anti probdnf  (Alomone Labs)


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    Alomone Labs anti probdnf
    Dexmedetomidine could decrease the level of <t>proBDNF</t> and restore the ratio of proBDNF/mBDNF and alleviates activation of the proBDNF-P75NRT-RHOA pathway after sevoflurane. (a) Western blot band. (b) ProBDNF/mBDNF. (c–e) Bar graph of Western blot. (f) Immunofluorescence of proBDNF (scale bar = 50 μ m). ∗ Compare with the control group, P
    Anti Probdnf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti probdnf/product/Alomone Labs
    Average 95 stars, based on 10 article reviews
    Price from $9.99 to $1999.99
    anti probdnf - by Bioz Stars, 2022-12
    95/100 stars

    Images

    1) Product Images from "Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway"

    Article Title: Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway

    Journal: Mediators of Inflammation

    doi: 10.1155/2020/5458061

    Dexmedetomidine could decrease the level of proBDNF and restore the ratio of proBDNF/mBDNF and alleviates activation of the proBDNF-P75NRT-RHOA pathway after sevoflurane. (a) Western blot band. (b) ProBDNF/mBDNF. (c–e) Bar graph of Western blot. (f) Immunofluorescence of proBDNF (scale bar = 50 μ m). ∗ Compare with the control group, P
    Figure Legend Snippet: Dexmedetomidine could decrease the level of proBDNF and restore the ratio of proBDNF/mBDNF and alleviates activation of the proBDNF-P75NRT-RHOA pathway after sevoflurane. (a) Western blot band. (b) ProBDNF/mBDNF. (c–e) Bar graph of Western blot. (f) Immunofluorescence of proBDNF (scale bar = 50 μ m). ∗ Compare with the control group, P

    Techniques Used: Activation Assay, Western Blot, Immunofluorescence

    2) Product Images from "Proneurotrophins Induce Apoptotic Neuronal Death After Controlled Cortical Impact Injury in Adult Mice"

    Article Title: Proneurotrophins Induce Apoptotic Neuronal Death After Controlled Cortical Impact Injury in Adult Mice

    Journal: ASN NEURO

    doi: 10.1177/1759091420930865

    proBDNF Is Induced in Astrocytes After TBI. Adult mice were subjected to CCI and perfused 3 days after injury. Representative sections through the injury site 3 days after CCI show increased proBDNF labeling (red), some of which colocalizes with GFAP (green) adjacent to the area of tissue damage. In contrast, sections through the contralateral side 3 days after the injury show little expression of proBDNF. (A) Arrows indicate colocalization of proBDNF and GFAP-positive cells. (B) Arrowheads indicate GFAP-positive cells that do not express proBDNF. Scale bar = 50 µm. GFAP = glial fibrillary acidic protein; proBDNF = pro-brain-derived neurotrophic factor.
    Figure Legend Snippet: proBDNF Is Induced in Astrocytes After TBI. Adult mice were subjected to CCI and perfused 3 days after injury. Representative sections through the injury site 3 days after CCI show increased proBDNF labeling (red), some of which colocalizes with GFAP (green) adjacent to the area of tissue damage. In contrast, sections through the contralateral side 3 days after the injury show little expression of proBDNF. (A) Arrows indicate colocalization of proBDNF and GFAP-positive cells. (B) Arrowheads indicate GFAP-positive cells that do not express proBDNF. Scale bar = 50 µm. GFAP = glial fibrillary acidic protein; proBDNF = pro-brain-derived neurotrophic factor.

