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k channel blocker 4 aminopyridine  (Tocris)


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    Structured Review

    Tocris k channel blocker 4 aminopyridine
    K Channel Blocker 4 Aminopyridine, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 452 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/k+channel+blocker+4+aminopyridine/4-Aminopyridine/pm38992824-65-8-14
    Average 95 stars, based on 452 article reviews
    k channel blocker 4 aminopyridine - by Bioz Stars, 2026-10
    95/100 stars

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    Related Articles

    Morphology:

    Article Title: Compromised Hippocampal Neuroplasticity in the Interferon-α and Toll-like Receptor-3 Activation-Induced Mouse Depression Model
    Article Snippet: .. To study the effects of IFN-α and poly(I:C) on neuronal morphology, synapse formation, and depolarization in vitro, IFN-α (100 IU/mL), poly(I:C) (1 μg/mL), or IFN-α (100 IU/mL) and poly(I:C) (1 μg/mL) dissolved in Neurobasal medium were administered over 24 h. A subset of cells were additionally treated with K + channel blocker 4-aminopyridine (4-AP; 2.5 mM; Tocris Bioscience, Wiesbaden-Nordenstadt, Germany) [ ] for 1 h before protein extraction or fixation for immunocytochemistry studies. ..

    Article Title: Compromised Hippocampal Neuroplasticity in the Interferon-α and Toll-like Receptor-3 Activation-Induced Mouse Depression Model.
    Article Snippet: .. To study the effects of IFN-α and poly(I:C) on neuronal morphology, synapse formation, and depolarization in vitro, IFN-α (100 IU/mL), poly(I:C) (1 μg/mL), or IFN-α (100 IU/mL) and poly(I:C) (1 μg/mL) dissolved in Neurobasal medium were administered over 24 h. A subset of cells were additionally treated with K+ channel blocker 4-aminopyridine (4-AP; 2.5 mM; Tocris Bioscience, Wiesbaden-Nordenstadt, Germany) [16] for 1 h before protein extraction or fixation for immunocytochemistry studies. ..

    In Vitro:

    Article Title: Compromised Hippocampal Neuroplasticity in the Interferon-α and Toll-like Receptor-3 Activation-Induced Mouse Depression Model
    Article Snippet: .. To study the effects of IFN-α and poly(I:C) on neuronal morphology, synapse formation, and depolarization in vitro, IFN-α (100 IU/mL), poly(I:C) (1 μg/mL), or IFN-α (100 IU/mL) and poly(I:C) (1 μg/mL) dissolved in Neurobasal medium were administered over 24 h. A subset of cells were additionally treated with K + channel blocker 4-aminopyridine (4-AP; 2.5 mM; Tocris Bioscience, Wiesbaden-Nordenstadt, Germany) [ ] for 1 h before protein extraction or fixation for immunocytochemistry studies. ..

    Article Title: Compromised Hippocampal Neuroplasticity in the Interferon-α and Toll-like Receptor-3 Activation-Induced Mouse Depression Model.
    Article Snippet: .. To study the effects of IFN-α and poly(I:C) on neuronal morphology, synapse formation, and depolarization in vitro, IFN-α (100 IU/mL), poly(I:C) (1 μg/mL), or IFN-α (100 IU/mL) and poly(I:C) (1 μg/mL) dissolved in Neurobasal medium were administered over 24 h. A subset of cells were additionally treated with K+ channel blocker 4-aminopyridine (4-AP; 2.5 mM; Tocris Bioscience, Wiesbaden-Nordenstadt, Germany) [16] for 1 h before protein extraction or fixation for immunocytochemistry studies. ..

    Protein Extraction:

    Article Title: Compromised Hippocampal Neuroplasticity in the Interferon-α and Toll-like Receptor-3 Activation-Induced Mouse Depression Model
    Article Snippet: .. To study the effects of IFN-α and poly(I:C) on neuronal morphology, synapse formation, and depolarization in vitro, IFN-α (100 IU/mL), poly(I:C) (1 μg/mL), or IFN-α (100 IU/mL) and poly(I:C) (1 μg/mL) dissolved in Neurobasal medium were administered over 24 h. A subset of cells were additionally treated with K + channel blocker 4-aminopyridine (4-AP; 2.5 mM; Tocris Bioscience, Wiesbaden-Nordenstadt, Germany) [ ] for 1 h before protein extraction or fixation for immunocytochemistry studies. ..

