β pompilidotoxin  (Alomone Labs)


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    Alomone Labs β pompilidotoxin
    β Pompilidotoxin, 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
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    94/100 stars

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    β pompilidotoxin  (Alomone Labs)


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    Alomone Labs β pompilidotoxin
    β Pompilidotoxin, 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
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    β pompilidotoxin pomp  (Alomone Labs)


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    Alomone Labs β pompilidotoxin pomp
    Effect of tefluthin, β-pompilidoxin, tefluthrin plus sparsentan, <t>β-pompilidotoxin</t> plus sparsentan on I Na in GH 3 cells. The voltage-clamp experiments were undertaken, as cells were voltage-clamped at −80 mV and the depolarizing pulse to −10 mV was imposed to them. ( A ) Representative current traces obtained in the control period (a, sparsentan was not present), and during exposure to 3 μM sparsentan (b) or to 3 μM sparsentan plus 3 μM tefluthrin (c). The top panel indicates the voltage-clamp protocol applied. Of note, the deactivating I Na was additionally detected as membrane potential was returned to −50 mV with a duration of 40 ms. ( B ) Summary bar graph demonstrating effect of 3 μM tefluthrin, 3 μM β-pompilidotoxn, 3 μM tefluthrin plus 3 μM sparsentan and 3 μM β-pompilidotoxin plus 3 μM sparsentan on the peak amplitude of I Na (mean ± SEM; n = 8 for each bar). The peak amplitude was measured at the start of 40 ms depolarizing command voltage from −80 to −10 mV. Tef: tefluthrin; Pomp: β-pompilidotoxin; Spar, sparsentan. Statistical analysis was performed by one-way ANOVA ( p < 0.05). * Significantly different from controls ( p < 0.05) and ** significantly different from Tef (3 μM) or Pomp (3 μM) alone group ( p < 0.05).
    β Pompilidotoxin Pomp, 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
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    94/100 stars

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    1) Product Images from "The Evidence for Sparsentan-Mediated Inhibition of I Na and I K(erg) : Possibly Unlinked to Its Antagonism of Angiotensin II or Endothelin Type a Receptor"

    Article Title: The Evidence for Sparsentan-Mediated Inhibition of I Na and I K(erg) : Possibly Unlinked to Its Antagonism of Angiotensin II or Endothelin Type a Receptor

    Journal: Biomedicines

    doi: 10.3390/biomedicines10010086

    Effect of tefluthin, β-pompilidoxin, tefluthrin plus sparsentan, β-pompilidotoxin plus sparsentan on I Na in GH 3 cells. The voltage-clamp experiments were undertaken, as cells were voltage-clamped at −80 mV and the depolarizing pulse to −10 mV was imposed to them. ( A ) Representative current traces obtained in the control period (a, sparsentan was not present), and during exposure to 3 μM sparsentan (b) or to 3 μM sparsentan plus 3 μM tefluthrin (c). The top panel indicates the voltage-clamp protocol applied. Of note, the deactivating I Na was additionally detected as membrane potential was returned to −50 mV with a duration of 40 ms. ( B ) Summary bar graph demonstrating effect of 3 μM tefluthrin, 3 μM β-pompilidotoxn, 3 μM tefluthrin plus 3 μM sparsentan and 3 μM β-pompilidotoxin plus 3 μM sparsentan on the peak amplitude of I Na (mean ± SEM; n = 8 for each bar). The peak amplitude was measured at the start of 40 ms depolarizing command voltage from −80 to −10 mV. Tef: tefluthrin; Pomp: β-pompilidotoxin; Spar, sparsentan. Statistical analysis was performed by one-way ANOVA ( p < 0.05). * Significantly different from controls ( p < 0.05) and ** significantly different from Tef (3 μM) or Pomp (3 μM) alone group ( p < 0.05).
    Figure Legend Snippet: Effect of tefluthin, β-pompilidoxin, tefluthrin plus sparsentan, β-pompilidotoxin plus sparsentan on I Na in GH 3 cells. The voltage-clamp experiments were undertaken, as cells were voltage-clamped at −80 mV and the depolarizing pulse to −10 mV was imposed to them. ( A ) Representative current traces obtained in the control period (a, sparsentan was not present), and during exposure to 3 μM sparsentan (b) or to 3 μM sparsentan plus 3 μM tefluthrin (c). The top panel indicates the voltage-clamp protocol applied. Of note, the deactivating I Na was additionally detected as membrane potential was returned to −50 mV with a duration of 40 ms. ( B ) Summary bar graph demonstrating effect of 3 μM tefluthrin, 3 μM β-pompilidotoxn, 3 μM tefluthrin plus 3 μM sparsentan and 3 μM β-pompilidotoxin plus 3 μM sparsentan on the peak amplitude of I Na (mean ± SEM; n = 8 for each bar). The peak amplitude was measured at the start of 40 ms depolarizing command voltage from −80 to −10 mV. Tef: tefluthrin; Pomp: β-pompilidotoxin; Spar, sparsentan. Statistical analysis was performed by one-way ANOVA ( p < 0.05). * Significantly different from controls ( p < 0.05) and ** significantly different from Tef (3 μM) or Pomp (3 μM) alone group ( p < 0.05).

