes/macrophages in peripheral blood in LPS-injected mice were detected. n = 9 in Con group, n = 8 in the LPS1d group, n = 4 in the LPS 5d group. Data b – k were analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Article Snippet: 4 × 105 cells were put in each well of a 96-well flat-bottom plate and stimulated with 100, 200, or 500 ng ml−1 proBDNF protein (Alomone Labs, Israel, catalog: B243) as introduced by our previous studies [ ], respectively.

    Techniques: Expressing, Mouse Assay, Injection, Immunofluorescence, Staining, Flow Cytometry

    Effect of i.c.v. injection of anti-proBDNF antibody on fear memory and meningeal immune activity in the septic mice. Mice were bilateral i.c.v. injected with 1 μg McAb-proB 3 days before LPS injection. Behavior tests were performed 1 day after LPS injection. a Representative images showed the broad and thorough diffusion of drugs in cerebroventricular lumen following i.c.v. injection with methylene blue. b McAb-proB i.c.v. injection did not influence weight of mice. c–e There was no difference of c fear conditioning acquiring performance in each group, nor McAb-proB increased the freezing time of d contextual or e cued fear conditioning test as compared to IgG control after LPS injection. n = 6 in each group. Data b , c , and e were analyzed by repeated measures ANOVA and followed by Bonferroni post hoc test and data d was analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Journal: Journal of Neuroinflammation

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    doi: 10.1186/s12974-020-01850-0

    Figure Lengend Snippet: Effect of i.c.v. injection of anti-proBDNF antibody on fear memory and meningeal immune activity in the septic mice. Mice were bilateral i.c.v. injected with 1 μg McAb-proB 3 days before LPS injection. Behavior tests were performed 1 day after LPS injection. a Representative images showed the broad and thorough diffusion of drugs in cerebroventricular lumen following i.c.v. injection with methylene blue. b McAb-proB i.c.v. injection did not influence weight of mice. c–e There was no difference of c fear conditioning acquiring performance in each group, nor McAb-proB increased the freezing time of d contextual or e cued fear conditioning test as compared to IgG control after LPS injection. n = 6 in each group. Data b , c , and e were analyzed by repeated measures ANOVA and followed by Bonferroni post hoc test and data d was analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Article Snippet: 4 × 105 cells were put in each well of a 96-well flat-bottom plate and stimulated with 100, 200, or 500 ng ml−1 proBDNF protein (Alomone Labs, Israel, catalog: B243) as introduced by our previous studies [ ], respectively.

    Techniques: Injection, Activity Assay, Mouse Assay, Diffusion-based Assay

    Systemic blockade of proBDNF ameliorated cognitive dysfunction and restored meningeal and peripheral CD4 + T cell ratio in septic mice. Mice were i.p. injected with proBDNF 30 min before LPS (5 mg kg −1 ) injection. Fear conditioning testing was performed 1 day after LPS injection. Meninges and peripheral blood were harvested 5 days after LPS injection for flow cytometry. a McAb-proB did not influence the weight of mice or b fear conditioning acquiring. c , d McAb-proB greatly alleviated memory deficit induced by LPS injection in mice as indicated by the increased freezing time in ( c ) contextual and ( d ) cued fear conditioning tests in the McAb-proB group relative to the IgG control. n = 8 in each group. Data a , b , and d were analyzed by repeated measures ANOVA and followed by Bonferroni post hoc tests. Data c was analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Journal: Journal of Neuroinflammation

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    doi: 10.1186/s12974-020-01850-0

    Figure Lengend Snippet: Systemic blockade of proBDNF ameliorated cognitive dysfunction and restored meningeal and peripheral CD4 + T cell ratio in septic mice. Mice were i.p. injected with proBDNF 30 min before LPS (5 mg kg −1 ) injection. Fear conditioning testing was performed 1 day after LPS injection. Meninges and peripheral blood were harvested 5 days after LPS injection for flow cytometry. a McAb-proB did not influence the weight of mice or b fear conditioning acquiring. c , d McAb-proB greatly alleviated memory deficit induced by LPS injection in mice as indicated by the increased freezing time in ( c ) contextual and ( d ) cued fear conditioning tests in the McAb-proB group relative to the IgG control. n = 8 in each group. Data a , b , and d were analyzed by repeated measures ANOVA and followed by Bonferroni post hoc tests. Data c was analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Article Snippet: 4 × 105 cells were put in each well of a 96-well flat-bottom plate and stimulated with 100, 200, or 500 ng ml−1 proBDNF protein (Alomone Labs, Israel, catalog: B243) as introduced by our previous studies [ ], respectively.