    Techniques Used: Mouse Assay, Labeling, Expressing, Derivative Assay

    Behavioral Analysis of Mice Receiving Intranasal Neutralizing Antibodies to proNGF or proBDNF Following CCI. (A) Outline of the experimental paradigm of CCI injury and behavioral testing. Control IgG, anti-proNGF, or anti-proBDNF was infused intranasally to each nostril every 2 min for a total of 20 µl immediately after CCI. (B) The mNSS score showed behavioral sparing of mice that received either anti-proNGF or anti-proBDNF compared with mice that received control IgG following CCI. Data were collected across 5 to 8 animals per group. Asterisks indicate significant difference from IgG control by Kruskal–Wallis test followed by Dunn’s multiple comparison test for nonparametric values, with p = .0204 for IgG control versus proNGF-treated mice; p = .045 for IgG control versus proBDNF-treated mice. CCI = controlled cortical impact; mNSS = modified neurological severity scoring; IgG = immunoglobulin G; BDNF = brain-derived neurotrophic factor; NGF = nerve growth factor.
    Figure Legend Snippet: Behavioral Analysis of Mice Receiving Intranasal Neutralizing Antibodies to proNGF or proBDNF Following CCI. (A) Outline of the experimental paradigm of CCI injury and behavioral testing. Control IgG, anti-proNGF, or anti-proBDNF was infused intranasally to each nostril every 2 min for a total of 20 µl immediately after CCI. (B) The mNSS score showed behavioral sparing of mice that received either anti-proNGF or anti-proBDNF compared with mice that received control IgG following CCI. Data were collected across 5 to 8 animals per group. Asterisks indicate significant difference from IgG control by Kruskal–Wallis test followed by Dunn’s multiple comparison test for nonparametric values, with p = .0204 for IgG control versus proNGF-treated mice; p = .045 for IgG control versus proBDNF-treated mice. CCI = controlled cortical impact; mNSS = modified neurological severity scoring; IgG = immunoglobulin G; BDNF = brain-derived neurotrophic factor; NGF = nerve growth factor.

    Techniques Used: Mouse Assay, Modification, Derivative Assay

    Neutralizing Antibodies to proNGF and proBDNF Provide Neuroprotection. (A) Mice were infused intranasally with anti-proNGF, anti-proBDNF, or control IgG immediately after the CCI. At 3 days of recovery, sections were stained for NeuN and counterstained with DAPI to reveal the area of damage. (B) The area of total damage comprised of the area of tissue loss and the penumbra (dotted line), where the density of DAPI and NeuN staining was reduced. The percentage of the total area of damage (relative to the contralateral hemisphere) was significantly reduced by the antiproneurotrophin antibodies. Scale bar = 200 µm. (C) Representative images of TUNEL staining in the penumbra showed fewer apoptotic cells in the mice that received anti-proNGF or anti-proBDNF. Scale bar = 50 µm. Data were collected from 3 to 4 animals per group. Graphs depict the means ± SEM. Asterisks indicate significance by one-way analysis of variance followed by Tukey’s post hoc analysis with p
    Figure Legend Snippet: Neutralizing Antibodies to proNGF and proBDNF Provide Neuroprotection. (A) Mice were infused intranasally with anti-proNGF, anti-proBDNF, or control IgG immediately after the CCI. At 3 days of recovery, sections were stained for NeuN and counterstained with DAPI to reveal the area of damage. (B) The area of total damage comprised of the area of tissue loss and the penumbra (dotted line), where the density of DAPI and NeuN staining was reduced. The percentage of the total area of damage (relative to the contralateral hemisphere) was significantly reduced by the antiproneurotrophin antibodies. Scale bar = 200 µm. (C) Representative images of TUNEL staining in the penumbra showed fewer apoptotic cells in the mice that received anti-proNGF or anti-proBDNF. Scale bar = 50 µm. Data were collected from 3 to 4 animals per group. Graphs depict the means ± SEM. Asterisks indicate significance by one-way analysis of variance followed by Tukey’s post hoc analysis with p

    Techniques Used: Mouse Assay, Staining, TUNEL Assay

    3) Product Images from "Extracellular Vesicles Derived from Lactobacillus plantarum Increase BDNF Expression in Cultured Hippocampal Neurons and Produce Antidepressant-like Effects in Mice"

    Article Title: Extracellular Vesicles Derived from Lactobacillus plantarum Increase BDNF Expression in Cultured Hippocampal Neurons and Produce Antidepressant-like Effects in Mice