    Techniques Used:

    βpompilidotoxin  (Alomone Labs)


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    Alomone Labs βpompilidotoxin
    βpompilidotoxin, 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
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    Average 94 stars, based on 1 article reviews
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    94/100 stars

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    25 6981 maleate  (Alomone Labs)


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    Alomone Labs 25 6981 maleate
    AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits (GluN2A and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or <t>Ro-25-6981</t> vs. Vehicle)
    25 6981 Maleate, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Chronic AdipoRon Treatment Mimics the Effects of Physical Exercise on Restoring Hippocampal Neuroplasticity in Diabetic Mice"

    Article Title: Chronic AdipoRon Treatment Mimics the Effects of Physical Exercise on Restoring Hippocampal Neuroplasticity in Diabetic Mice

    Journal: Molecular Neurobiology

    doi: 10.1007/s12035-021-02441-7

    AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits (GluN2A and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or Ro-25-6981 vs. Vehicle)
    Figure Legend Snippet: AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits (GluN2A and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or Ro-25-6981 vs. Vehicle)

    Techniques Used: Slice Preparation, Inhibition

    intraperitoneal β pompilidotoxin  (Alomone Labs)


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    Alomone Labs intraperitoneal β pompilidotoxin
    Intraperitoneal β Pompilidotoxin, 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
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    amg9810  (Alomone Labs)


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    Alomone Labs amg9810
    Amg9810, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    pbs 180  (Alomone Labs)


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    Alomone Labs pbs 180
    Pbs 180, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    180 n m ω agatoxin iva  (Alomone Labs)


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    Alomone Labs 180 n m ω agatoxin iva
    Specificity of Ca v 2‐type calcium channels deficit in MAP6 KO neurons. (A) Left panel, examples of KCl‐stimulated fluo‐4‐loaded WT cortical neurons in the absence (black line) or presence (yellow line) of 20 μ m nimodipine. Right panels, ratios of KCl‐elicited fluorescence intensity peaks, recorded from WT (white squares) and MAP6 KO (grey squares) cortical neurons in the presence or absence of 20 μ m nimodipine (yellow curves), <t>180</t> <t>n</t> <t>m</t> <t>ω‐agatoxin</t> <t>IVA</t> <t>(red</t> curves) or 320 n m ω‐conotoxin GVIA (green curves). n represents the total number of wells recorded from eight independent neuronal cultures. ns, P > 0.05, *, P < 0.05 and **, P < 0.01 against the corresponding WT, using paired nonparametric t ‐tests. Note that Wilcoxon t ‐tests have been performed to account for technical data pairing between neighbouring MAP6 KO and WT culture wells and this pairing was deemed as highly significant ( P < 0.01) for each panel. (B) Left panel, example of identified axons (yellow arrowheads) from a neuronal culture with immunolabelled microtubules (red), tau (green) and nuclei (blue). Right panel, measurements of axonal length of WT (white symbols) and MAP6 KO (grey symbols) hippocampal neurons after 48 h in the absence (sham, discs) or presence (conotox, diamonds) of 320 n m ω‐conotoxin GVIA. n represents the total number of neurons measured from three independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding sham, using unpaired nonparametric t ‐tests. Scale bar = 10 μm. (C) Left panel, examples of spontaneous calcium activity recorded from fluo‐4‐loaded WT (black line) and MAP6 KO (grey line) hippocampal neurons. Right panel, quantification of mean peak intensity during spontaneous calcium activity of fluo‐4‐loaded WT (white discs) and MAP6 KO (grey discs) hippocampal neurons, recorded in cell bodies and neurites, independently, normalized by that of WT (dashed grey line = 100%). n represents the total number of fields recorded from six independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding WT, using unpaired parametric t ‐tests.[Colour figure can be viewed at wileyonlinelibrary.com ].
    180 N M ω Agatoxin Iva, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "MAP6 interacts with Tctex1 and Ca v 2.2/N‐type calcium channels to regulate calcium signalling in neurons"