    Techniques: Mouse Assay, Injection, Flow Cytometry

    Systemic blockade of proBDNF restored meningeal pro-inflammatory microenvironment in septic mice. Mice were i.p. injected with proBDNF 30 min before LPS (5 mg kg −1 ) injection. Meninges were harvested 5 days after LPS injection for qPCR. a The level of CD4 gene expression was higher in the meninges of the McAb-proB group than in IgG controls in septic mice. b–f Gene levels were significantly lower in b IL-1β and c IL-6 but higher in d IL-4, e IFN-γ, and f IL-13 in the meninges after LPS injection in the McAb-proB group as compared to IgG control. n = 5 in each group. All experiments were performed at least in triplicate. Data were analyzed by unpaired T test, * P

    Journal: Journal of Neuroinflammation

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    doi: 10.1186/s12974-020-01850-0

    Figure Lengend Snippet: Systemic blockade of proBDNF restored meningeal pro-inflammatory microenvironment in septic mice. Mice were i.p. injected with proBDNF 30 min before LPS (5 mg kg −1 ) injection. Meninges were harvested 5 days after LPS injection for qPCR. a The level of CD4 gene expression was higher in the meninges of the McAb-proB group than in IgG controls in septic mice. b–f Gene levels were significantly lower in b IL-1β and c IL-6 but higher in d IL-4, e IFN-γ, and f IL-13 in the meninges after LPS injection in the McAb-proB group as compared to IgG control. n = 5 in each group. All experiments were performed at least in triplicate. Data were analyzed by unpaired T test, * P

    Article Snippet: 4 × 105 cells were put in each well of a 96-well flat-bottom plate and stimulated with 100, 200, or 500 ng ml−1 proBDNF protein (Alomone Labs, Israel, catalog: B243) as introduced by our previous studies [ ], respectively.

    Techniques: Mouse Assay, Injection, Real-time Polymerase Chain Reaction, Expressing

    The increase proBDNF alters synaptic currents, promotes LFS-induced synaptic depression and strengthens the theta phase-gamma amplitude coupling during the PR-LTM test. (A) Schematic describing the timeline for morphological analysis (Top-left). Illustration of the region of interest in prelimbic images (Top-middle), and dendritic segment analysis for spine quantification (Top-right). Red circles indicated the mushroom type spine, yellow circles indicated thin type spine and blue circles indicated stubby type spine. Sample images were projected at minimal intensity and inverted, background was then subtracted, followed by brightness/contrast adjustment. Scale bars, 5 μm. Quantification of spine density (Bottom-left) and the proportion of spine (Bottom-right). No statistical difference in spine density was found between juvenile and adult groups. However, a significant higher proportion of thin type spine but a lower mushroom type spine was observed in juveniles compared with adults. (B) Schematic describing the timeline for EPSCs recordings (Top-left). Representative continuous traces (Top-middle) and average waveform (Top-right) of the pharmacologically isolated NMDA EPSCs in the prelimbic neurons of adult, juvenile and juvenile+anti groups. No change in the amplitude of EPSCs (Bottom-left) was found but the frequency (Bottom-middle) and decay time (Bottom-right) were significantly increased in juvenile group. The enhanced frequency and decay time of NMDA currents in juvenile group were inhibited after infusions of anti-proBDNF antibody. (* P

