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kv1 2 channel blocker rtityustoxin kα  (Alomone Labs)


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    Structured Review

    Alomone Labs kv1 2 channel blocker rtityustoxin kα
    Application of <t>the</t> <t>Kv1.2</t> antagonist Tityustoxin‐Κα partially decrease effects of sevoflurane. (A) Voltage responses to hyperpolarizing and depolarizing current steps in control conditions, after sevoflurane and after additional Tityustoxin Κα (100 nM, sevo + TsTX‐Κα) application for type A (red; TsTX‐Κα, n = 8) and type B (blue; TsTX‐Κα, n = 5) L5 PNs. Arrow depicts hyperpolarization magnitude, arrowhead points to the sag or rebound AP. (B) Tityustoxin‐Κα application increased the firing frequency initially decreased by sevoflurane marginally for type A PNs but more so in type B PNs, but could not recover firing frequency to baseline frequency. Asterisks (*) show significant difference between aCSF and sevoflurane + TsTX‐Κα; significance levels * p < 0.05, ** p < 0.01, ** p < 0.001. (C) Boxplots showing that the average membrane potential depolarization of type A PNs could not be recovered by TsTX‐Κα. (D) Boxplots showing that the average input resistance of type B PNs was recovered by TsTX‐Κα. (E) Boxplots of average Δsag also show TsTX‐Κα to reverse sevoflurane effects. Boxplots show median (horizontal bar), interquartile range (IQR, box), and 1.5× IQR values. Full statistical report in Table .
    Kv1 2 Channel Blocker Rtityustoxin Kα, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Sevoflurane Inhibits Layer 5 Pyramidal Neurons via Kv1.2‐Dependent Modulation of Subthreshold Currents"

    Article Title: Sevoflurane Inhibits Layer 5 Pyramidal Neurons via Kv1.2‐Dependent Modulation of Subthreshold Currents

    Journal: Journal of Neurochemistry

    doi: 10.1111/jnc.70360

    Application of the Kv1.2 antagonist Tityustoxin‐Κα partially decrease effects of sevoflurane. (A) Voltage responses to hyperpolarizing and depolarizing current steps in control conditions, after sevoflurane and after additional Tityustoxin Κα (100 nM, sevo + TsTX‐Κα) application for type A (red; TsTX‐Κα, n = 8) and type B (blue; TsTX‐Κα, n = 5) L5 PNs. Arrow depicts hyperpolarization magnitude, arrowhead points to the sag or rebound AP. (B) Tityustoxin‐Κα application increased the firing frequency initially decreased by sevoflurane marginally for type A PNs but more so in type B PNs, but could not recover firing frequency to baseline frequency. Asterisks (*) show significant difference between aCSF and sevoflurane + TsTX‐Κα; significance levels * p < 0.05, ** p < 0.01, ** p < 0.001. (C) Boxplots showing that the average membrane potential depolarization of type A PNs could not be recovered by TsTX‐Κα. (D) Boxplots showing that the average input resistance of type B PNs was recovered by TsTX‐Κα. (E) Boxplots of average Δsag also show TsTX‐Κα to reverse sevoflurane effects. Boxplots show median (horizontal bar), interquartile range (IQR, box), and 1.5× IQR values. Full statistical report in Table .
    Figure Legend Snippet: Application of the Kv1.2 antagonist Tityustoxin‐Κα partially decrease effects of sevoflurane. (A) Voltage responses to hyperpolarizing and depolarizing current steps in control conditions, after sevoflurane and after additional Tityustoxin Κα (100 nM, sevo + TsTX‐Κα) application for type A (red; TsTX‐Κα, n = 8) and type B (blue; TsTX‐Κα, n = 5) L5 PNs. Arrow depicts hyperpolarization magnitude, arrowhead points to the sag or rebound AP. (B) Tityustoxin‐Κα application increased the firing frequency initially decreased by sevoflurane marginally for type A PNs but more so in type B PNs, but could not recover firing frequency to baseline frequency. Asterisks (*) show significant difference between aCSF and sevoflurane + TsTX‐Κα; significance levels * p < 0.05, ** p < 0.01, ** p < 0.001. (C) Boxplots showing that the average membrane potential depolarization of type A PNs could not be recovered by TsTX‐Κα. (D) Boxplots showing that the average input resistance of type B PNs was recovered by TsTX‐Κα. (E) Boxplots of average Δsag also show TsTX‐Κα to reverse sevoflurane effects. Boxplots show median (horizontal bar), interquartile range (IQR, box), and 1.5× IQR values. Full statistical report in Table .