    Article Title: MAP6 interacts with Tctex1 and Ca v 2.2/N‐type calcium channels to regulate calcium signalling in neurons

    Journal: The European Journal of Neuroscience

    doi: 10.1111/ejn.13766

    Specificity of Ca v 2‐type calcium channels deficit in MAP6 KO neurons. (A) Left panel, examples of KCl‐stimulated fluo‐4‐loaded WT cortical neurons in the absence (black line) or presence (yellow line) of 20 μ m nimodipine. Right panels, ratios of KCl‐elicited fluorescence intensity peaks, recorded from WT (white squares) and MAP6 KO (grey squares) cortical neurons in the presence or absence of 20 μ m nimodipine (yellow curves), 180 n m ω‐agatoxin IVA (red curves) or 320 n m ω‐conotoxin GVIA (green curves). n represents the total number of wells recorded from eight independent neuronal cultures. ns, P > 0.05, *, P < 0.05 and **, P < 0.01 against the corresponding WT, using paired nonparametric t ‐tests. Note that Wilcoxon t ‐tests have been performed to account for technical data pairing between neighbouring MAP6 KO and WT culture wells and this pairing was deemed as highly significant ( P < 0.01) for each panel. (B) Left panel, example of identified axons (yellow arrowheads) from a neuronal culture with immunolabelled microtubules (red), tau (green) and nuclei (blue). Right panel, measurements of axonal length of WT (white symbols) and MAP6 KO (grey symbols) hippocampal neurons after 48 h in the absence (sham, discs) or presence (conotox, diamonds) of 320 n m ω‐conotoxin GVIA. n represents the total number of neurons measured from three independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding sham, using unpaired nonparametric t ‐tests. Scale bar = 10 μm. (C) Left panel, examples of spontaneous calcium activity recorded from fluo‐4‐loaded WT (black line) and MAP6 KO (grey line) hippocampal neurons. Right panel, quantification of mean peak intensity during spontaneous calcium activity of fluo‐4‐loaded WT (white discs) and MAP6 KO (grey discs) hippocampal neurons, recorded in cell bodies and neurites, independently, normalized by that of WT (dashed grey line = 100%). n represents the total number of fields recorded from six independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding WT, using unpaired parametric t ‐tests.[Colour figure can be viewed at wileyonlinelibrary.com ].
    Figure Legend Snippet: Specificity of Ca v 2‐type calcium channels deficit in MAP6 KO neurons. (A) Left panel, examples of KCl‐stimulated fluo‐4‐loaded WT cortical neurons in the absence (black line) or presence (yellow line) of 20 μ m nimodipine. Right panels, ratios of KCl‐elicited fluorescence intensity peaks, recorded from WT (white squares) and MAP6 KO (grey squares) cortical neurons in the presence or absence of 20 μ m nimodipine (yellow curves), 180 n m ω‐agatoxin IVA (red curves) or 320 n m ω‐conotoxin GVIA (green curves). n represents the total number of wells recorded from eight independent neuronal cultures. ns, P > 0.05, *, P < 0.05 and **, P < 0.01 against the corresponding WT, using paired nonparametric t ‐tests. Note that Wilcoxon t ‐tests have been performed to account for technical data pairing between neighbouring MAP6 KO and WT culture wells and this pairing was deemed as highly significant ( P < 0.01) for each panel. (B) Left panel, example of identified axons (yellow arrowheads) from a neuronal culture with immunolabelled microtubules (red), tau (green) and nuclei (blue). Right panel, measurements of axonal length of WT (white symbols) and MAP6 KO (grey symbols) hippocampal neurons after 48 h in the absence (sham, discs) or presence (conotox, diamonds) of 320 n m ω‐conotoxin GVIA. n represents the total number of neurons measured from three independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding sham, using unpaired nonparametric t ‐tests. Scale bar = 10 μm. (C) Left panel, examples of spontaneous calcium activity recorded from fluo‐4‐loaded WT (black line) and MAP6 KO (grey line) hippocampal neurons. Right panel, quantification of mean peak intensity during spontaneous calcium activity of fluo‐4‐loaded WT (white discs) and MAP6 KO (grey discs) hippocampal neurons, recorded in cell bodies and neurites, independently, normalized by that of WT (dashed grey line = 100%). n represents the total number of fields recorded from six independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding WT, using unpaired parametric t ‐tests.[Colour figure can be viewed at wileyonlinelibrary.com ].