    Article Title: Compromised Hippocampal Neuroplasticity in the Interferon-α and Toll-like Receptor-3 Activation-Induced Mouse Depression Model.
    Article Snippet: .. To study the effects of IFN-α and poly(I:C) on neuronal morphology, synapse formation, and depolarization in vitro, IFN-α (100 IU/mL), poly(I:C) (1 μg/mL), or IFN-α (100 IU/mL) and poly(I:C) (1 μg/mL) dissolved in Neurobasal medium were administered over 24 h. A subset of cells were additionally treated with K+ channel blocker 4-aminopyridine (4-AP; 2.5 mM; Tocris Bioscience, Wiesbaden-Nordenstadt, Germany) [16] for 1 h before protein extraction or fixation for immunocytochemistry studies. ..

    Immunocytochemistry:

    Article Title: Compromised Hippocampal Neuroplasticity in the Interferon-α and Toll-like Receptor-3 Activation-Induced Mouse Depression Model
    Article Snippet: .. To study the effects of IFN-α and poly(I:C) on neuronal morphology, synapse formation, and depolarization in vitro, IFN-α (100 IU/mL), poly(I:C) (1 μg/mL), or IFN-α (100 IU/mL) and poly(I:C) (1 μg/mL) dissolved in Neurobasal medium were administered over 24 h. A subset of cells were additionally treated with K + channel blocker 4-aminopyridine (4-AP; 2.5 mM; Tocris Bioscience, Wiesbaden-Nordenstadt, Germany) [ ] for 1 h before protein extraction or fixation for immunocytochemistry studies. ..

    Article Title: Compromised Hippocampal Neuroplasticity in the Interferon-α and Toll-like Receptor-3 Activation-Induced Mouse Depression Model.
    Article Snippet: .. To study the effects of IFN-α and poly(I:C) on neuronal morphology, synapse formation, and depolarization in vitro, IFN-α (100 IU/mL), poly(I:C) (1 μg/mL), or IFN-α (100 IU/mL) and poly(I:C) (1 μg/mL) dissolved in Neurobasal medium were administered over 24 h. A subset of cells were additionally treated with K+ channel blocker 4-aminopyridine (4-AP; 2.5 mM; Tocris Bioscience, Wiesbaden-Nordenstadt, Germany) [16] for 1 h before protein extraction or fixation for immunocytochemistry studies. ..

    other:

    Article Title: Activity-dependent extracellular potassium changes in unmyelinated versus myelinated areas in olfactory regions of the isolated female guinea-pig brain.
    Article Snippet: The potassium released in the extracellular space during neuronal activity is rapidly removed by glia and neurons to maintain tissue homeostasis.. Oligodendrocyte-derived myelin axonal coating contributes to potassium buffering and is therefore crucial to control brain excitability.. We studied activity-dependent extracellular potassium ([K]o) changes in the piriform cortex (PC), a region that features highly segregated bundles of myelinated and unmyelinated fibers.