    Journal: bioRxiv

    Article Title: Prelimbic proBDNF facilitates memory destabilization by regulation of neuronal function in juveniles

    doi: 10.1101/2021.12.30.474526

    Figure Lengend Snippet: The increase proBDNF alters synaptic currents, promotes LFS-induced synaptic depression and strengthens the theta phase-gamma amplitude coupling during the PR-LTM test. (A) Schematic describing the timeline for morphological analysis (Top-left). Illustration of the region of interest in prelimbic images (Top-middle), and dendritic segment analysis for spine quantification (Top-right). Red circles indicated the mushroom type spine, yellow circles indicated thin type spine and blue circles indicated stubby type spine. Sample images were projected at minimal intensity and inverted, background was then subtracted, followed by brightness/contrast adjustment. Scale bars, 5 μm. Quantification of spine density (Bottom-left) and the proportion of spine (Bottom-right). No statistical difference in spine density was found between juvenile and adult groups. However, a significant higher proportion of thin type spine but a lower mushroom type spine was observed in juveniles compared with adults. (B) Schematic describing the timeline for EPSCs recordings (Top-left). Representative continuous traces (Top-middle) and average waveform (Top-right) of the pharmacologically isolated NMDA EPSCs in the prelimbic neurons of adult, juvenile and juvenile+anti groups. No change in the amplitude of EPSCs (Bottom-left) was found but the frequency (Bottom-middle) and decay time (Bottom-right) were significantly increased in juvenile group. The enhanced frequency and decay time of NMDA currents in juvenile group were inhibited after infusions of anti-proBDNF antibody. (* P

    Article Snippet: Needles were inserted into bilateral cannulae and then cleavage-resistant proBDNF (2 ng/ml; Cat#B257 Alomone Labs), anti-proBDNF antibody (10 μg/μL; Cat#ANT-006, Alomone Labs), TAT-Pep5 (4 ng/μL; Cat#506181, EMD Millipore), K252a (25 μg/μL; Cat#82497; Sigma-Aldrich), 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP; 32 ng/μL; Cat#01773, Tocris Bioscience), NVP-AAM077 (0.8 ng/μL; Cat#P1999, Sigma-Aldrich), Ro25-6981 (2.0 ng/μL; Cat#1594, Tocris Bioscience), mature BDNF (1.5 μg/mL; Cat#B250; Alomone Labs) or artificial CSF (ACSF, Cat#3525, Tocris Bioscience) into prelimbic area (at a rate of 0.5 μL/min/side for 2 min) was infused immediately or one day following memory retrieval.

    Techniques: Isolation

    The higher prelimbic proBDNF expression during the juvenile period facilitates retrieval-dependent memory destabilization. Quantification of the proBDNF (A) and its receptor p75 NTR (B) levels in prelimbic cortex of juvenile and adult rats. Representative immunoblots the expression of proBDNF and p75 NTR (Top). A significant increase in the proBDNF levels was detected in juvenile group, as well the p75 NTR levels (Bottom). (* P

    Journal: bioRxiv

    Article Title: Prelimbic proBDNF facilitates memory destabilization by regulation of neuronal function in juveniles

    doi: 10.1101/2021.12.30.474526

    Figure Lengend Snippet: The higher prelimbic proBDNF expression during the juvenile period facilitates retrieval-dependent memory destabilization. Quantification of the proBDNF (A) and its receptor p75 NTR (B) levels in prelimbic cortex of juvenile and adult rats. Representative immunoblots the expression of proBDNF and p75 NTR (Top). A significant increase in the proBDNF levels was detected in juvenile group, as well the p75 NTR levels (Bottom). (* P

    Article Snippet: Needles were inserted into bilateral cannulae and then cleavage-resistant proBDNF (2 ng/ml; Cat#B257 Alomone Labs), anti-proBDNF antibody (10 μg/μL; Cat#ANT-006, Alomone Labs), TAT-Pep5 (4 ng/μL; Cat#506181, EMD Millipore), K252a (25 μg/μL; Cat#82497; Sigma-Aldrich), 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP; 32 ng/μL; Cat#01773, Tocris Bioscience), NVP-AAM077 (0.8 ng/μL; Cat#P1999, Sigma-Aldrich), Ro25-6981 (2.0 ng/μL; Cat#1594, Tocris Bioscience), mature BDNF (1.5 μg/mL; Cat#B250; Alomone Labs) or artificial CSF (ACSF, Cat#3525, Tocris Bioscience) into prelimbic area (at a rate of 0.5 μL/min/side for 2 min) was infused immediately or one day following memory retrieval.