    Techniques Used: Control, Membrane

    Sevoflurane shifts Kv1.2 activation to more hyperpolarized voltages, suppressing subthreshold currents in L5 pyramidal neurons. (A) Pharmacology schematics. (B) Current responses to 7 subthreshold voltage steps (−77 to −47 mV, 5 mV increments, 500 ms duration) of type A (all groups, n = 7 neurons) and type B (all groups, n = 5 neurons) PNs in the presence of aCSF, sevoflurane and sevoflurane + Tityustoxin‐Kα. Bottom: The digitally subtracted trace of sevoflurane trace from the Sevo + TsTX‐Κα trace, showing the TsTX‐Κα current enhancement was similar for the two subtypes. (C) Current voltage‐dependency (I–V) plots for average steady state currents ( I ss ) in response to subthreshold voltage steps in aCSF, after application of sevoflurane and after additional application of Tityustoxin‐Kα (TsTX‐Kα). Arrows denote reversal potential of subthreshold currents in the presence of aCSF (type A—red, type B—blue) and sevo (black). Arrowheads show no difference in average current in response to a −50 mV step in aCSF vs. Sevo + TsTX‐Κα. (D) I–V plots as in ‘C’ for type B PNs. (E) Z ‐scores and −log 10 (P FDR ) plots from mixed effects linear model for each 5 mV voltage bin (1: −77 to −72 mV; 6: −52 to −47 mV) for current amplitudes, and 15 mV bin comparisons (−77 to −62 mV and −62 to −47 mV) for I–V slope analysis. Dotted lines indicate standard significance thresholds and the line at z = 0, which represents no effect of the treatment. All error bars represent SEM. Full statistical report in Table .
    Figure Legend Snippet: Sevoflurane shifts Kv1.2 activation to more hyperpolarized voltages, suppressing subthreshold currents in L5 pyramidal neurons. (A) Pharmacology schematics. (B) Current responses to 7 subthreshold voltage steps (−77 to −47 mV, 5 mV increments, 500 ms duration) of type A (all groups, n = 7 neurons) and type B (all groups, n = 5 neurons) PNs in the presence of aCSF, sevoflurane and sevoflurane + Tityustoxin‐Kα. Bottom: The digitally subtracted trace of sevoflurane trace from the Sevo + TsTX‐Κα trace, showing the TsTX‐Κα current enhancement was similar for the two subtypes. (C) Current voltage‐dependency (I–V) plots for average steady state currents ( I ss ) in response to subthreshold voltage steps in aCSF, after application of sevoflurane and after additional application of Tityustoxin‐Kα (TsTX‐Kα). Arrows denote reversal potential of subthreshold currents in the presence of aCSF (type A—red, type B—blue) and sevo (black). Arrowheads show no difference in average current in response to a −50 mV step in aCSF vs. Sevo + TsTX‐Κα. (D) I–V plots as in ‘C’ for type B PNs. (E) Z ‐scores and −log 10 (P FDR ) plots from mixed effects linear model for each 5 mV voltage bin (1: −77 to −72 mV; 6: −52 to −47 mV) for current amplitudes, and 15 mV bin comparisons (−77 to −62 mV and −62 to −47 mV) for I–V slope analysis. Dotted lines indicate standard significance thresholds and the line at z = 0, which represents no effect of the treatment. All error bars represent SEM. Full statistical report in Table .