    Journal: Experimental Neurobiology

    doi: 10.5607/en.2019.28.2.158

    L -EV treatment during the stress-treatment period blocked the stress-induced decrease in the expression of neurotrophic factors in the hippocampus and inhibited stress-induced depressive-like behaviors. (A) Experimental design (Exp. 1). Mice were treated with restraint for 2-h daily for 14 days (2h×14 d RST). Saline or L -EV (0.1 µg/kg) were i.p. injected 30 min before restraint treatment each day. Behavioral tests were performed on post-stress days 1-3 ( p 1~ p 3) and mice were sacrificed on post-stress day 7 ( p 7). Control mice injected with saline (CON+veh), mice treated with L -EV (CON+ L -EV), mice treated with repeated restraint and injected with saline (CRST+veh), and mice treated with repeated restraint and injected with L -EV (CRST+ L -EV) were prepared. (B) Body weight (g) changes of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=8~12 animals per group). (C) Expression levels of Ngf , t Bdnf , Bdnf1 , Bdnf4 , Nt3 , Nt4/5 , and Trkb in the hippocampus of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=6 animals and 4~8 PCR repeats per group). Two-way ANOVA followed by Bonferroni post hoc test ( Ngf , F (1,28) =2.900 and p=0.0997 for CRST main effect, F (1,28) =0.6187 and p=0.4381 for L -EV main effect, and F (1,28) =1.024 and p=0.3202 for CRST× L -EV; t Bdnf , F (1,25) =0.2452 and p=0.6248 for CRST main effect, F (1,25) =15.43 and p=0.0006 for L -EV main effect, and F (1,25) =1.932 and p=0.1768 for CRST× L -EV; Bdnf1 , F (1,12) =9.542 and p=0.0094 for CRST main effect, F (1,12) =15.01 and p=0.0022 for L -EV main effect, and F (1,12) =2.324 and p=0.1533 for CRST× L -EV; Bdnf4 , F (1,12) =13.95 and p=0.0028 for CRST main effect, F (1,12) =9.418 and p=0.0097 for L -EV main effect, and F (1,12) =8.003 and p=0.0152 for CRST× L -EV; Nt3 , F (1,28) 0.9424 and p=0.3400 for CRST main effect, F (1,28) =0.1996 and p=0.6585 for L -EV main effect, and F (1,28) =1.974 and p=0.1710 for CRST× L -EV; Nt4/5 , F (1,24) =14.45 and p=0.0009 for CRST main effect, F (1,24) =1.654 and p=0.2106 for L -EV main effect, and F (1,24) =8.419 and p=0.0078 for CRST× L -EV; Trkb , F (1,14) =0.0650 and p=0.8025 for CRST main effect, F (1,14) =1.768 and p=0.2049 for L -EV main effect, and F (1,14) =2.969 and p=0.1069 for CRST× L -EV). (D) Western blot data showing the expression level of proBDNF in the hippocampus of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=6 animals and 4 WB repeats per group). Two-way ANOVA followed by Bonferroni post hoc test (F (1,12) =12.29 and p=0.0043 for CRST main effect, F (1,12) =1.697 and p=0.2172 for L -EV main effect, and F (1,12) =8.952 and p=0.0112 for CRST× L -EV). (E) Expression levels of Sirt1 , Hdac2 , and Creb1 in the hippocampus of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=6 animals and 6–10 PCR repeats per group). Two-way ANOVA followed by Bonferroni post hoc test ( Sirt1 , F (1,23) =6.483 and p=0.0181 for CRST main effect, F (1,23) =12.17 and p=0.0020 for L -EV main effect, and F (1,23) =2.365 and p=0.1377 for CRST× L -EV; Hdac2 , F (1,25) =10.31 and p=0.0036 for CRST main effect, F (1,25) =5.110 and p=0.0327 for L -EV main effect, and F (1,25) =1.340 and p=0.2280 for CRST× L -EV; Creb1 , F (1,22) =0.2456 and p=0.6251 for CRST main effect, F (1,22) =2.829 and p=0.1067 for L -EV main effect, and F (1,22) =1.358 and p=0.2564 for CRST× L -EV). (F, G) Immobility time in the tail suspension test (TST; F) and forced swim test (FST; G) of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=7~12 animals per group). Two-way ANOVA followed by Bonferroni post hoc test (TST, F (1,33) =11.90 and p=0.0016 for CRST main effect, F (1,33) =6.235 and p=0.0177 for L -EV main effect, and F (1,33) =1.665 and p=0.2059 for CRST× L -EV; FST, F (1,36) =23.84 and p
    Figure Legend Snippet: L -EV treatment during the stress-treatment period blocked the stress-induced decrease in the expression of neurotrophic factors in the hippocampus and inhibited stress-induced depressive-like behaviors. (A) Experimental design (Exp. 1). Mice were treated with restraint for 2-h daily for 14 days (2h×14 d RST). Saline or L -EV (0.1 µg/kg) were i.p. injected 30 min before restraint treatment each day. Behavioral tests were performed on post-stress days 1-3 ( p 1~ p 3) and mice were sacrificed on post-stress day 7 ( p 7). Control mice injected with saline (CON+veh), mice treated with L -EV (CON+ L -EV), mice treated with repeated restraint and injected with saline (CRST+veh), and mice treated with repeated restraint and injected with L -EV (CRST+ L -EV) were prepared. (B) Body weight (g) changes of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=8~12 animals per group). (C) Expression levels of Ngf , t Bdnf , Bdnf1 , Bdnf4 , Nt3 , Nt4/5 , and Trkb in the hippocampus of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=6 animals