    Techniques: Expressing, Western Blot

    Up-regulation of proBDNF-p75NTR signaling mediated by NMDA-GluN2B contributes to enhance the modulation of existing fear memory traces in juvenile rats. (A) Schematic describing the behavioral timeline for the retrieval-dependent memory destabilization experiment using rats conditioned with four tones (Top). Immediately following the memory retrieval, the rats infused with TAT-Pep5, K252a or vehicle into the prelimbic cortex 15 min prior to the mBDNF, proBDNF or vehicle infusion. Two days later, PR-LTM was assessed by exposed the rats to the novel context. Similar, no significant difference in the percentage freezing during the memory retrieval but the percentage freezing level during the PR-LTM test was significant lower in juvenile group than adult group (Bottom). No obvious effect of mBDNF on freeze behavior was found. Infusions of p75 NTR blocker TAT-Pep5 could significantly enhance the percentage of freeze behavior. Meanwhile, infusions of TAT-Pep5, but not K252a, markedly blocked the effects of proBDNF treatment. (* P

    Journal: bioRxiv

    Article Title: Prelimbic proBDNF facilitates memory destabilization by regulation of neuronal function in juveniles

    doi: 10.1101/2021.12.30.474526

    Figure Lengend Snippet: Up-regulation of proBDNF-p75NTR signaling mediated by NMDA-GluN2B contributes to enhance the modulation of existing fear memory traces in juvenile rats. (A) Schematic describing the behavioral timeline for the retrieval-dependent memory destabilization experiment using rats conditioned with four tones (Top). Immediately following the memory retrieval, the rats infused with TAT-Pep5, K252a or vehicle into the prelimbic cortex 15 min prior to the mBDNF, proBDNF or vehicle infusion. Two days later, PR-LTM was assessed by exposed the rats to the novel context. Similar, no significant difference in the percentage freezing during the memory retrieval but the percentage freezing level during the PR-LTM test was significant lower in juvenile group than adult group (Bottom). No obvious effect of mBDNF on freeze behavior was found. Infusions of p75 NTR blocker TAT-Pep5 could significantly enhance the percentage of freeze behavior. Meanwhile, infusions of TAT-Pep5, but not K252a, markedly blocked the effects of proBDNF treatment. (* P

    Article Snippet: Needles were inserted into bilateral cannulae and then cleavage-resistant proBDNF (2 ng/ml; Cat#B257 Alomone Labs), anti-proBDNF antibody (10 μg/μL; Cat#ANT-006, Alomone Labs), TAT-Pep5 (4 ng/μL; Cat#506181, EMD Millipore), K252a (25 μg/μL; Cat#82497; Sigma-Aldrich), 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP; 32 ng/μL; Cat#01773, Tocris Bioscience), NVP-AAM077 (0.8 ng/μL; Cat#P1999, Sigma-Aldrich), Ro25-6981 (2.0 ng/μL; Cat#1594, Tocris Bioscience), mature BDNF (1.5 μg/mL; Cat#B250; Alomone Labs) or artificial CSF (ACSF, Cat#3525, Tocris Bioscience) into prelimbic area (at a rate of 0.5 μL/min/side for 2 min) was infused immediately or one day following memory retrieval.

    Techniques:

    proBNDF-mediated p75NTR activation in cortical PV cells reduces their perisomatic boutons. A , Experimental approach. B , The intensity of perisomatic PV immunostaining (green) is reduced in the binocular visual cortex ipsilateral to the minipump-releasing mut-proBDNF (Ipsi) compared with the contralateral cortex (Contra) in the same animal. On the other hand, perisomatic PV intensity in the ipsilateral cortex of PV_Cre;p75 flx/flx mice is similar to that observed in the contralateral, untreated cortex. C , Low ( C1 ) and high ( C2 ) magnification of PNN (red, WFA staining) enwrapping PV cells (green) shows a dramatic reduction in both PNN density and intensity in the visual cortex infused with mut-proBFNF. This effect is abolished in PV_Cre;p75 flx/flx mice. Scale bars: C1 , 100 μm; B , C2 , 10 μm. D , Quantification of the mean intensity of perisomatic PV-positive puncta in ipsilateral compared with contralateral cortex. I/C ratio is obtained for each animal and then averaged between different animals. Mean I/C ratio is significantly reduced in Mut-proBDNF-infused p75 Ctrl mice compared with Mut-proBDNF-infused PV_Cre;p75 flx/flx mice (unpaired t test, df = 8, t = 6.077, p = 0.0003). E , The ratio of mean PNN intensity around PV cells in ipsilateral versus contralateral cortex is significantly lower in p75 Ctrl than PV_Cre;p75 flx/flx mice infused with mut-proBDNF (unpaired t test, df = 8, t = 15.33, p

    Journal: The Journal of Neuroscience

    Article Title: p75 Neurotrophin Receptor Activation Regulates the Timing of the Maturation of Cortical Parvalbumin Interneuron Connectivity and Promotes Juvenile-like Plasticity in Adult Visual Cortex

    doi: 10.1523/JNEUROSCI.2881-18.2019

    Figure Lengend Snippet: proBNDF-mediated p75NTR activation in cortical PV cells reduces their perisomatic boutons. A , Experimental approach. B , The intensity of perisomatic PV immunostaining (green) is reduced in the binocular visual cortex ipsilateral to the minipump-releasing mut-proBDNF (Ipsi) compared with the contralateral cortex (Contra) in the same animal. On the other hand, perisomatic PV intensity in the ipsilateral cortex of PV_Cre;p75 flx/flx mice is similar to that observed in the contralateral, untreated cortex. C , Low ( C1 ) and high ( C2 ) magnification of PNN (red, WFA staining) enwrapping PV cells (green) shows a dramatic reduction in both PNN density and intensity in the visual cortex infused with mut-proBFNF. This effect is abolished in PV_Cre;p75 flx/flx mice. Scale bars: C1 , 100 μm; B , C2 , 10 μm. D , Quantification of the mean intensity of perisomatic PV-positive puncta in ipsilateral compared with contralateral cortex. I/C ratio is obtained for each animal and then averaged between different animals. Mean I/C ratio is significantly reduced in Mut-proBDNF-infused p75 Ctrl mice compared with Mut-proBDNF-infused PV_Cre;p75 flx/flx mice (unpaired t test, df = 8, t = 6.077, p = 0.0003). E , The ratio of mean PNN intensity around PV cells in ipsilateral versus contralateral cortex is significantly lower in p75 Ctrl than PV_Cre;p75 flx/flx mice infused with mut-proBDNF (unpaired t test, df = 8, t = 15.33, p

    Article Snippet: Recombinant mouse proneurotrophin, proBDNF (wt-proBDNF, 10 ng/ml, Alomone Labs, catalog #B-240) and cleavage-resistant, recombinant mouse proBDNF (mut-proBDNF, 10 ng/ml, Alomone Labs, catalog #B-243) were, respectively, added with the culture medium during the specific time window indicated in Results.

    Techniques: Activation Assay, Immunostaining, Mouse Assay, Staining

    Modulation of tPA activity affects the formation of PV cell innervations during early postnatal development. A , Control EP18 PV cell ( A1 , green represents Ctrl). B , PV cell treated with the tPA inhibitor PPACK from EP10–EP18 shows simpler axonal arborization, contacting less potential targets ( B2 , blue represents NeuN-positive somata). C , PV cell treated with tPA in the same time window shows a very complex axonal arbor ( C2 ) and an increase in both terminal branching and perisomatic boutons ( C3 , arrowheads) compared with control cells ( A2 , A3 ). D , PV cell treated simultaneously with tPA and mut-proBDNF shows axonal branching and perisomatic innervation more similar to those formed by PV cell treated with mut-proBDNF alone, suggesting that the effects of tPA application may be mediated by a decrease in endogenous proBDNF/mBDNF ratio. Stars indicate NeuN-positive somata that are not innervated. Scale bars: A1–D1 , 50 μm; A2–D2 , 10 μm; A3–D3 , 5 μm. E , Perisomatic boutons density (one-way ANOVA, F (3,20) = 121.2, p

    Journal: The Journal of Neuroscience

    Article Title: p75 Neurotrophin Receptor Activation Regulates the Timing of the Maturation of Cortical Parvalbumin Interneuron Connectivity and Promotes Juvenile-like Plasticity in Adult Visual Cortex

    doi: 10.1523/JNEUROSCI.2881-18.2019

    Figure Lengend Snippet: Modulation of tPA activity affects the formation of PV cell innervations during early postnatal development. A , Control EP18 PV cell ( A1 , green represents Ctrl). B , PV cell treated with the tPA inhibitor PPACK from EP10–EP18 shows simpler axonal arborization, contacting less potential targets ( B2 , blue represents NeuN-positive somata). C , PV cell treated with tPA in the same time window shows a very complex axonal arbor ( C2 ) and an increase in both terminal branching and perisomatic boutons ( C3 , arrowheads) compared with control cells ( A2 , A3 ). D , PV cell treated simultaneously with tPA and mut-proBDNF shows axonal branching and perisomatic innervation more similar to those formed by PV cell treated with mut-proBDNF alone, suggesting that the effects of tPA application may be mediated by a decrease in endogenous proBDNF/mBDNF ratio. Stars indicate NeuN-positive somata that are not innervated. Scale bars: A1–D1 , 50 μm; A2–D2 , 10 μm; A3–D3 , 5 μm. E , Perisomatic boutons density (one-way ANOVA, F (3,20) = 121.2, p

    Article Snippet: Recombinant mouse proneurotrophin, proBDNF (wt-proBDNF, 10 ng/ml, Alomone Labs, catalog #B-240) and cleavage-resistant, recombinant mouse proBDNF (mut-proBDNF, 10 ng/ml, Alomone Labs, catalog #B-243) were, respectively, added with the culture medium during the specific time window indicated in Results.

    Techniques: Activity Assay

    proBNDF-mediated p75NTR activation in cortical PV cells restores ocular dominance plasticity in adult visual cortex in vivo . A , Typical VEP responses to the stimulation of either contralateral (blue) or ipsilateral (red) eye to the cortex in which the recording is performed in p75NTR Ctrl mice infused with either vehicle or mut-proBDNF, and PV_Cre;p75NTR flx/flx mice infused with mut-proBDNF. Calibration bars: 50 μV, 100 ms. B , C/I VEP ratio mean values. Three days of monocular deprivation do not affect the C/I VEP ratio in adult mice, although it leads to a significant decrease in the C/I VEP ratio in animals treated with mut-proBDNF. Mut-proBDNF effects are, however, abolished in PV_Cre;p75 flx/flx mice (one-way ANOVA, F (2,18) = 8.903, p = 0.0021). p75NTR Ctrl + vehicle: n = 9 mice; p75NTR Ctrl + mut-proBDNF: n = 5 mice; PV_Cre;p75 flx/flx +mut-proBDNF: n = 7 mice. C , ODI of p75NTR Ctrl mice infused with vehicle solution and PV_Cre;p75 flx/flx mice infused with mut-proBDNF are not significantly different from those of undeprived animals, whereas ODIs in p75 Ctrl mice treated with mut-proBDNF are significantly shifted toward the open eye (one-way ANOVA, F (2,443) = 5.203, p = 0.0058). D , Mean spontaneous discharge is significantly increased only in p75 Ctrl mice treated with mut-proBDNF (one-way ANOVA, F (2,443) = 4.580, p = 0.0107). p75NTR Ctrl + vehicle: n = 9 mice, 174 cells; p75NTR Ctrl + mut-proBDNF: n = 5 mice, 147 cells; PV_Cre;p75 flx/flx +mut-proBDNF: n = 6 mice, 125 cells. Gray area represents the C/I VEP ratio ( B ) or the ODI range ( C ) (mean ± SEM) in adult nondeprived animals ( n = 5 mice, 99 cells). * indicate p

    Journal: The Journal of Neuroscience

    Article Title: p75 Neurotrophin Receptor Activation Regulates the Timing of the Maturation of Cortical Parvalbumin Interneuron Connectivity and Promotes Juvenile-like Plasticity in Adult Visual Cortex