    Techniques Used: Fluorescence, Activity Assay

    p2x7 anti p2x1 receptor atto 488 180  (Alomone Labs)


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    Alomone Labs p2x7 anti p2x1 receptor atto 488 180
    P2x7 Anti P2x1 Receptor Atto 488 180, 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
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    β pmtx  (Alomone Labs)


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    Alomone Labs β pmtx
    β Pmtx, 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
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    Alomone Labs β pompilidotoxin
    β Pompilidotoxin, 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
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    Alomone Labs β pompilidotoxin pomp
    Effect of tefluthin, β-pompilidoxin, tefluthrin plus sparsentan, <t>β-pompilidotoxin</t> plus sparsentan on I Na in GH 3 cells. The voltage-clamp experiments were undertaken, as cells were voltage-clamped at −80 mV and the depolarizing pulse to −10 mV was imposed to them. ( A ) Representative current traces obtained in the control period (a, sparsentan was not present), and during exposure to 3 μM sparsentan (b) or to 3 μM sparsentan plus 3 μM tefluthrin (c). The top panel indicates the voltage-clamp protocol applied. Of note, the deactivating I Na was additionally detected as membrane potential was returned to −50 mV with a duration of 40 ms. ( B ) Summary bar graph demonstrating effect of 3 μM tefluthrin, 3 μM β-pompilidotoxn, 3 μM tefluthrin plus 3 μM sparsentan and 3 μM β-pompilidotoxin plus 3 μM sparsentan on the peak amplitude of I Na (mean ± SEM; n = 8 for each bar). The peak amplitude was measured at the start of 40 ms depolarizing command voltage from −80 to −10 mV. Tef: tefluthrin; Pomp: β-pompilidotoxin; Spar, sparsentan. Statistical analysis was performed by one-way ANOVA ( p < 0.05). * Significantly different from controls ( p < 0.05) and ** significantly different from Tef (3 μM) or Pomp (3 μM) alone group ( p < 0.05).
    β Pompilidotoxin Pomp, 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
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    Alomone Labs βpompilidotoxin
    Effect of tefluthin, β-pompilidoxin, tefluthrin plus sparsentan, <t>β-pompilidotoxin</t> plus sparsentan on I Na in GH 3 cells. The voltage-clamp experiments were undertaken, as cells were voltage-clamped at −80 mV and the depolarizing pulse to −10 mV was imposed to them. ( A ) Representative current traces obtained in the control period (a, sparsentan was not present), and during exposure to 3 μM sparsentan (b) or to 3 μM sparsentan plus 3 μM tefluthrin (c). The top panel indicates the voltage-clamp protocol applied. Of note, the deactivating I Na was additionally detected as membrane potential was returned to −50 mV with a duration of 40 ms. ( B ) Summary bar graph demonstrating effect of 3 μM tefluthrin, 3 μM β-pompilidotoxn, 3 μM tefluthrin plus 3 μM sparsentan and 3 μM β-pompilidotoxin plus 3 μM sparsentan on the peak amplitude of I Na (mean ± SEM; n = 8 for each bar). The peak amplitude was measured at the start of 40 ms depolarizing command voltage from −80 to −10 mV. Tef: tefluthrin; Pomp: β-pompilidotoxin; Spar, sparsentan. Statistical analysis was performed by one-way ANOVA ( p < 0.05). * Significantly different from controls ( p < 0.05) and ** significantly different from Tef (3 μM) or Pomp (3 μM) alone group ( p < 0.05).
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    AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits (GluN2A and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or <t>Ro-25-6981</t> vs. Vehicle)
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    AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits (GluN2A and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or <t>Ro-25-6981</t> vs. Vehicle)
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    AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits (GluN2A and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or <t>Ro-25-6981</t> vs. Vehicle)
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    AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits (GluN2A and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or <t>Ro-25-6981</t> vs. Vehicle)
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    Specificity of Ca v 2‐type calcium channels deficit in MAP6 KO neurons. (A) Left panel, examples of KCl‐stimulated fluo‐4‐loaded WT cortical neurons in the absence (black line) or presence (yellow line) of 20 μ m nimodipine. Right panels, ratios of KCl‐elicited fluorescence intensity peaks, recorded from WT (white squares) and MAP6 KO (grey squares) cortical neurons in the presence or absence of 20 μ m nimodipine (yellow curves), <t>180</t> <t>n</t> <t>m</t> <t>ω‐agatoxin</t> <t>IVA</t> <t>(red</t> curves) or 320 n m ω‐conotoxin GVIA (green curves). n represents the total number of wells recorded from eight independent neuronal cultures. ns, P > 0.05, *, P < 0.05 and **, P < 0.01 against the corresponding WT, using paired nonparametric t ‐tests. Note that Wilcoxon t ‐tests have been performed to account for technical data pairing between neighbouring MAP6 KO and WT culture wells and this pairing was deemed as highly significant ( P < 0.01) for each panel. (B) Left panel, example of identified axons (yellow arrowheads) from a neuronal culture with immunolabelled microtubules (red), tau (green) and nuclei (blue). Right panel, measurements of axonal length of WT (white symbols) and MAP6 KO (grey symbols) hippocampal neurons after 48 h in the absence (sham, discs) or presence (conotox, diamonds) of 320 n m ω‐conotoxin GVIA. n represents the total number of neurons measured from three independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding sham, using unpaired nonparametric t ‐tests. Scale bar = 10 μm. (C) Left panel, examples of spontaneous calcium activity recorded from fluo‐4‐loaded WT (black line) and MAP6 KO (grey line) hippocampal neurons. Right panel, quantification of mean peak intensity during spontaneous calcium activity of fluo‐4‐loaded WT (white discs) and MAP6 KO (grey discs) hippocampal neurons, recorded in cell bodies and neurites, independently, normalized by that of WT (dashed grey line = 100%). n represents the total number of fields recorded from six independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding WT, using unpaired parametric t ‐tests.[Colour figure can be viewed at wileyonlinelibrary.com ].
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    Specificity of Ca v 2‐type calcium channels deficit in MAP6 KO neurons. (A) Left panel, examples of KCl‐stimulated fluo‐4‐loaded WT cortical neurons in the absence (black line) or presence (yellow line) of 20 μ m nimodipine. Right panels, ratios of KCl‐elicited fluorescence intensity peaks, recorded from WT (white squares) and MAP6 KO (grey squares) cortical neurons in the presence or absence of 20 μ m nimodipine (yellow curves), <t>180</t> <t>n</t> <t>m</t> <t>ω‐agatoxin</t> <t>IVA</t> <t>(red</t> curves) or 320 n m ω‐conotoxin GVIA (green curves). n represents the total number of wells recorded from eight independent neuronal cultures. ns, P > 0.05, *, P < 0.05 and **, P < 0.01 against the corresponding WT, using paired nonparametric t ‐tests. Note that Wilcoxon t ‐tests have been performed to account for technical data pairing between neighbouring MAP6 KO and WT culture wells and this pairing was deemed as highly significant ( P < 0.01) for each panel. (B) Left panel, example of identified axons (yellow arrowheads) from a neuronal culture with immunolabelled microtubules (red), tau (green) and nuclei (blue). Right panel, measurements of axonal length of WT (white symbols) and MAP6 KO (grey symbols) hippocampal neurons after 48 h in the absence (sham, discs) or presence (conotox, diamonds) of 320 n m ω‐conotoxin GVIA. n represents the total number of neurons measured from three independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding sham, using unpaired nonparametric t ‐tests. Scale bar = 10 μm. (C) Left panel, examples of spontaneous calcium activity recorded from fluo‐4‐loaded WT (black line) and MAP6 KO (grey line) hippocampal neurons. Right panel, quantification of mean peak intensity during spontaneous calcium activity of fluo‐4‐loaded WT (white discs) and MAP6 KO (grey discs) hippocampal neurons, recorded in cell bodies and neurites, independently, normalized by that of WT (dashed grey line = 100%). n represents the total number of fields recorded from six independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding WT, using unpaired parametric t ‐tests.[Colour figure can be viewed at wileyonlinelibrary.com ].
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    Specificity of Ca v 2‐type calcium channels deficit in MAP6 KO neurons. (A) Left panel, examples of KCl‐stimulated fluo‐4‐loaded WT cortical neurons in the absence (black line) or presence (yellow line) of 20 μ m nimodipine. Right panels, ratios of KCl‐elicited fluorescence intensity peaks, recorded from WT (white squares) and MAP6 KO (grey squares) cortical neurons in the presence or absence of 20 μ m nimodipine (yellow curves), <t>180</t> <t>n</t> <t>m</t> <t>ω‐agatoxin</t> <t>IVA</t> <t>(red</t> curves) or 320 n m ω‐conotoxin GVIA (green curves). n represents the total number of wells recorded from eight independent neuronal cultures. ns, P > 0.05, *, P < 0.05 and **, P < 0.01 against the corresponding WT, using paired nonparametric t ‐tests. Note that Wilcoxon t ‐tests have been performed to account for technical data pairing between neighbouring MAP6 KO and WT culture wells and this pairing was deemed as highly significant ( P < 0.01) for each panel. (B) Left panel, example of identified axons (yellow arrowheads) from a neuronal culture with immunolabelled microtubules (red), tau (green) and nuclei (blue). Right panel, measurements of axonal length of WT (white symbols) and MAP6 KO (grey symbols) hippocampal neurons after 48 h in the absence (sham, discs) or presence (conotox, diamonds) of 320 n m ω‐conotoxin GVIA. n represents the total number of neurons measured from three independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding sham, using unpaired nonparametric t ‐tests. Scale bar = 10 μm. (C) Left panel, examples of spontaneous calcium activity recorded from fluo‐4‐loaded WT (black line) and MAP6 KO (grey line) hippocampal neurons. Right panel, quantification of mean peak intensity during spontaneous calcium activity of fluo‐4‐loaded WT (white discs) and MAP6 KO (grey discs) hippocampal neurons, recorded in cell bodies and neurites, independently, normalized by that of WT (dashed grey line = 100%). n represents the total number of fields recorded from six independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding WT, using unpaired parametric t ‐tests.[Colour figure can be viewed at wileyonlinelibrary.com ].
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    Image Search Results


    Effect of tefluthin, β-pompilidoxin, tefluthrin plus sparsentan, β-pompilidotoxin plus sparsentan on I Na in GH 3 cells. The voltage-clamp experiments were undertaken, as cells were voltage-clamped at −80 mV and the depolarizing pulse to −10 mV was imposed to them. ( A ) Representative current traces obtained in the control period (a, sparsentan was not present), and during exposure to 3 μM sparsentan (b) or to 3 μM sparsentan plus 3 μM tefluthrin (c). The top panel indicates the voltage-clamp protocol applied. Of note, the deactivating I Na was additionally detected as membrane potential was returned to −50 mV with a duration of 40 ms. ( B ) Summary bar graph demonstrating effect of 3 μM tefluthrin, 3 μM β-pompilidotoxn, 3 μM tefluthrin plus 3 μM sparsentan and 3 μM β-pompilidotoxin plus 3 μM sparsentan on the peak amplitude of I Na (mean ± SEM; n = 8 for each bar). The peak amplitude was measured at the start of 40 ms depolarizing command voltage from −80 to −10 mV. Tef: tefluthrin; Pomp: β-pompilidotoxin; Spar, sparsentan. Statistical analysis was performed by one-way ANOVA ( p < 0.05). * Significantly different from controls ( p < 0.05) and ** significantly different from Tef (3 μM) or Pomp (3 μM) alone group ( p < 0.05).

    Journal: Biomedicines

    Article Title: The Evidence for Sparsentan-Mediated Inhibition of I Na and I K(erg) : Possibly Unlinked to Its Antagonism of Angiotensin II or Endothelin Type a Receptor

    doi: 10.3390/biomedicines10010086

    Figure Lengend Snippet: Effect of tefluthin, β-pompilidoxin, tefluthrin plus sparsentan, β-pompilidotoxin plus sparsentan on I Na in GH 3 cells. The voltage-clamp experiments were undertaken, as cells were voltage-clamped at −80 mV and the depolarizing pulse to −10 mV was imposed to them. ( A ) Representative current traces obtained in the control period (a, sparsentan was not present), and during exposure to 3 μM sparsentan (b) or to 3 μM sparsentan plus 3 μM tefluthrin (c). The top panel indicates the voltage-clamp protocol applied. Of note, the deactivating I Na was additionally detected as membrane potential was returned to −50 mV with a duration of 40 ms. ( B ) Summary bar graph demonstrating effect of 3 μM tefluthrin, 3 μM β-pompilidotoxn, 3 μM tefluthrin plus 3 μM sparsentan and 3 μM β-pompilidotoxin plus 3 μM sparsentan on the peak amplitude of I Na (mean ± SEM; n = 8 for each bar). The peak amplitude was measured at the start of 40 ms depolarizing command voltage from −80 to −10 mV. Tef: tefluthrin; Pomp: β-pompilidotoxin; Spar, sparsentan. Statistical analysis was performed by one-way ANOVA ( p < 0.05). * Significantly different from controls ( p < 0.05) and ** significantly different from Tef (3 μM) or Pomp (3 μM) alone group ( p < 0.05).

    Article Snippet: Angiotensin II (AngII), endothelin 1, tefluthrin (Tef), tetraethylammonium chloride (TEA) were supplied by Sigma-Aldrich (Merck, Taipei, Taiwan) and β-pompilidotoxin (Pomp) and tetrodotoxin (TTX) were by Alomone (Jerusalem, Israel).

    Techniques:

    AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits (GluN2A and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or Ro-25-6981 vs. Vehicle)

    Journal: Molecular Neurobiology

    Article Title: Chronic AdipoRon Treatment Mimics the Effects of Physical Exercise on Restoring Hippocampal Neuroplasticity in Diabetic Mice

    doi: 10.1007/s12035-021-02441-7

    Figure Lengend Snippet: AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits (GluN2A and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or Ro-25-6981 vs. Vehicle)

    Article Snippet: In pharmacological intervention, brain slices were acutely perfused in PEAQX tetrasodium hydrate (0.1 μM; NVP-AAM077) (Sigma-Aldrich, MO, USA) to inhibit GluN2A subunit ( ) or in Ro 25-6981 maleate (0.5 μM) (Alomone Labs, Israel) to inhibit GluN2B subunit ( ) for 30 min before HFS.

    Techniques: Slice Preparation, Inhibition

    Specificity of Ca v 2‐type calcium channels deficit in MAP6 KO neurons. (A) Left panel, examples of KCl‐stimulated fluo‐4‐loaded WT cortical neurons in the absence (black line) or presence (yellow line) of 20 μ m nimodipine. Right panels, ratios of KCl‐elicited fluorescence intensity peaks, recorded from WT (white squares) and MAP6 KO (grey squares) cortical neurons in the presence or absence of 20 μ m nimodipine (yellow curves), 180 n m ω‐agatoxin IVA (red curves) or 320 n m ω‐conotoxin GVIA (green curves). n represents the total number of wells recorded from eight independent neuronal cultures. ns, P > 0.05, *, P < 0.05 and **, P < 0.01 against the corresponding WT, using paired nonparametric t ‐tests. Note that Wilcoxon t ‐tests have been performed to account for technical data pairing between neighbouring MAP6 KO and WT culture wells and this pairing was deemed as highly significant ( P < 0.01) for each panel. (B) Left panel, example of identified axons (yellow arrowheads) from a neuronal culture with immunolabelled microtubules (red), tau (green) and nuclei (blue). Right panel, measurements of axonal length of WT (white symbols) and MAP6 KO (grey symbols) hippocampal neurons after 48 h in the absence (sham, discs) or presence (conotox, diamonds) of 320 n m ω‐conotoxin GVIA. n represents the total number of neurons measured from three independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding sham, using unpaired nonparametric t ‐tests. Scale bar = 10 μm. (C) Left panel, examples of spontaneous calcium activity recorded from fluo‐4‐loaded WT (black line) and MAP6 KO (grey line) hippocampal neurons. Right panel, quantification of mean peak intensity during spontaneous calcium activity of fluo‐4‐loaded WT (white discs) and MAP6 KO (grey discs) hippocampal neurons, recorded in cell bodies and neurites, independently, normalized by that of WT (dashed grey line = 100%). n represents the total number of fields recorded from six independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding WT, using unpaired parametric t ‐tests.[Colour figure can be viewed at wileyonlinelibrary.com ].

    Journal: The European Journal of Neuroscience

    Article Title: MAP6 interacts with Tctex1 and Ca v 2.2/N‐type calcium channels to regulate calcium signalling in neurons

    doi: 10.1111/ejn.13766

    Figure Lengend Snippet: Specificity of Ca v 2‐type calcium channels deficit in MAP6 KO neurons. (A) Left panel, examples of KCl‐stimulated fluo‐4‐loaded WT cortical neurons in the absence (black line) or presence (yellow line) of 20 μ m nimodipine. Right panels, ratios of KCl‐elicited fluorescence intensity peaks, recorded from WT (white squares) and MAP6 KO (grey squares) cortical neurons in the presence or absence of 20 μ m nimodipine (yellow curves), 180 n m ω‐agatoxin IVA (red curves) or 320 n m ω‐conotoxin GVIA (green curves). n represents the total number of wells recorded from eight independent neuronal cultures. ns, P > 0.05, *, P < 0.05 and **, P < 0.01 against the corresponding WT, using paired nonparametric t ‐tests. Note that Wilcoxon t ‐tests have been performed to account for technical data pairing between neighbouring MAP6 KO and WT culture wells and this pairing was deemed as highly significant ( P < 0.01) for each panel. (B) Left panel, example of identified axons (yellow arrowheads) from a neuronal culture with immunolabelled microtubules (red), tau (green) and nuclei (blue). Right panel, measurements of axonal length of WT (white symbols) and MAP6 KO (grey symbols) hippocampal neurons after 48 h in the absence (sham, discs) or presence (conotox, diamonds) of 320 n m ω‐conotoxin GVIA. n represents the total number of neurons measured from three independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding sham, using unpaired nonparametric t ‐tests. Scale bar = 10 μm. (C) Left panel, examples of spontaneous calcium activity recorded from fluo‐4‐loaded WT (black line) and MAP6 KO (grey line) hippocampal neurons. Right panel, quantification of mean peak intensity during spontaneous calcium activity of fluo‐4‐loaded WT (white discs) and MAP6 KO (grey discs) hippocampal neurons, recorded in cell bodies and neurites, independently, normalized by that of WT (dashed grey line = 100%). n represents the total number of fields recorded from six independent neuronal cultures. ns, P > 0.05 and *, P < 0.05 as compared to corresponding WT, using unpaired parametric t ‐tests.[Colour figure can be viewed at wileyonlinelibrary.com ].

    Article Snippet: Twenty‐four‐well plates of cortical cultures after 7–8 DIV were incubated at 37 °C without CO 2 , in the presence of 1 μ m Fluo‐4 (Thermo Fisher Scientific, France) in warm aCSF containing LiCl + KA, in the absence [nimo] or presence [toxins] of 20 μ m nimodipine (see above, ), during 20 min. Each well was rinsed with aCSF containing LiCl + KA, without [nimo] or with [toxins] 20 m m nimodipine and 450 μL of fresh medium containing also DMSO or 20 μ m nimodipine [nimo] on the one hand or DMSO, 320 n m ω‐conotoxin GVIA (STC‐750, Alomone Labs, Israel, diluted to 160 μ m in DMSO) or 180 n m ω‐agatoxin IVA (STC‐750, Alomone Labs, Israel, diluted to 90 μ m in DMSO) [toxins] on the other hand, was added to the corresponding wells.

    Techniques: Fluorescence, Activity Assay