    Techniques Used: Activation Assay



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    Application of <t>the</t> <t>Kv1.2</t> antagonist Tityustoxin‐Κα partially decrease effects of sevoflurane. (A) Voltage responses to hyperpolarizing and depolarizing current steps in control conditions, after sevoflurane and after additional Tityustoxin Κα (100 nM, sevo + TsTX‐Κα) application for type A (red; TsTX‐Κα, n = 8) and type B (blue; TsTX‐Κα, n = 5) L5 PNs. Arrow depicts hyperpolarization magnitude, arrowhead points to the sag or rebound AP. (B) Tityustoxin‐Κα application increased the firing frequency initially decreased by sevoflurane marginally for type A PNs but more so in type B PNs, but could not recover firing frequency to baseline frequency. Asterisks (*) show significant difference between aCSF and sevoflurane + TsTX‐Κα; significance levels * p < 0.05, ** p < 0.01, ** p < 0.001. (C) Boxplots showing that the average membrane potential depolarization of type A PNs could not be recovered by TsTX‐Κα. (D) Boxplots showing that the average input resistance of type B PNs was recovered by TsTX‐Κα. (E) Boxplots of average Δsag also show TsTX‐Κα to reverse sevoflurane effects. Boxplots show median (horizontal bar), interquartile range (IQR, box), and 1.5× IQR values. Full statistical report in Table .
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    Image Search Results


    Application of the Kv1.2 antagonist Tityustoxin‐Κα partially decrease effects of sevoflurane. (A) Voltage responses to hyperpolarizing and depolarizing current steps in control conditions, after sevoflurane and after additional Tityustoxin Κα (100 nM, sevo + TsTX‐Κα) application for type A (red; TsTX‐Κα, n = 8) and type B (blue; TsTX‐Κα, n = 5) L5 PNs. Arrow depicts hyperpolarization magnitude, arrowhead points to the sag or rebound AP. (B) Tityustoxin‐Κα application increased the firing frequency initially decreased by sevoflurane marginally for type A PNs but more so in type B PNs, but could not recover firing frequency to baseline frequency. Asterisks (*) show significant difference between aCSF and sevoflurane + TsTX‐Κα; significance levels * p < 0.05, ** p < 0.01, ** p < 0.001. (C) Boxplots showing that the average membrane potential depolarization of type A PNs could not be recovered by TsTX‐Κα. (D) Boxplots showing that the average input resistance of type B PNs was recovered by TsTX‐Κα. (E) Boxplots of average Δsag also show TsTX‐Κα to reverse sevoflurane effects. Boxplots show median (horizontal bar), interquartile range (IQR, box), and 1.5× IQR values. Full statistical report in Table .

    Journal: Journal of Neurochemistry

    Article Title: Sevoflurane Inhibits Layer 5 Pyramidal Neurons via Kv1.2‐Dependent Modulation of Subthreshold Currents

    doi: 10.1111/jnc.70360

    Figure Lengend Snippet: Application of the Kv1.2 antagonist Tityustoxin‐Κα partially decrease effects of sevoflurane. (A) Voltage responses to hyperpolarizing and depolarizing current steps in control conditions, after sevoflurane and after additional Tityustoxin Κα (100 nM, sevo + TsTX‐Κα) application for type A (red; TsTX‐Κα, n = 8) and type B (blue; TsTX‐Κα, n = 5) L5 PNs. Arrow depicts hyperpolarization magnitude, arrowhead points to the sag or rebound AP. (B) Tityustoxin‐Κα application increased the firing frequency initially decreased by sevoflurane marginally for type A PNs but more so in type B PNs, but could not recover firing frequency to baseline frequency. Asterisks (*) show significant difference between aCSF and sevoflurane + TsTX‐Κα; significance levels * p < 0.05, ** p < 0.01, ** p < 0.001. (C) Boxplots showing that the average membrane potential depolarization of type A PNs could not be recovered by TsTX‐Κα. (D) Boxplots showing that the average input resistance of type B PNs was recovered by TsTX‐Κα. (E) Boxplots of average Δsag also show TsTX‐Κα to reverse sevoflurane effects. Boxplots show median (horizontal bar), interquartile range (IQR, box), and 1.5× IQR values. Full statistical report in Table .

    Article Snippet: In some experiments, the Kv1.2 channel blocker rTityustoxin‐Kα (TsTX‐Kα, Alomone Labs, Cat#: STT‐360, 100 nM) was added to aCSF pre‐bubbled with sevoflurane.

    Techniques: Control, Membrane

    Sevoflurane shifts Kv1.2 activation to more hyperpolarized voltages, suppressing subthreshold currents in L5 pyramidal neurons. (A) Pharmacology schematics. (B) Current responses to 7 subthreshold voltage steps (−77 to −47 mV, 5 mV increments, 500 ms duration) of type A (all groups, n = 7 neurons) and type B (all groups, n = 5 neurons) PNs in the presence of aCSF, sevoflurane and sevoflurane + Tityustoxin‐Kα. Bottom: The digitally subtracted trace of sevoflurane trace from the Sevo + TsTX‐Κα trace, showing the TsTX‐Κα current enhancement was similar for the two subtypes. (C) Current voltage‐dependency (I–V) plots for average steady state currents ( I ss ) in response to subthreshold voltage steps in aCSF, after application of sevoflurane and after additional application of Tityustoxin‐Kα (TsTX‐Kα). Arrows denote reversal potential of subthreshold currents in the presence of aCSF (type A—red, type B—blue) and sevo (black). Arrowheads show no difference in average current in response to a −50 mV step in aCSF vs. Sevo + TsTX‐Κα. (D) I–V plots as in ‘C’ for type B PNs. (E) Z ‐scores and −log 10 (P FDR ) plots from mixed effects linear model for each 5 mV voltage bin (1: −77 to −72 mV; 6: −52 to −47 mV) for current amplitudes, and 15 mV bin comparisons (−77 to −62 mV and −62 to −47 mV) for I–V slope analysis. Dotted lines indicate standard significance thresholds and the line at z = 0, which represents no effect of the treatment. All error bars represent SEM. Full statistical report in Table .

    Journal: Journal of Neurochemistry

    Article Title: Sevoflurane Inhibits Layer 5 Pyramidal Neurons via Kv1.2‐Dependent Modulation of Subthreshold Currents

    doi: 10.1111/jnc.70360

    Figure Lengend Snippet: Sevoflurane shifts Kv1.2 activation to more hyperpolarized voltages, suppressing subthreshold currents in L5 pyramidal neurons. (A) Pharmacology schematics. (B) Current responses to 7 subthreshold voltage steps (−77 to −47 mV, 5 mV increments, 500 ms duration) of type A (all groups, n = 7 neurons) and type B (all groups, n = 5 neurons) PNs in the presence of aCSF, sevoflurane and sevoflurane + Tityustoxin‐Kα. Bottom: The digitally subtracted trace of sevoflurane trace from the Sevo + TsTX‐Κα trace, showing the TsTX‐Κα current enhancement was similar for the two subtypes. (C) Current voltage‐dependency (I–V) plots for average steady state currents ( I ss ) in response to subthreshold voltage steps in aCSF, after application of sevoflurane and after additional application of Tityustoxin‐Kα (TsTX‐Kα). Arrows denote reversal potential of subthreshold currents in the presence of aCSF (type A—red, type B—blue) and sevo (black). Arrowheads show no difference in average current in response to a −50 mV step in aCSF vs. Sevo + TsTX‐Κα. (D) I–V plots as in ‘C’ for type B PNs. (E) Z ‐scores and −log 10 (P FDR ) plots from mixed effects linear model for each 5 mV voltage bin (1: −77 to −72 mV; 6: −52 to −47 mV) for current amplitudes, and 15 mV bin comparisons (−77 to −62 mV and −62 to −47 mV) for I–V slope analysis. Dotted lines indicate standard significance thresholds and the line at z = 0, which represents no effect of the treatment. All error bars represent SEM. Full statistical report in Table .

    Article Snippet: In some experiments, the Kv1.2 channel blocker rTityustoxin‐Kα (TsTX‐Kα, Alomone Labs, Cat#: STT‐360, 100 nM) was added to aCSF pre‐bubbled with sevoflurane.

    Techniques: Activation Assay