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    ( A ) Tau4R-GFP biosensor zebrafish larvae subjected to TBI and treated with the convulsant <t>4-AP</t> show no brain puncta. Scale bar = 200 μm. ( B ) 4-AP significantly reduced (apparently eliminated) the abundance of GFP+ puncta in the brain and spinal cord compared to untreated TBI control. Results from alternative doses and timings of 4-AP are reported in . The impact of 4-AP on tauopathy appears to be independent of its actions on post-traumatic seizures because reducing the latter with anti-convulsant retigabine (RTG) had no measurable effect. ( C-F ) Pharmacological inhibition of endocytosis reduced tauopathy following TBI. ( C ) Blocking endocytosis with Pyrimidyn-7 (P7) treatments significantly inhibited the formation of Tau4R-GFP+ puncta following TBI in zebrafish larvae (***p=0.001). ( D ) Dyngo 4a treatment significantly reduced Tau aggregates in the spinal cord (**p=0.0025) in a manner similar to P7. ( E ) 4-AP treatment significantly inhibited the formation of Tau4R-GFP+ puncta in the spinal cord (***p=0.0003) of Tau biosensor line that also express human Tau (0N4R) after traumatic brain injury compared to untreated TBI control group. ( F ) A notable reduction in Tau aggregates was observed in the same line after treatment with P7 drug. Statistical analysis shows no significance difference (ns, p=0.2223) between groups. n = number of larvae. ****p<0.0001, Kruskal-Wallis ANOVA with Dunn’s multiple comparison test used throughout this Figure.
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    ( A ) Tau4R-GFP biosensor zebrafish larvae subjected to TBI and treated with the convulsant <t>4-AP</t> show no brain puncta. Scale bar = 200 μm. ( B ) 4-AP significantly reduced (apparently eliminated) the abundance of GFP+ puncta in the brain and spinal cord compared to untreated TBI control. Results from alternative doses and timings of 4-AP are reported in . The impact of 4-AP on tauopathy appears to be independent of its actions on post-traumatic seizures because reducing the latter with anti-convulsant retigabine (RTG) had no measurable effect. ( C-F ) Pharmacological inhibition of endocytosis reduced tauopathy following TBI. ( C ) Blocking endocytosis with Pyrimidyn-7 (P7) treatments significantly inhibited the formation of Tau4R-GFP+ puncta following TBI in zebrafish larvae (***p=0.001). ( D ) Dyngo 4a treatment significantly reduced Tau aggregates in the spinal cord (**p=0.0025) in a manner similar to P7. ( E ) 4-AP treatment significantly inhibited the formation of Tau4R-GFP+ puncta in the spinal cord (***p=0.0003) of Tau biosensor line that also express human Tau (0N4R) after traumatic brain injury compared to untreated TBI control group. ( F ) A notable reduction in Tau aggregates was observed in the same line after treatment with P7 drug. Statistical analysis shows no significance difference (ns, p=0.2223) between groups. n = number of larvae. ****p<0.0001, Kruskal-Wallis ANOVA with Dunn’s multiple comparison test used throughout this Figure.
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    ( A ) Tau4R-GFP biosensor zebrafish larvae subjected to TBI and treated with the convulsant <t>4-AP</t> show no brain puncta. Scale bar = 200 μm. ( B ) 4-AP significantly reduced (apparently eliminated) the abundance of GFP+ puncta in the brain and spinal cord compared to untreated TBI control. Results from alternative doses and timings of 4-AP are reported in . The impact of 4-AP on tauopathy appears to be independent of its actions on post-traumatic seizures because reducing the latter with anti-convulsant retigabine (RTG) had no measurable effect. ( C-F ) Pharmacological inhibition of endocytosis reduced tauopathy following TBI. ( C ) Blocking endocytosis with Pyrimidyn-7 (P7) treatments significantly inhibited the formation of Tau4R-GFP+ puncta following TBI in zebrafish larvae (***p=0.001). ( D ) Dyngo 4a treatment significantly reduced Tau aggregates in the spinal cord (**p=0.0025) in a manner similar to P7. ( E ) 4-AP treatment significantly inhibited the formation of Tau4R-GFP+ puncta in the spinal cord (***p=0.0003) of Tau biosensor line that also express human Tau (0N4R) after traumatic brain injury compared to untreated TBI control group. ( F ) A notable reduction in Tau aggregates was observed in the same line after treatment with P7 drug. Statistical analysis shows no significance difference (ns, p=0.2223) between groups. n = number of larvae. ****p<0.0001, Kruskal-Wallis ANOVA with Dunn’s multiple comparison test used throughout this Figure.
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    ( A ) Tau4R-GFP biosensor zebrafish larvae subjected to TBI and treated with the convulsant <t>4-AP</t> show no brain puncta. Scale bar = 200 μm. ( B ) 4-AP significantly reduced (apparently eliminated) the abundance of GFP+ puncta in the brain and spinal cord compared to untreated TBI control. Results from alternative doses and timings of 4-AP are reported in . The impact of 4-AP on tauopathy appears to be independent of its actions on post-traumatic seizures because reducing the latter with anti-convulsant retigabine (RTG) had no measurable effect. ( C-F ) Pharmacological inhibition of endocytosis reduced tauopathy following TBI. ( C ) Blocking endocytosis with Pyrimidyn-7 (P7) treatments significantly inhibited the formation of Tau4R-GFP+ puncta following TBI in zebrafish larvae (***p=0.001). ( D ) Dyngo 4a treatment significantly reduced Tau aggregates in the spinal cord (**p=0.0025) in a manner similar to P7. ( E ) 4-AP treatment significantly inhibited the formation of Tau4R-GFP+ puncta in the spinal cord (***p=0.0003) of Tau biosensor line that also express human Tau (0N4R) after traumatic brain injury compared to untreated TBI control group. ( F ) A notable reduction in Tau aggregates was observed in the same line after treatment with P7 drug. Statistical analysis shows no significance difference (ns, p=0.2223) between groups. n = number of larvae. ****p<0.0001, Kruskal-Wallis ANOVA with Dunn’s multiple comparison test used throughout this Figure.
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    ( A ) Tau4R-GFP biosensor zebrafish larvae subjected to TBI and treated with the convulsant <t>4-AP</t> show no brain puncta. Scale bar = 200 μm. ( B ) 4-AP significantly reduced (apparently eliminated) the abundance of GFP+ puncta in the brain and spinal cord compared to untreated TBI control. Results from alternative doses and timings of 4-AP are reported in . The impact of 4-AP on tauopathy appears to be independent of its actions on post-traumatic seizures because reducing the latter with anti-convulsant retigabine (RTG) had no measurable effect. ( C-F ) Pharmacological inhibition of endocytosis reduced tauopathy following TBI. ( C ) Blocking endocytosis with Pyrimidyn-7 (P7) treatments significantly inhibited the formation of Tau4R-GFP+ puncta following TBI in zebrafish larvae (***p=0.001). ( D ) Dyngo 4a treatment significantly reduced Tau aggregates in the spinal cord (**p=0.0025) in a manner similar to P7. ( E ) 4-AP treatment significantly inhibited the formation of Tau4R-GFP+ puncta in the spinal cord (***p=0.0003) of Tau biosensor line that also express human Tau (0N4R) after traumatic brain injury compared to untreated TBI control group. ( F ) A notable reduction in Tau aggregates was observed in the same line after treatment with P7 drug. Statistical analysis shows no significance difference (ns, p=0.2223) between groups. n = number of larvae. ****p<0.0001, Kruskal-Wallis ANOVA with Dunn’s multiple comparison test used throughout this Figure.
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    ( A ) Tau4R-GFP biosensor zebrafish larvae subjected to TBI and treated with the convulsant <t>4-AP</t> show no brain puncta. Scale bar = 200 μm. ( B ) 4-AP significantly reduced (apparently eliminated) the abundance of GFP+ puncta in the brain and spinal cord compared to untreated TBI control. Results from alternative doses and timings of 4-AP are reported in . The impact of 4-AP on tauopathy appears to be independent of its actions on post-traumatic seizures because reducing the latter with anti-convulsant retigabine (RTG) had no measurable effect. ( C-F ) Pharmacological inhibition of endocytosis reduced tauopathy following TBI. ( C ) Blocking endocytosis with Pyrimidyn-7 (P7) treatments significantly inhibited the formation of Tau4R-GFP+ puncta following TBI in zebrafish larvae (***p=0.001). ( D ) Dyngo 4a treatment significantly reduced Tau aggregates in the spinal cord (**p=0.0025) in a manner similar to P7. ( E ) 4-AP treatment significantly inhibited the formation of Tau4R-GFP+ puncta in the spinal cord (***p=0.0003) of Tau biosensor line that also express human Tau (0N4R) after traumatic brain injury compared to untreated TBI control group. ( F ) A notable reduction in Tau aggregates was observed in the same line after treatment with P7 drug. Statistical analysis shows no significance difference (ns, p=0.2223) between groups. n = number of larvae. ****p<0.0001, Kruskal-Wallis ANOVA with Dunn’s multiple comparison test used throughout this Figure.
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    Image Search Results