and 4~8 PCR repeats per group). Two-way ANOVA followed by Bonferroni post hoc test ( Ngf , F (1,28) =2.900 and p=0.0997 for CRST main effect, F (1,28) =0.6187 and p=0.4381 for L -EV main effect, and F (1,28) =1.024 and p=0.3202 for CRST× L -EV; t Bdnf , F (1,25) =0.2452 and p=0.6248 for CRST main effect, F (1,25) =15.43 and p=0.0006 for L -EV main effect, and F (1,25) =1.932 and p=0.1768 for CRST× L -EV; Bdnf1 , F (1,12) =9.542 and p=0.0094 for CRST main effect, F (1,12) =15.01 and p=0.0022 for L -EV main effect, and F (1,12) =2.324 and p=0.1533 for CRST× L -EV; Bdnf4 , F (1,12) =13.95 and p=0.0028 for CRST main effect, F (1,12) =9.418 and p=0.0097 for L -EV main effect, and F (1,12) =8.003 and p=0.0152 for CRST× L -EV; Nt3 , F (1,28) 0.9424 and p=0.3400 for CRST main effect, F (1,28) =0.1996 and p=0.6585 for L -EV main effect, and F (1,28) =1.974 and p=0.1710 for CRST× L -EV; Nt4/5 , F (1,24) =14.45 and p=0.0009 for CRST main effect, F (1,24) =1.654 and p=0.2106 for L -EV main effect, and F (1,24) =8.419 and p=0.0078 for CRST× L -EV; Trkb , F (1,14) =0.0650 and p=0.8025 for CRST main effect, F (1,14) =1.768 and p=0.2049 for L -EV main effect, and F (1,14) =2.969 and p=0.1069 for CRST× L -EV). (D) Western blot data showing the expression level of proBDNF in the hippocampus of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=6 animals and 4 WB repeats per group). Two-way ANOVA followed by Bonferroni post hoc test (F (1,12) =12.29 and p=0.0043 for CRST main effect, F (1,12) =1.697 and p=0.2172 for L -EV main effect, and F (1,12) =8.952 and p=0.0112 for CRST× L -EV). (E) Expression levels of Sirt1 , Hdac2 , and Creb1 in the hippocampus of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=6 animals and 6–10 PCR repeats per group). Two-way ANOVA followed by Bonferroni post hoc test ( Sirt1 , F (1,23) =6.483 and p=0.0181 for CRST main effect, F (1,23) =12.17 and p=0.0020 for L -EV main effect, and F (1,23) =2.365 and p=0.1377 for CRST× L -EV; Hdac2 , F (1,25) =10.31 and p=0.0036 for CRST main effect, F (1,25) =5.110 and p=0.0327 for L -EV main effect, and F (1,25) =1.340 and p=0.2280 for CRST× L -EV; Creb1 , F (1,22) =0.2456 and p=0.6251 for CRST main effect, F (1,22) =2.829 and p=0.1067 for L -EV main effect, and F (1,22) =1.358 and p=0.2564 for CRST× L -EV). (F, G) Immobility time in the tail suspension test (TST; F) and forced swim test (FST; G) of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=7~12 animals per group). Two-way ANOVA followed by Bonferroni post hoc test (TST, F (1,33) =11.90 and p=0.0016 for CRST main effect, F (1,33) =6.235 and p=0.0177 for L -EV main effect, and F (1,33) =1.665 and p=0.2059 for CRST× L -EV; FST, F (1,36) =23.84 and p

    Techniques Used: Expressing, Mouse Assay, Injection, Polymerase Chain Reaction, Western Blot

    4) Product Images from "Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior"

    Article Title: Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2018.00863

    Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p
    Figure Legend Snippet: Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    5) Product Images from "Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior"

    Article Title: Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2018.00863

    Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p
    Figure Legend Snippet: Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    6) Product Images from "Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior"

    Article Title: Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2018.00863

    Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p
    Figure Legend Snippet: Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    7) Product Images from "Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior"

    Article Title: Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2018.00863

    Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p
    Figure Legend Snippet: Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p

    Techniques Used: Western Blot, Expressing, Mouse Assay

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    Alomone Labs b 257 human probdnf
    B 257 Human Probdnf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/b 257 human probdnf/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    b 257 human probdnf - by Bioz Stars, 2022-12
    94/100 stars
      Buy from Supplier

    94
    Alomone Labs anti probdnf antibody
    The increase <t>proBDNF</t> 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
    Anti Probdnf Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti probdnf antibody/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti probdnf antibody - by Bioz Stars, 2022-12
    94/100 stars
      Buy from Supplier

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    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: