retigabine  (Alomone Labs)


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    Alomone Labs retigabine
    Retigabine, 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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    retigabine  (Alomone Labs)


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    Alomone Labs retigabine
    Retigabine, 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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    retigabine  (Alomone Labs)


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    Alomone Labs retigabine
    Retigabine’s effect on excitability of cKO PV-INs. A: representative voltage responses to a ramp protocol in CA1 PV-INs from WT and cKO slices before and after bath application of RTG (10 µM). ( B) : summary graphs showing the effect of 10 µM <t>retigabine</t> (RTG) on action potential number (WT, n = 19; cKO, n = 19; ** p < 0.01, Genotype x Treatment interaction: F=9.5, p <0.01 with two-way ANOVA). ( C ) Bath application of RTG in hippocampal slices significantly hyperpolarized the RMP of PV-INs from both WT and cKO mice, but RTG had a smaller effect on RMP from cKO mice (WT, n = 19; cKO, n = 18; ** p < 0.01; interaction: p = 0.046 with two-way ANOVA). (D) Bath application of RTG significantly increased the rheobase of PV-INs from both WT and cKO mice, but RTG had less effects on cKO mice (WT, n = 19; cKO, n = 18; ** p < 0.01, interaction: p= 0.046 with two-way ANOVA).
    Retigabine, 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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    1) Product Images from "Removal of KCNQ2 from Parvalbumin-expressing Interneurons Improves Anti-Seizure Efficacy of Retigabine"

    Article Title: Removal of KCNQ2 from Parvalbumin-expressing Interneurons Improves Anti-Seizure Efficacy of Retigabine

    Journal: bioRxiv

    doi: 10.1101/2020.12.09.417295

    Retigabine’s effect on excitability of cKO PV-INs. A: representative voltage responses to a ramp protocol in CA1 PV-INs from WT and cKO slices before and after bath application of RTG (10 µM). ( B) : summary graphs showing the effect of 10 µM retigabine (RTG) on action potential number (WT, n = 19; cKO, n = 19; ** p < 0.01, Genotype x Treatment interaction: F=9.5, p <0.01 with two-way ANOVA). ( C ) Bath application of RTG in hippocampal slices significantly hyperpolarized the RMP of PV-INs from both WT and cKO mice, but RTG had a smaller effect on RMP from cKO mice (WT, n = 19; cKO, n = 18; ** p < 0.01; interaction: p = 0.046 with two-way ANOVA). (D) Bath application of RTG significantly increased the rheobase of PV-INs from both WT and cKO mice, but RTG had less effects on cKO mice (WT, n = 19; cKO, n = 18; ** p < 0.01, interaction: p= 0.046 with two-way ANOVA).
    Figure Legend Snippet: Retigabine’s effect on excitability of cKO PV-INs. A: representative voltage responses to a ramp protocol in CA1 PV-INs from WT and cKO slices before and after bath application of RTG (10 µM). ( B) : summary graphs showing the effect of 10 µM retigabine (RTG) on action potential number (WT, n = 19; cKO, n = 19; ** p < 0.01, Genotype x Treatment interaction: F=9.5, p <0.01 with two-way ANOVA). ( C ) Bath application of RTG in hippocampal slices significantly hyperpolarized the RMP of PV-INs from both WT and cKO mice, but RTG had a smaller effect on RMP from cKO mice (WT, n = 19; cKO, n = 18; ** p < 0.01; interaction: p = 0.046 with two-way ANOVA). (D) Bath application of RTG significantly increased the rheobase of PV-INs from both WT and cKO mice, but RTG had less effects on cKO mice (WT, n = 19; cKO, n = 18; ** p < 0.01, interaction: p= 0.046 with two-way ANOVA).

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    conditioning paradigm with retigabine  (Alomone Labs)


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    Alomone Labs conditioning paradigm with retigabine
    (a) Schematic of spared nerve injury and tissues of interest. (b, c) Once neuropathic pain was established on day 7 after SNI, male (n=6) and female (n=6) mice were treated with oral 1c (350 μmol/kg/day), diroximel fumarate (350 μmol/kg/day), or vehicle every day for 3 days (gray box). (b) Mechanical allodynia and (c) dynamic allodynia were assessed. Relative to vehicle: * P <0.05, ** P <0.01, *** P <0.001; 1c vs. diroximel fumarate: ## P <0.01, ### P <0.001. (d) Seven days after SNI, male (n=3) and female (n=3) mice were treated with oral 1c (350 μmol/kg/day) or subcutaneous morphine (3 mg/kg, b.i.d.). Relative to 1c Day 0 (D0, prior to surgery): ** P <0.01, *** P <0.001; relative to morphine D0: # P <0.05, ### P <0.001. (e) Male (n=3) and female (n=3) mice were treated with oral 1c (350 µmol/kg/day), diroximel fumarate (350 µmol/kg/day) or vehicle every day for 7 days, beginning 7 days after SNI or sham surgery. Presence of ongoing pain was interpreted as an increase in time spent in <t>retigabine-paired</t> chamber (conditioning stimulus) after 7 days of treatment, relative to baseline. Relative to sham-vehicle: †† P <0.01; relative to SNI-vehicle: * P <0.05, *** P <0.001. (f) Male and female Nfe2l2 -/- and wildtype control mice (n=3/sex/group) were treated with oral 1c (350 μmol/kg/day), beginning 7 days after SNI, and mechanical allodynia assessed. Relative to wildtype controls: *** P <0.001. (g) L4/5 DRG from 3 mice were pooled after 3 days of treatment, and nuclear extracts were probed for Nrf2 (n=2 males, n=2 females). Relative to ipsilateral vehicle: *** P <0.001; relative to contralateral vehicle and 1c : ††† P <0.001. (h) Antioxidant gene expression L4/5 DRG was determined after 3 days of treatment (n=3 males, n=3 females). Relative to ipsilateral vehicle: * P <0.05, ** P <0.01; relative to contralateral vehicle: # P <0.05; relative to contralateral 1c : † P <0.05; †† P <0.01, ††† P <0.001. ( i ) Naive male (n=3) and female (n = 3) mice were orally treated with 1c (350 µmol/kg), diroximel fumarate (350 µmol/kg), or vehicle daily for 10 days. Blood was collected by cardiac puncture and leukocytes were manually counted. Relative to vehicle: * P <0.05. Individual replicates are presented in spaghetti plots or grey dots.
    Conditioning Paradigm With Retigabine, 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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    1) Product Images from "Drug targeting to sites of oxidative stress using the Baeyer-Villiger reaction"

    Article Title: Drug targeting to sites of oxidative stress using the Baeyer-Villiger reaction

    Journal: bioRxiv

    doi: 10.1101/2021.09.03.458872

    (a) Schematic of spared nerve injury and tissues of interest. (b, c) Once neuropathic pain was established on day 7 after SNI, male (n=6) and female (n=6) mice were treated with oral 1c (350 μmol/kg/day), diroximel fumarate (350 μmol/kg/day), or vehicle every day for 3 days (gray box). (b) Mechanical allodynia and (c) dynamic allodynia were assessed. Relative to vehicle: * P <0.05, ** P <0.01, *** P <0.001; 1c vs. diroximel fumarate: ## P <0.01, ### P <0.001. (d) Seven days after SNI, male (n=3) and female (n=3) mice were treated with oral 1c (350 μmol/kg/day) or subcutaneous morphine (3 mg/kg, b.i.d.). Relative to 1c Day 0 (D0, prior to surgery): ** P <0.01, *** P <0.001; relative to morphine D0: # P <0.05, ### P <0.001. (e) Male (n=3) and female (n=3) mice were treated with oral 1c (350 µmol/kg/day), diroximel fumarate (350 µmol/kg/day) or vehicle every day for 7 days, beginning 7 days after SNI or sham surgery. Presence of ongoing pain was interpreted as an increase in time spent in retigabine-paired chamber (conditioning stimulus) after 7 days of treatment, relative to baseline. Relative to sham-vehicle: †† P <0.01; relative to SNI-vehicle: * P <0.05, *** P <0.001. (f) Male and female Nfe2l2 -/- and wildtype control mice (n=3/sex/group) were treated with oral 1c (350 μmol/kg/day), beginning 7 days after SNI, and mechanical allodynia assessed. Relative to wildtype controls: *** P <0.001. (g) L4/5 DRG from 3 mice were pooled after 3 days of treatment, and nuclear extracts were probed for Nrf2 (n=2 males, n=2 females). Relative to ipsilateral vehicle: *** P <0.001; relative to contralateral vehicle and 1c : ††† P <0.001. (h) Antioxidant gene expression L4/5 DRG was determined after 3 days of treatment (n=3 males, n=3 females). Relative to ipsilateral vehicle: * P <0.05, ** P <0.01; relative to contralateral vehicle: # P <0.05; relative to contralateral 1c : † P <0.05; †† P <0.01, ††† P <0.001. ( i ) Naive male (n=3) and female (n = 3) mice were orally treated with 1c (350 µmol/kg), diroximel fumarate (350 µmol/kg), or vehicle daily for 10 days. Blood was collected by cardiac puncture and leukocytes were manually counted. Relative to vehicle: * P <0.05. Individual replicates are presented in spaghetti plots or grey dots.
    Figure Legend Snippet: (a) Schematic of spared nerve injury and tissues of interest. (b, c) Once neuropathic pain was established on day 7 after SNI, male (n=6) and female (n=6) mice were treated with oral 1c (350 μmol/kg/day), diroximel fumarate (350 μmol/kg/day), or vehicle every day for 3 days (gray box). (b) Mechanical allodynia and (c) dynamic allodynia were assessed. Relative to vehicle: * P <0.05, ** P <0.01, *** P <0.001; 1c vs. diroximel fumarate: ## P <0.01, ### P <0.001. (d) Seven days after SNI, male (n=3) and female (n=3) mice were treated with oral 1c (350 μmol/kg/day) or subcutaneous morphine (3 mg/kg, b.i.d.). Relative to 1c Day 0 (D0, prior to surgery): ** P <0.01, *** P <0.001; relative to morphine D0: # P <0.05, ### P <0.001. (e) Male (n=3) and female (n=3) mice were treated with oral 1c (350 µmol/kg/day), diroximel fumarate (350 µmol/kg/day) or vehicle every day for 7 days, beginning 7 days after SNI or sham surgery. Presence of ongoing pain was interpreted as an increase in time spent in retigabine-paired chamber (conditioning stimulus) after 7 days of treatment, relative to baseline. Relative to sham-vehicle: †† P <0.01; relative to SNI-vehicle: * P <0.05, *** P <0.001. (f) Male and female Nfe2l2 -/- and wildtype control mice (n=3/sex/group) were treated with oral 1c (350 μmol/kg/day), beginning 7 days after SNI, and mechanical allodynia assessed. Relative to wildtype controls: *** P <0.001. (g) L4/5 DRG from 3 mice were pooled after 3 days of treatment, and nuclear extracts were probed for Nrf2 (n=2 males, n=2 females). Relative to ipsilateral vehicle: *** P <0.001; relative to contralateral vehicle and 1c : ††† P <0.001. (h) Antioxidant gene expression L4/5 DRG was determined after 3 days of treatment (n=3 males, n=3 females). Relative to ipsilateral vehicle: * P <0.05, ** P <0.01; relative to contralateral vehicle: # P <0.05; relative to contralateral 1c : † P <0.05; †† P <0.01, ††† P <0.001. ( i ) Naive male (n=3) and female (n = 3) mice were orally treated with 1c (350 µmol/kg), diroximel fumarate (350 µmol/kg), or vehicle daily for 10 days. Blood was collected by cardiac puncture and leukocytes were manually counted. Relative to vehicle: * P <0.05. Individual replicates are presented in spaghetti plots or grey dots.

    Techniques Used: Expressing

    retigabine  (Alomone Labs)


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    Alomone Labs retigabine
    Effects of <t>retigabine</t> on the sensory and motor behaviors following oxaliplatin treatment. Oxaliplatin (oxa, 5 mg/kg, ip) was administrated at Day 0. Retigabine (10 mg/kg, ip, daily) was treated at Day –2, Day –1, Day 0, Day 1, and Day 2. The same groups of animals were tested for mechanical and cold behaviors at Day 3, and were tested for heat and motor behaviors at Day 4. (A) Paw withdrawal threshold to Von-Frey filament; (B) Score of withdrawal response to acetone; (C) Paw withdrawal latency to radiant heat; and (D) Time stayed on rod at different speeds in rotarod tests ( n = 6 for all groups). *, P < 0.05; **, P < 0.01; ****, P < 0.0001; two-way repeated measure ANOVA.
    Retigabine, 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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    1) Product Images from "Oxaliplatin Depolarizes the IB4 – Dorsal Root Ganglion Neurons to Drive the Development of Neuropathic Pain Through TRPM8 in Mice"

    Article Title: Oxaliplatin Depolarizes the IB4 – Dorsal Root Ganglion Neurons to Drive the Development of Neuropathic Pain Through TRPM8 in Mice

    Journal: Frontiers in Molecular Neuroscience

    doi: 10.3389/fnmol.2021.690858

    Effects of retigabine on the sensory and motor behaviors following oxaliplatin treatment. Oxaliplatin (oxa, 5 mg/kg, ip) was administrated at Day 0. Retigabine (10 mg/kg, ip, daily) was treated at Day –2, Day –1, Day 0, Day 1, and Day 2. The same groups of animals were tested for mechanical and cold behaviors at Day 3, and were tested for heat and motor behaviors at Day 4. (A) Paw withdrawal threshold to Von-Frey filament; (B) Score of withdrawal response to acetone; (C) Paw withdrawal latency to radiant heat; and (D) Time stayed on rod at different speeds in rotarod tests ( n = 6 for all groups). *, P < 0.05; **, P < 0.01; ****, P < 0.0001; two-way repeated measure ANOVA.
    Figure Legend Snippet: Effects of retigabine on the sensory and motor behaviors following oxaliplatin treatment. Oxaliplatin (oxa, 5 mg/kg, ip) was administrated at Day 0. Retigabine (10 mg/kg, ip, daily) was treated at Day –2, Day –1, Day 0, Day 1, and Day 2. The same groups of animals were tested for mechanical and cold behaviors at Day 3, and were tested for heat and motor behaviors at Day 4. (A) Paw withdrawal threshold to Von-Frey filament; (B) Score of withdrawal response to acetone; (C) Paw withdrawal latency to radiant heat; and (D) Time stayed on rod at different speeds in rotarod tests ( n = 6 for all groups). *, P < 0.05; **, P < 0.01; ****, P < 0.0001; two-way repeated measure ANOVA.

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    Effects of TC-I on the sensory and motor behaviors following oxaliplatin treatment. The administration of oxaliplatin, the schedule for TC-I (10 mg/kg, ip) treatment (same to the Retigabine treatment), the testing schedule for different types of behaviors were described in the Legend of . (A) Paw withdrawal threshold to Von-Frey filament; (B) Score of withdrawal response to acetone; (C) Paw withdrawal latency to radiant heat; and (D) Time stayed on rod at different speeds in rotarod tests ( n = 6 for all groups). **, P < 0.01; ****, P < 0.0001; two-way repeated measure ANOVA.
    Figure Legend Snippet: Effects of TC-I on the sensory and motor behaviors following oxaliplatin treatment. The administration of oxaliplatin, the schedule for TC-I (10 mg/kg, ip) treatment (same to the Retigabine treatment), the testing schedule for different types of behaviors were described in the Legend of . (A) Paw withdrawal threshold to Von-Frey filament; (B) Score of withdrawal response to acetone; (C) Paw withdrawal latency to radiant heat; and (D) Time stayed on rod at different speeds in rotarod tests ( n = 6 for all groups). **, P < 0.01; ****, P < 0.0001; two-way repeated measure ANOVA.

    Techniques Used:

    Effects of A-967079 on the sensory and motor behaviors following oxaliplatin treatment. The administration of oxaliplatin, the schedule for A-967079 (A-96, 100 mg/kg, po) treatment (same to the Retigabine and TC-I treatment), the testing schedule for different types of behaviors were described in the Legend of . (A) Paw withdrawal threshold to Von-Frey filament; (B) Score of withdrawal response to acetone; (C) Paw withdrawal latency to radiant heat; and (D) Time stayed on rod at different speeds in rotarod tests ( n = 6 for all groups).
    Figure Legend Snippet: Effects of A-967079 on the sensory and motor behaviors following oxaliplatin treatment. The administration of oxaliplatin, the schedule for A-967079 (A-96, 100 mg/kg, po) treatment (same to the Retigabine and TC-I treatment), the testing schedule for different types of behaviors were described in the Legend of . (A) Paw withdrawal threshold to Von-Frey filament; (B) Score of withdrawal response to acetone; (C) Paw withdrawal latency to radiant heat; and (D) Time stayed on rod at different speeds in rotarod tests ( n = 6 for all groups).

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    retigabine  (Alomone Labs)


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    Alomone Labs retigabine
    Retigabine, 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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    retigabine  (Alomone Labs)


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    Alomone Labs retigabine
    PI(4,5)P 2 regulates the action of <t>Retigabine.</t> (A–C) K + -currents were activated with a +40 mV pulses of variable duration in Xenopus oocytes expression K V 7.2/K V 7.3 channels. Subsequently, the currents were deactivated at −90 mV. These recordings were performed in the absence (A) and the presence of 1 µM (blue diamonds, n = 6) and 5 µM of Retigabine (red triangles, n = 7) (C) . (D–F) A two-exponential function was fitted to deactivating currents and the yielded τ 1 , τ 2 and the fractional contribution of the second component (fraction of τ 2 ) were plotted against t PULSE . ( D–F , respectively). (G–I) Semi-logarithmic version of the plot in (D–F) , detailing τ DEACT for t PULSE up to 1 second. For reference, the equivalent values from were plotted as small black square and small red circles. Black arrows in panels (D–I) indicate the range of t PULSE values at which values were statistically different between the recordings in the presence of 1 µM and 5 µM Retigabine.
    Retigabine, 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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    1) Product Images from "Modulation of K V 7 Channel Deactivation by PI(4,5)P 2"

    Article Title: Modulation of K V 7 Channel Deactivation by PI(4,5)P 2

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2020.00895

    PI(4,5)P 2 regulates the action of Retigabine. (A–C) K + -currents were activated with a +40 mV pulses of variable duration in Xenopus oocytes expression K V 7.2/K V 7.3 channels. Subsequently, the currents were deactivated at −90 mV. These recordings were performed in the absence (A) and the presence of 1 µM (blue diamonds, n = 6) and 5 µM of Retigabine (red triangles, n = 7) (C) . (D–F) A two-exponential function was fitted to deactivating currents and the yielded τ 1 , τ 2 and the fractional contribution of the second component (fraction of τ 2 ) were plotted against t PULSE . ( D–F , respectively). (G–I) Semi-logarithmic version of the plot in (D–F) , detailing τ DEACT for t PULSE up to 1 second. For reference, the equivalent values from were plotted as small black square and small red circles. Black arrows in panels (D–I) indicate the range of t PULSE values at which values were statistically different between the recordings in the presence of 1 µM and 5 µM Retigabine.
    Figure Legend Snippet: PI(4,5)P 2 regulates the action of Retigabine. (A–C) K + -currents were activated with a +40 mV pulses of variable duration in Xenopus oocytes expression K V 7.2/K V 7.3 channels. Subsequently, the currents were deactivated at −90 mV. These recordings were performed in the absence (A) and the presence of 1 µM (blue diamonds, n = 6) and 5 µM of Retigabine (red triangles, n = 7) (C) . (D–F) A two-exponential function was fitted to deactivating currents and the yielded τ 1 , τ 2 and the fractional contribution of the second component (fraction of τ 2 ) were plotted against t PULSE . ( D–F , respectively). (G–I) Semi-logarithmic version of the plot in (D–F) , detailing τ DEACT for t PULSE up to 1 second. For reference, the equivalent values from were plotted as small black square and small red circles. Black arrows in panels (D–I) indicate the range of t PULSE values at which values were statistically different between the recordings in the presence of 1 µM and 5 µM Retigabine.

    Techniques Used: Expressing

    Overall deactivation kinetics as a function of the t PULSE . (A) As before, to consolidate the analysis of the deactivation kinetics, τ DEACT was plotted against the duration of the +40-mV Pulse (t PULSE ) for currents recorded in the presence of 1 μM and 5 μM Retigabine (blue open diamonds and red oepn hexagons, respectively). (B) The values of τ DEACT were significantly different for t PULSE longer than 61 ms. For reference, the equivalent values from were plotted as black solid square and red solid circles. (C, D) Equivalent τ DEACT -t PULSE plots generated from Wortmannin-treated oocytes.
    Figure Legend Snippet: Overall deactivation kinetics as a function of the t PULSE . (A) As before, to consolidate the analysis of the deactivation kinetics, τ DEACT was plotted against the duration of the +40-mV Pulse (t PULSE ) for currents recorded in the presence of 1 μM and 5 μM Retigabine (blue open diamonds and red oepn hexagons, respectively). (B) The values of τ DEACT were significantly different for t PULSE longer than 61 ms. For reference, the equivalent values from were plotted as black solid square and red solid circles. (C, D) Equivalent τ DEACT -t PULSE plots generated from Wortmannin-treated oocytes.

    Techniques Used: Generated

    To determine whether the decrease in the rate of deactivation was a unique property of the heteromeric K V 7.2/K V 7.3 channel. (A, B) K + -current recordings from oocytes expressing K V 7.2 in the absence and presence of 10μM Retigabine (RTG). (C) τ DEACT was plotted as a function of t PULSE for the homomeric K V 7.2. It was found that the slow down of the deactvation kinetics still occurs when K V 7.2 was expressed alone, suggesting that the hysteretic behavior of these K V 7 channels was not a property emerging from heteromerization ( n = 5). (D) τ DEACT -t PULSE plots in C, replotted with a logarithmic t PULSE to highlight the behavior of τ DEACT at short t PULSE values.
    Figure Legend Snippet: To determine whether the decrease in the rate of deactivation was a unique property of the heteromeric K V 7.2/K V 7.3 channel. (A, B) K + -current recordings from oocytes expressing K V 7.2 in the absence and presence of 10μM Retigabine (RTG). (C) τ DEACT was plotted as a function of t PULSE for the homomeric K V 7.2. It was found that the slow down of the deactvation kinetics still occurs when K V 7.2 was expressed alone, suggesting that the hysteretic behavior of these K V 7 channels was not a property emerging from heteromerization ( n = 5). (D) τ DEACT -t PULSE plots in C, replotted with a logarithmic t PULSE to highlight the behavior of τ DEACT at short t PULSE values.

    Techniques Used: Expressing

    retigabine  (Alomone Labs)


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    Alomone Labs retigabine
    Retigabine, 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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    retigabine  (Alomone Labs)


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    Alomone Labs retigabine
    Retigabine, 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 retigabine
    A) Current injection data from layer II/III PLC pyramidal cells of HFD-exposed mice before and after bath application of 100 μM <t>retigabine,</t> with representative traces shown on the left and summary data on the right. We observed significant main effects of current injected (F(20,160) = 23.07, p < 0.001) and drug (F(20,160) = 23.07, p < 0.001) and an interaction of drug and current (F(1,8) = 39.8, p < 0.001, 2-way RM ANOVA). Retigabine reduced the number of action potentials in response to currents of 20 pA to 200 pA (20 pA, p = 0.037; 30 pA: p = 0.01; 40 pA, p = 0.006; 50 pA, p = 0.001; 60 pA, p = 0.002; 70–200 pA: p < 0.001, n = 5 cells per condition, Fisher’s LSD). B) Representative traces and current injection data from layer II/III PLC pyramidal cells from vehicle injected CD- or HFD-exposed mice, in comparison to retigabine treated HFD mice, using slices isolated 24 h after the last of eight daily doses of retigabine. A two-way RM ANOVA revealed a main effect of current injected (F(1.544,44.78) = 69.63, p < 0.001), treatment (F(2,29) = 3.79, p = 0.035) and an interaction of current and treatment (F(40,580) = 5.16, p < 0.001). HFD exposure (vs. CD) increased the number of action potentials in response to currents of 180 pA to 200 pA (180 pA, p = 0.035; 190 pA, p = 0.047; 200 pA, p = 0.042, Fisher’s LSD). Retigabine increased the number of action potentials in response to currents of 60 pA to 120 pA (60 pA–80 pA, p < 0.01; 90 pA, p = 0.011; 100 pA, p = 0.022; 110 pA, p < 0.01; 120 pA, p = 0.027; Fisher’s LSD, n = 6–14 cells from at least four animals per condition). C) Representative traces and summary data of Ih currents recorded from layer II/III PLC pyramidal cells from behaviorally naïve CD- or HFD-exposed mice, using slices isolated 24 h after the last of eight daily doses of retigabine or vehicle. A two-way RM ANOVA revealed a main effect of V step (F(5,125) = 6.75, p < 0.001) and an interaction of diet and voltage (F(10,125) = 2.73, p = 0.005, 2-way RM ANOVA). HFD exposure (vs. CD) increased Ih currents in response to V-steps of −110 mV to −120 mV (−110 mV, p = 0.026; −120 mV, p = 0.002, n = 7–12 cells from at least four animals per condition). Retigabine (vs vehicle) reduced Ih currents of HFD-exposed mice in response to V steps of −100 mV to −120 mV (−100 mV, p = 0.03; −110 mV, p = 0.002; −120 mV, p = 0.001; n = 9–12 cells from at least four animals per condition, Fisher’s LSD). Error bars, SEMs; *,$p < 0.05, **,$ $p < 0.01.
    Retigabine, 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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    1) Product Images from "Reversal of a treatment-resistant, depression-related brain state with the Kv7 channel opener retigabine"

    Article Title: Reversal of a treatment-resistant, depression-related brain state with the Kv7 channel opener retigabine

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2019.03.003

    A) Current injection data from layer II/III PLC pyramidal cells of HFD-exposed mice before and after bath application of 100 μM retigabine, with representative traces shown on the left and summary data on the right. We observed significant main effects of current injected (F(20,160) = 23.07, p < 0.001) and drug (F(20,160) = 23.07, p < 0.001) and an interaction of drug and current (F(1,8) = 39.8, p < 0.001, 2-way RM ANOVA). Retigabine reduced the number of action potentials in response to currents of 20 pA to 200 pA (20 pA, p = 0.037; 30 pA: p = 0.01; 40 pA, p = 0.006; 50 pA, p = 0.001; 60 pA, p = 0.002; 70–200 pA: p < 0.001, n = 5 cells per condition, Fisher’s LSD). B) Representative traces and current injection data from layer II/III PLC pyramidal cells from vehicle injected CD- or HFD-exposed mice, in comparison to retigabine treated HFD mice, using slices isolated 24 h after the last of eight daily doses of retigabine. A two-way RM ANOVA revealed a main effect of current injected (F(1.544,44.78) = 69.63, p < 0.001), treatment (F(2,29) = 3.79, p = 0.035) and an interaction of current and treatment (F(40,580) = 5.16, p < 0.001). HFD exposure (vs. CD) increased the number of action potentials in response to currents of 180 pA to 200 pA (180 pA, p = 0.035; 190 pA, p = 0.047; 200 pA, p = 0.042, Fisher’s LSD). Retigabine increased the number of action potentials in response to currents of 60 pA to 120 pA (60 pA–80 pA, p < 0.01; 90 pA, p = 0.011; 100 pA, p = 0.022; 110 pA, p < 0.01; 120 pA, p = 0.027; Fisher’s LSD, n = 6–14 cells from at least four animals per condition). C) Representative traces and summary data of Ih currents recorded from layer II/III PLC pyramidal cells from behaviorally naïve CD- or HFD-exposed mice, using slices isolated 24 h after the last of eight daily doses of retigabine or vehicle. A two-way RM ANOVA revealed a main effect of V step (F(5,125) = 6.75, p < 0.001) and an interaction of diet and voltage (F(10,125) = 2.73, p = 0.005, 2-way RM ANOVA). HFD exposure (vs. CD) increased Ih currents in response to V-steps of −110 mV to −120 mV (−110 mV, p = 0.026; −120 mV, p = 0.002, n = 7–12 cells from at least four animals per condition). Retigabine (vs vehicle) reduced Ih currents of HFD-exposed mice in response to V steps of −100 mV to −120 mV (−100 mV, p = 0.03; −110 mV, p = 0.002; −120 mV, p = 0.001; n = 9–12 cells from at least four animals per condition, Fisher’s LSD). Error bars, SEMs; *,$p < 0.05, **,$ $p < 0.01.
    Figure Legend Snippet: A) Current injection data from layer II/III PLC pyramidal cells of HFD-exposed mice before and after bath application of 100 μM retigabine, with representative traces shown on the left and summary data on the right. We observed significant main effects of current injected (F(20,160) = 23.07, p < 0.001) and drug (F(20,160) = 23.07, p < 0.001) and an interaction of drug and current (F(1,8) = 39.8, p < 0.001, 2-way RM ANOVA). Retigabine reduced the number of action potentials in response to currents of 20 pA to 200 pA (20 pA, p = 0.037; 30 pA: p = 0.01; 40 pA, p = 0.006; 50 pA, p = 0.001; 60 pA, p = 0.002; 70–200 pA: p < 0.001, n = 5 cells per condition, Fisher’s LSD). B) Representative traces and current injection data from layer II/III PLC pyramidal cells from vehicle injected CD- or HFD-exposed mice, in comparison to retigabine treated HFD mice, using slices isolated 24 h after the last of eight daily doses of retigabine. A two-way RM ANOVA revealed a main effect of current injected (F(1.544,44.78) = 69.63, p < 0.001), treatment (F(2,29) = 3.79, p = 0.035) and an interaction of current and treatment (F(40,580) = 5.16, p < 0.001). HFD exposure (vs. CD) increased the number of action potentials in response to currents of 180 pA to 200 pA (180 pA, p = 0.035; 190 pA, p = 0.047; 200 pA, p = 0.042, Fisher’s LSD). Retigabine increased the number of action potentials in response to currents of 60 pA to 120 pA (60 pA–80 pA, p < 0.01; 90 pA, p = 0.011; 100 pA, p = 0.022; 110 pA, p < 0.01; 120 pA, p = 0.027; Fisher’s LSD, n = 6–14 cells from at least four animals per condition). C) Representative traces and summary data of Ih currents recorded from layer II/III PLC pyramidal cells from behaviorally naïve CD- or HFD-exposed mice, using slices isolated 24 h after the last of eight daily doses of retigabine or vehicle. A two-way RM ANOVA revealed a main effect of V step (F(5,125) = 6.75, p < 0.001) and an interaction of diet and voltage (F(10,125) = 2.73, p = 0.005, 2-way RM ANOVA). HFD exposure (vs. CD) increased Ih currents in response to V-steps of −110 mV to −120 mV (−110 mV, p = 0.026; −120 mV, p = 0.002, n = 7–12 cells from at least four animals per condition). Retigabine (vs vehicle) reduced Ih currents of HFD-exposed mice in response to V steps of −100 mV to −120 mV (−100 mV, p = 0.03; −110 mV, p = 0.002; −120 mV, p = 0.001; n = 9–12 cells from at least four animals per condition, Fisher’s LSD). Error bars, SEMs; *,$p < 0.05, **,$ $p < 0.01.

    Techniques Used: Injection, Isolation

    A) Mice exposed to HFD starting from 5-weeks of age were subjected to a daily injection of retigabine or vehicle, starting at the end of the 18th week of diet exposure. CD-exposed mice were vehicle injected and analyzed in parallel. Behavioral testing was initiated on the 8th day of drug treatment, 1 h (B–G, N) or 12 h (H–M) after drug injection, with one behavioral test every 2–3 days. B) In the OFT, retigabine (Ret) had no effect on distance traveled (F(2,30) = 9.75, p < 0.001, ANOVA, p = 0.87, Fisher’s LSD). C) In the NSFT, HFD exposure increased the latency to feed (F(2,31) = 11.09, p < 0.001, ANOVA), and retigabine treatment partially reversed this effect (p = 0.040, Fisher’s LSD). D) Caloric intake in HCF tests was unaffected by diet and retigabine (F(2,32) = 0.81, p = 0.45, ANOVA). E) In the SST, retigabine partially reversed the HFD-exposure-induced reduction in grooming duration (F(2,31) = 44.27, p < 0.001, ANOVA; CD-Veh vs HFD-Veh, p < 0.001; HFD-Veh vs HFD-Ret, p < 0.001, Fisher’s LSD). F) In the FUST, neither diet nor retigabine had significant effects on grooming duration (F(2,31) = 2.17, p = 0.13, ANOVA). G) In the Y-Maze, retigabine reversed HFD-exposure-induced reductions in % alternations (F(2,32) = 3.82, p = 0.03 for diet and p = 0.049 for drug effects, ANOVA, Fisher’s LSD). H) In the OFT, retigabine had no effect on distance traveled, independent of diet (Diet, F(1,44) = 22.59, p < 0.001; Drug, F(1,44) = 3.81, p = 0.06; Interaction, F(1,44) = 0.007, p = 0.94, ANOVA). I) In the NSFT, the HFD increased the latency to feed (Diet, F(1,44) = 147.5, p < 0.001, ANOVA), and retigabine partially reversed this effect (Drug, F(1,44) = 0.19, p = 0.67;Interaction, F(1,44) = 5.86, p = 0.020, ANOVA, p = 0.0499, Fisher’s LSD), without effect on CD mice (p = 0.17, Fisher’s LSD). J) In the HCF test, caloric intake was increased in HFD-exposed animals but was unaffected by retigabine (Diet, F(1,44) = 22.59, p < 0.001; Drug, F(1,44) = 0.15, p = 0.70; Interaction, F(1,44) = 3.64, p = 0.063, ANOVA). K) In the SST, the grooming duration of HFD-exposed animals was reduced but unaffected by retigabine (Diet, F(1,44) = 39.34, p < 0.001; Drug, F(1,44) = 0.045, p = 0.83; Interaction, F(1,44) = 1.31, p = 0.26, ANOVA). L) In the FUST, the duration spent sniffing was reduced in HFD-exposed mice and unaffected by retigabine (Diet, F(1,44) = 30.49, p < 0.001; Drug, F(1,44) = 1.34, p = 0.25; Interaction, F(1,44) = 0.048, p = 0.83, ANOVA). M) In the Y-maze, retigabine reversed the HFD-induced reduction in % alternations but had no effect in CD mice (Diet, F(1,43) = 6.30, p = 0.016; Drug, F(1,43) = 3.55, p = 0.067; Interaction, F(1,43) = 3.92, p = 0.054, ANOVA; CD-Veh vs HFD-Veh, p = 0.003; CD-Ret vs HFD-Veh, p = 0.004; HFD-Veh vs HFD-Ret, p = 0.0098, Fisher’s LSD). N) Some of the mice tested in (H–M) were taken off retigabine or vehicle for 6 weeks and then tested again in the SST [untreated controls (Unt)]. The same mice were then subjected to daily retigabine injections for 8 days and retested 1 h after the last injection. Retigabine partially reversed HFD-induced reductions in grooming duration without effects in CD mice (Diet, F(1,25) = 38.58, p < 0.001; Drug, F(1,25) = 7.24, p = 0.013; Interaction, F(1,25) = 0.29, p = 0.59, two-way RM ANOVA; CD-Veh vs CD-Ret, p = 0.13; HFD-Veh vs HFD-Ret, p = 0.034, Fisher’s LSD). Error bars, SEMs; *p < 0.05, **p < 0.01, ***p < 0.001.
    Figure Legend Snippet: A) Mice exposed to HFD starting from 5-weeks of age were subjected to a daily injection of retigabine or vehicle, starting at the end of the 18th week of diet exposure. CD-exposed mice were vehicle injected and analyzed in parallel. Behavioral testing was initiated on the 8th day of drug treatment, 1 h (B–G, N) or 12 h (H–M) after drug injection, with one behavioral test every 2–3 days. B) In the OFT, retigabine (Ret) had no effect on distance traveled (F(2,30) = 9.75, p < 0.001, ANOVA, p = 0.87, Fisher’s LSD). C) In the NSFT, HFD exposure increased the latency to feed (F(2,31) = 11.09, p < 0.001, ANOVA), and retigabine treatment partially reversed this effect (p = 0.040, Fisher’s LSD). D) Caloric intake in HCF tests was unaffected by diet and retigabine (F(2,32) = 0.81, p = 0.45, ANOVA). E) In the SST, retigabine partially reversed the HFD-exposure-induced reduction in grooming duration (F(2,31) = 44.27, p < 0.001, ANOVA; CD-Veh vs HFD-Veh, p < 0.001; HFD-Veh vs HFD-Ret, p < 0.001, Fisher’s LSD). F) In the FUST, neither diet nor retigabine had significant effects on grooming duration (F(2,31) = 2.17, p = 0.13, ANOVA). G) In the Y-Maze, retigabine reversed HFD-exposure-induced reductions in % alternations (F(2,32) = 3.82, p = 0.03 for diet and p = 0.049 for drug effects, ANOVA, Fisher’s LSD). H) In the OFT, retigabine had no effect on distance traveled, independent of diet (Diet, F(1,44) = 22.59, p < 0.001; Drug, F(1,44) = 3.81, p = 0.06; Interaction, F(1,44) = 0.007, p = 0.94, ANOVA). I) In the NSFT, the HFD increased the latency to feed (Diet, F(1,44) = 147.5, p < 0.001, ANOVA), and retigabine partially reversed this effect (Drug, F(1,44) = 0.19, p = 0.67;Interaction, F(1,44) = 5.86, p = 0.020, ANOVA, p = 0.0499, Fisher’s LSD), without effect on CD mice (p = 0.17, Fisher’s LSD). J) In the HCF test, caloric intake was increased in HFD-exposed animals but was unaffected by retigabine (Diet, F(1,44) = 22.59, p < 0.001; Drug, F(1,44) = 0.15, p = 0.70; Interaction, F(1,44) = 3.64, p = 0.063, ANOVA). K) In the SST, the grooming duration of HFD-exposed animals was reduced but unaffected by retigabine (Diet, F(1,44) = 39.34, p < 0.001; Drug, F(1,44) = 0.045, p = 0.83; Interaction, F(1,44) = 1.31, p = 0.26, ANOVA). L) In the FUST, the duration spent sniffing was reduced in HFD-exposed mice and unaffected by retigabine (Diet, F(1,44) = 30.49, p < 0.001; Drug, F(1,44) = 1.34, p = 0.25; Interaction, F(1,44) = 0.048, p = 0.83, ANOVA). M) In the Y-maze, retigabine reversed the HFD-induced reduction in % alternations but had no effect in CD mice (Diet, F(1,43) = 6.30, p = 0.016; Drug, F(1,43) = 3.55, p = 0.067; Interaction, F(1,43) = 3.92, p = 0.054, ANOVA; CD-Veh vs HFD-Veh, p = 0.003; CD-Ret vs HFD-Veh, p = 0.004; HFD-Veh vs HFD-Ret, p = 0.0098, Fisher’s LSD). N) Some of the mice tested in (H–M) were taken off retigabine or vehicle for 6 weeks and then tested again in the SST [untreated controls (Unt)]. The same mice were then subjected to daily retigabine injections for 8 days and retested 1 h after the last injection. Retigabine partially reversed HFD-induced reductions in grooming duration without effects in CD mice (Diet, F(1,25) = 38.58, p < 0.001; Drug, F(1,25) = 7.24, p = 0.013; Interaction, F(1,25) = 0.29, p = 0.59, two-way RM ANOVA; CD-Veh vs CD-Ret, p = 0.13; HFD-Veh vs HFD-Ret, p = 0.034, Fisher’s LSD). Error bars, SEMs; *p < 0.05, **p < 0.01, ***p < 0.001.

    Techniques Used: Injection

    r 100  (Alomone Labs)


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    R 100, 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 retigabine
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    Alomone Labs conditioning paradigm with retigabine
    (a) Schematic of spared nerve injury and tissues of interest. (b, c) Once neuropathic pain was established on day 7 after SNI, male (n=6) and female (n=6) mice were treated with oral 1c (350 μmol/kg/day), diroximel fumarate (350 μmol/kg/day), or vehicle every day for 3 days (gray box). (b) Mechanical allodynia and (c) dynamic allodynia were assessed. Relative to vehicle: * P <0.05, ** P <0.01, *** P <0.001; 1c vs. diroximel fumarate: ## P <0.01, ### P <0.001. (d) Seven days after SNI, male (n=3) and female (n=3) mice were treated with oral 1c (350 μmol/kg/day) or subcutaneous morphine (3 mg/kg, b.i.d.). Relative to 1c Day 0 (D0, prior to surgery): ** P <0.01, *** P <0.001; relative to morphine D0: # P <0.05, ### P <0.001. (e) Male (n=3) and female (n=3) mice were treated with oral 1c (350 µmol/kg/day), diroximel fumarate (350 µmol/kg/day) or vehicle every day for 7 days, beginning 7 days after SNI or sham surgery. Presence of ongoing pain was interpreted as an increase in time spent in <t>retigabine-paired</t> chamber (conditioning stimulus) after 7 days of treatment, relative to baseline. Relative to sham-vehicle: †† P <0.01; relative to SNI-vehicle: * P <0.05, *** P <0.001. (f) Male and female Nfe2l2 -/- and wildtype control mice (n=3/sex/group) were treated with oral 1c (350 μmol/kg/day), beginning 7 days after SNI, and mechanical allodynia assessed. Relative to wildtype controls: *** P <0.001. (g) L4/5 DRG from 3 mice were pooled after 3 days of treatment, and nuclear extracts were probed for Nrf2 (n=2 males, n=2 females). Relative to ipsilateral vehicle: *** P <0.001; relative to contralateral vehicle and 1c : ††† P <0.001. (h) Antioxidant gene expression L4/5 DRG was determined after 3 days of treatment (n=3 males, n=3 females). Relative to ipsilateral vehicle: * P <0.05, ** P <0.01; relative to contralateral vehicle: # P <0.05; relative to contralateral 1c : † P <0.05; †† P <0.01, ††† P <0.001. ( i ) Naive male (n=3) and female (n = 3) mice were orally treated with 1c (350 µmol/kg), diroximel fumarate (350 µmol/kg), or vehicle daily for 10 days. Blood was collected by cardiac puncture and leukocytes were manually counted. Relative to vehicle: * P <0.05. Individual replicates are presented in spaghetti plots or grey dots.
    Conditioning Paradigm With Retigabine, 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 r 100
    (a) Schematic of spared nerve injury and tissues of interest. (b, c) Once neuropathic pain was established on day 7 after SNI, male (n=6) and female (n=6) mice were treated with oral 1c (350 μmol/kg/day), diroximel fumarate (350 μmol/kg/day), or vehicle every day for 3 days (gray box). (b) Mechanical allodynia and (c) dynamic allodynia were assessed. Relative to vehicle: * P <0.05, ** P <0.01, *** P <0.001; 1c vs. diroximel fumarate: ## P <0.01, ### P <0.001. (d) Seven days after SNI, male (n=3) and female (n=3) mice were treated with oral 1c (350 μmol/kg/day) or subcutaneous morphine (3 mg/kg, b.i.d.). Relative to 1c Day 0 (D0, prior to surgery): ** P <0.01, *** P <0.001; relative to morphine D0: # P <0.05, ### P <0.001. (e) Male (n=3) and female (n=3) mice were treated with oral 1c (350 µmol/kg/day), diroximel fumarate (350 µmol/kg/day) or vehicle every day for 7 days, beginning 7 days after SNI or sham surgery. Presence of ongoing pain was interpreted as an increase in time spent in <t>retigabine-paired</t> chamber (conditioning stimulus) after 7 days of treatment, relative to baseline. Relative to sham-vehicle: †† P <0.01; relative to SNI-vehicle: * P <0.05, *** P <0.001. (f) Male and female Nfe2l2 -/- and wildtype control mice (n=3/sex/group) were treated with oral 1c (350 μmol/kg/day), beginning 7 days after SNI, and mechanical allodynia assessed. Relative to wildtype controls: *** P <0.001. (g) L4/5 DRG from 3 mice were pooled after 3 days of treatment, and nuclear extracts were probed for Nrf2 (n=2 males, n=2 females). Relative to ipsilateral vehicle: *** P <0.001; relative to contralateral vehicle and 1c : ††† P <0.001. (h) Antioxidant gene expression L4/5 DRG was determined after 3 days of treatment (n=3 males, n=3 females). Relative to ipsilateral vehicle: * P <0.05, ** P <0.01; relative to contralateral vehicle: # P <0.05; relative to contralateral 1c : † P <0.05; †† P <0.01, ††† P <0.001. ( i ) Naive male (n=3) and female (n = 3) mice were orally treated with 1c (350 µmol/kg), diroximel fumarate (350 µmol/kg), or vehicle daily for 10 days. Blood was collected by cardiac puncture and leukocytes were manually counted. Relative to vehicle: * P <0.05. Individual replicates are presented in spaghetti plots or grey dots.