    ( A ) Tau4R-GFP biosensor zebrafish larvae subjected to TBI and treated with the convulsant 4-AP show no brain puncta. Scale bar = 200 μm. ( B ) 4-AP significantly reduced (apparently eliminated) the abundance of GFP+ puncta in the brain and spinal cord compared to untreated TBI control. Results from alternative doses and timings of 4-AP are reported in . The impact of 4-AP on tauopathy appears to be independent of its actions on post-traumatic seizures because reducing the latter with anti-convulsant retigabine (RTG) had no measurable effect. ( C-F ) Pharmacological inhibition of endocytosis reduced tauopathy following TBI. ( C ) Blocking endocytosis with Pyrimidyn-7 (P7) treatments significantly inhibited the formation of Tau4R-GFP+ puncta following TBI in zebrafish larvae (***p=0.001). ( D ) Dyngo 4a treatment significantly reduced Tau aggregates in the spinal cord (**p=0.0025) in a manner similar to P7. ( E ) 4-AP treatment significantly inhibited the formation of Tau4R-GFP+ puncta in the spinal cord (***p=0.0003) of Tau biosensor line that also express human Tau (0N4R) after traumatic brain injury compared to untreated TBI control group. ( F ) A notable reduction in Tau aggregates was observed in the same line after treatment with P7 drug. Statistical analysis shows no significance difference (ns, p=0.2223) between groups. n = number of larvae. ****p<0.0001, Kruskal-Wallis ANOVA with Dunn’s multiple comparison test used throughout this Figure.

    Journal: eLife

    Article Title: Seizures are a druggable mechanistic link between TBI and subsequent tauopathy

    doi: 10.7554/eLife.58744

    Figure Lengend Snippet: ( A ) Tau4R-GFP biosensor zebrafish larvae subjected to TBI and treated with the convulsant 4-AP show no brain puncta. Scale bar = 200 μm. ( B ) 4-AP significantly reduced (apparently eliminated) the abundance of GFP+ puncta in the brain and spinal cord compared to untreated TBI control. Results from alternative doses and timings of 4-AP are reported in . The impact of 4-AP on tauopathy appears to be independent of its actions on post-traumatic seizures because reducing the latter with anti-convulsant retigabine (RTG) had no measurable effect. ( C-F ) Pharmacological inhibition of endocytosis reduced tauopathy following TBI. ( C ) Blocking endocytosis with Pyrimidyn-7 (P7) treatments significantly inhibited the formation of Tau4R-GFP+ puncta following TBI in zebrafish larvae (***p=0.001). ( D ) Dyngo 4a treatment significantly reduced Tau aggregates in the spinal cord (**p=0.0025) in a manner similar to P7. ( E ) 4-AP treatment significantly inhibited the formation of Tau4R-GFP+ puncta in the spinal cord (***p=0.0003) of Tau biosensor line that also express human Tau (0N4R) after traumatic brain injury compared to untreated TBI control group. ( F ) A notable reduction in Tau aggregates was observed in the same line after treatment with P7 drug. Statistical analysis shows no significance difference (ns, p=0.2223) between groups. n = number of larvae. ****p<0.0001, Kruskal-Wallis ANOVA with Dunn’s multiple comparison test used throughout this Figure.

    Article Snippet: Chemical compound, drug , 4-Aminopyridine (4AP) K+ channel blocker , Sigma , Cat# 275875–1G , .

    Techniques: Inhibition, Blocking Assay

    ( A ) Tau4R-GFP biosensor zebrafish larvae subjected to TBI and treated with the convulsant 4-AP show no brain puncta. 4-AP was added to the TBI larvae 1 day post-traumatic brain injury (dpti) and left for 38 hr as displayed in timeline at top. ( A,B ) 4-AP significantly reduced (apparently eliminated) the abundance of GFP+ puncta in the brain and spinal cord compared to untreated TBI control (**p<0.009 at 3dpti and ***p<0.0003 at 4dpti) at two different doses. ( C ) All larvae treated with 4-AP failed to display any GFP+ puncta (# of aggregates is 0), displayed as distribution of larvae binned into the number of GFP+ puncta they exhibited. ( D,E ) Timing and duration of 4-AP treatments following TBI had no appreciable effect on 4-AP abrogating the TBI-induced Tau aggregates. Symbols and colors for all panels are consistent with the legend at the top right of the Figure.

    Journal: eLife

    Article Title: Seizures are a druggable mechanistic link between TBI and subsequent tauopathy

    doi: 10.7554/eLife.58744

    Figure Lengend Snippet: ( A ) Tau4R-GFP biosensor zebrafish larvae subjected to TBI and treated with the convulsant 4-AP show no brain puncta. 4-AP was added to the TBI larvae 1 day post-traumatic brain injury (dpti) and left for 38 hr as displayed in timeline at top. ( A,B ) 4-AP significantly reduced (apparently eliminated) the abundance of GFP+ puncta in the brain and spinal cord compared to untreated TBI control (**p<0.009 at 3dpti and ***p<0.0003 at 4dpti) at two different doses. ( C ) All larvae treated with 4-AP failed to display any GFP+ puncta (# of aggregates is 0), displayed as distribution of larvae binned into the number of GFP+ puncta they exhibited. ( D,E ) Timing and duration of 4-AP treatments following TBI had no appreciable effect on 4-AP abrogating the TBI-induced Tau aggregates. Symbols and colors for all panels are consistent with the legend at the top right of the Figure.

    Article Snippet: Chemical compound, drug , 4-Aminopyridine (4AP) K+ channel blocker , Sigma , Cat# 275875–1G , .

    Techniques:

    Journal: eLife

    Article Title: Seizures are a druggable mechanistic link between TBI and subsequent tauopathy

    doi: 10.7554/eLife.58744

    Figure Lengend Snippet:

    Article Snippet: Chemical compound, drug , 4-Aminopyridine (4AP) K+ channel blocker , Sigma , Cat# 275875–1G , .

    Techniques: Expressing, Sequencing, Isolation, Recombinant, Concentration Assay, Software, Blocking Assay, Transfection, Staining