    doi: 10.1523/JNEUROSCI.2881-18.2019

    Figure Lengend Snippet: proBNDF-mediated p75NTR activation in cortical PV cells restores ocular dominance plasticity in adult visual cortex in vivo . A , Typical VEP responses to the stimulation of either contralateral (blue) or ipsilateral (red) eye to the cortex in which the recording is performed in p75NTR Ctrl mice infused with either vehicle or mut-proBDNF, and PV_Cre;p75NTR flx/flx mice infused with mut-proBDNF. Calibration bars: 50 μV, 100 ms. B , C/I VEP ratio mean values. Three days of monocular deprivation do not affect the C/I VEP ratio in adult mice, although it leads to a significant decrease in the C/I VEP ratio in animals treated with mut-proBDNF. Mut-proBDNF effects are, however, abolished in PV_Cre;p75 flx/flx mice (one-way ANOVA, F (2,18) = 8.903, p = 0.0021). p75NTR Ctrl + vehicle: n = 9 mice; p75NTR Ctrl + mut-proBDNF: n = 5 mice; PV_Cre;p75 flx/flx +mut-proBDNF: n = 7 mice. C , ODI of p75NTR Ctrl mice infused with vehicle solution and PV_Cre;p75 flx/flx mice infused with mut-proBDNF are not significantly different from those of undeprived animals, whereas ODIs in p75 Ctrl mice treated with mut-proBDNF are significantly shifted toward the open eye (one-way ANOVA, F (2,443) = 5.203, p = 0.0058). D , Mean spontaneous discharge is significantly increased only in p75 Ctrl mice treated with mut-proBDNF (one-way ANOVA, F (2,443) = 4.580, p = 0.0107). p75NTR Ctrl + vehicle: n = 9 mice, 174 cells; p75NTR Ctrl + mut-proBDNF: n = 5 mice, 147 cells; PV_Cre;p75 flx/flx +mut-proBDNF: n = 6 mice, 125 cells. Gray area represents the C/I VEP ratio ( B ) or the ODI range ( C ) (mean ± SEM) in adult nondeprived animals ( n = 5 mice, 99 cells). * indicate p

    Article Snippet: Recombinant mouse proneurotrophin, proBDNF (wt-proBDNF, 10 ng/ml, Alomone Labs, catalog #B-240) and cleavage-resistant, recombinant mouse proBDNF (mut-proBDNF, 10 ng/ml, Alomone Labs, catalog #B-243) were, respectively, added with the culture medium during the specific time window indicated in Results.

    Techniques: Activation Assay, In Vivo, Mouse Assay

    mut-proBDNF destabilizes PV cell innervation, even after it has reached maturity. A , Control PV cell ( A1 , Ctrl, green) at EP32 with exuberant innervation field characterized by extensive branching contacting the majority of potential targets, dense boutons along axons ( A2 ), and terminal branches with prominent and clustered boutons ( A3 ; arrowheads) around NeuN-positive somata (blue). B , PV cell treated with wt-proBDNF from EP26-EP32 shows overall similar axon size ( B1 ), percentage of potentially targeted neurons ( B2 ), and perisomatic innervations ( B3 ) as control, untreated PV cells. C , PV cell treated with mut-proBDNF from EP26-EP32 shows a drastic reduction both in percentage of innervated cells ( C2 ) and perisomatic innervation ( C3 ). Stars indicate NeuN-positive somata that are not innervated. Scale bars: A1–C1 , 50 μm; A2–C2 , 10 μm; A3–C3 , 5 μm. D , Perisomatic bouton density (one-way ANOVA, F (2,18) = 93.34, p

    Journal: The Journal of Neuroscience

    Article Title: p75 Neurotrophin Receptor Activation Regulates the Timing of the Maturation of Cortical Parvalbumin Interneuron Connectivity and Promotes Juvenile-like Plasticity in Adult Visual Cortex

    doi: 10.1523/JNEUROSCI.2881-18.2019

    Figure Lengend Snippet: mut-proBDNF destabilizes PV cell innervation, even after it has reached maturity. A , Control PV cell ( A1 , Ctrl, green) at EP32 with exuberant innervation field characterized by extensive branching contacting the majority of potential targets, dense boutons along axons ( A2 ), and terminal branches with prominent and clustered boutons ( A3 ; arrowheads) around NeuN-positive somata (blue). B , PV cell treated with wt-proBDNF from EP26-EP32 shows overall similar axon size ( B1 ), percentage of potentially targeted neurons ( B2 ), and perisomatic innervations ( B3 ) as control, untreated PV cells. C , PV cell treated with mut-proBDNF from EP26-EP32 shows a drastic reduction both in percentage of innervated cells ( C2 ) and perisomatic innervation ( C3 ). Stars indicate NeuN-positive somata that are not innervated. Scale bars: A1–C1 , 50 μm; A2–C2 , 10 μm; A3–C3 , 5 μm. D , Perisomatic bouton density (one-way ANOVA, F (2,18) = 93.34, p

    Article Snippet: Recombinant mouse proneurotrophin, proBDNF (wt-proBDNF, 10 ng/ml, Alomone Labs, catalog #B-240) and cleavage-resistant, recombinant mouse proBDNF (mut-proBDNF, 10 ng/ml, Alomone Labs, catalog #B-243) were, respectively, added with the culture medium during the specific time window indicated in Results.

    Techniques:

    Paracrine actions of proBDNF on GABAergic synaptic activity. Schematic representation of the steps leading to the p75 NTR -dependent LLP GABA-A and LLD GABA-A . CA3 pyramidal cells release proBDNF in response to the activation of L-type Ca 2+ channel during

    Journal: Cerebral Cortex (New York, NY)

    Article Title: NMDA-Dependent Switch of proBDNF Actions on Developing GABAergic Synapses

    doi: 10.1093/cercor/bhs071

    Figure Lengend Snippet: Paracrine actions of proBDNF on GABAergic synaptic activity. Schematic representation of the steps leading to the p75 NTR -dependent LLP GABA-A and LLD GABA-A . CA3 pyramidal cells release proBDNF in response to the activation of L-type Ca 2+ channel during

    Article Snippet: 1,2,3,4-Tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamide (NBQX), Gabazin, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate (MK801) and D-2-amino-5-phosphovaleric acid (D-AP5) (Tocris Cookson); k252a, TAT-pep5 (Calbiochem); Nifedipine, aprotinin (Sigma); p75NTR antibody (ab1554, Millipore); cleavage-resistant (CR) proBDNF, mBDNF (Alomone labs); TrkA-IgG, TrkB-IgG (R & D system).

    Techniques: Activity Assay, Activation Assay

    Endogenous activation of p75 NTR is required for LLD GABA-A induction. ( A ) Immunofluorescence detection of proBDNF and p75 NTR in a 4-days-old rat hippocampi (red signal, upper images), superimposed on neuro-tracer immunofluorescence (Nt, green signal, lower

    Journal: Cerebral Cortex (New York, NY)

    Article Title: NMDA-Dependent Switch of proBDNF Actions on Developing GABAergic Synapses

    doi: 10.1093/cercor/bhs071

    Figure Lengend Snippet: Endogenous activation of p75 NTR is required for LLD GABA-A induction. ( A ) Immunofluorescence detection of proBDNF and p75 NTR in a 4-days-old rat hippocampi (red signal, upper images), superimposed on neuro-tracer immunofluorescence (Nt, green signal, lower

    Article Snippet: 1,2,3,4-Tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamide (NBQX), Gabazin, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate (MK801) and D-2-amino-5-phosphovaleric acid (D-AP5) (Tocris Cookson); k252a, TAT-pep5 (Calbiochem); Nifedipine, aprotinin (Sigma); p75NTR antibody (ab1554, Millipore); cleavage-resistant (CR) proBDNF, mBDNF (Alomone labs); TrkA-IgG, TrkB-IgG (R & D system).

    Techniques: Activation Assay, Immunofluorescence

    Regulated secretion of proBDNF is required for LLD GABA-A induction. ( A ) Average time course of sGABA A -PSCs frequency before and after activity recovery with aprotinin and nifedipine (10 μM) in the absence (control, open symbol, n = 6) or the presence

    Journal: Cerebral Cortex (New York, NY)

    Article Title: NMDA-Dependent Switch of proBDNF Actions on Developing GABAergic Synapses

    doi: 10.1093/cercor/bhs071

    Figure Lengend Snippet: Regulated secretion of proBDNF is required for LLD GABA-A induction. ( A ) Average time course of sGABA A -PSCs frequency before and after activity recovery with aprotinin and nifedipine (10 μM) in the absence (control, open symbol, n = 6) or the presence

    Article Snippet: 1,2,3,4-Tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamide (NBQX), Gabazin, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate (MK801) and D-2-amino-5-phosphovaleric acid (D-AP5) (Tocris Cookson); k252a, TAT-pep5 (Calbiochem); Nifedipine, aprotinin (Sigma); p75NTR antibody (ab1554, Millipore); cleavage-resistant (CR) proBDNF, mBDNF (Alomone labs); TrkA-IgG, TrkB-IgG (R & D system).

    Techniques: Activity Assay