    R 100, 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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    (a) Schematic of spared nerve injury and tissues of interest. (b, c) Once neuropathic pain was established on day 7 after SNI, male (n=6) and female (n=6) mice were treated with oral 1c (350 μmol/kg/day), diroximel fumarate (350 μmol/kg/day), or vehicle every day for 3 days (gray box). (b) Mechanical allodynia and (c) dynamic allodynia were assessed. Relative to vehicle: * P <0.05, ** P <0.01, *** P <0.001; 1c vs. diroximel fumarate: ## P <0.01, ### P <0.001. (d) Seven days after SNI, male (n=3) and female (n=3) mice were treated with oral 1c (350 μmol/kg/day) or subcutaneous morphine (3 mg/kg, b.i.d.). Relative to 1c Day 0 (D0, prior to surgery): ** P <0.01, *** P <0.001; relative to morphine D0: # P <0.05, ### P <0.001. (e) Male (n=3) and female (n=3) mice were treated with oral 1c (350 µmol/kg/day), diroximel fumarate (350 µmol/kg/day) or vehicle every day for 7 days, beginning 7 days after SNI or sham surgery. Presence of ongoing pain was interpreted as an increase in time spent in retigabine-paired chamber (conditioning stimulus) after 7 days of treatment, relative to baseline. Relative to sham-vehicle: †† P <0.01; relative to SNI-vehicle: * P <0.05, *** P <0.001. (f) Male and female Nfe2l2 -/- and wildtype control mice (n=3/sex/group) were treated with oral 1c (350 μmol/kg/day), beginning 7 days after SNI, and mechanical allodynia assessed. Relative to wildtype controls: *** P <0.001. (g) L4/5 DRG from 3 mice were pooled after 3 days of treatment, and nuclear extracts were probed for Nrf2 (n=2 males, n=2 females). Relative to ipsilateral vehicle: *** P <0.001; relative to contralateral vehicle and 1c : ††† P <0.001. (h) Antioxidant gene expression L4/5 DRG was determined after 3 days of treatment (n=3 males, n=3 females). Relative to ipsilateral vehicle: * P <0.05, ** P <0.01; relative to contralateral vehicle: # P <0.05; relative to contralateral 1c : † P <0.05; †† P <0.01, ††† P <0.001. ( i ) Naive male (n=3) and female (n = 3) mice were orally treated with 1c (350 µmol/kg), diroximel fumarate (350 µmol/kg), or vehicle daily for 10 days. Blood was collected by cardiac puncture and leukocytes were manually counted. Relative to vehicle: * P <0.05. Individual replicates are presented in spaghetti plots or grey dots.

    Journal: bioRxiv

    Article Title: Drug targeting to sites of oxidative stress using the Baeyer-Villiger reaction

    doi: 10.1101/2021.09.03.458872

    Figure Lengend Snippet: (a) Schematic of spared nerve injury and tissues of interest. (b, c) Once neuropathic pain was established on day 7 after SNI, male (n=6) and female (n=6) mice were treated with oral 1c (350 μmol/kg/day), diroximel fumarate (350 μmol/kg/day), or vehicle every day for 3 days (gray box). (b) Mechanical allodynia and (c) dynamic allodynia were assessed. Relative to vehicle: * P <0.05, ** P <0.01, *** P <0.001; 1c vs. diroximel fumarate: ## P <0.01, ### P <0.001. (d) Seven days after SNI, male (n=3) and female (n=3) mice were treated with oral 1c (350 μmol/kg/day) or subcutaneous morphine (3 mg/kg, b.i.d.). Relative to 1c Day 0 (D0, prior to surgery): ** P <0.01, *** P <0.001; relative to morphine D0: # P <0.05, ### P <0.001. (e) Male (n=3) and female (n=3) mice were treated with oral 1c (350 µmol/kg/day), diroximel fumarate (350 µmol/kg/day) or vehicle every day for 7 days, beginning 7 days after SNI or sham surgery. Presence of ongoing pain was interpreted as an increase in time spent in retigabine-paired chamber (conditioning stimulus) after 7 days of treatment, relative to baseline. Relative to sham-vehicle: †† P <0.01; relative to SNI-vehicle: * P <0.05, *** P <0.001. (f) Male and female Nfe2l2 -/- and wildtype control mice (n=3/sex/group) were treated with oral 1c (350 μmol/kg/day), beginning 7 days after SNI, and mechanical allodynia assessed. Relative to wildtype controls: *** P <0.001. (g) L4/5 DRG from 3 mice were pooled after 3 days of treatment, and nuclear extracts were probed for Nrf2 (n=2 males, n=2 females). Relative to ipsilateral vehicle: *** P <0.001; relative to contralateral vehicle and 1c : ††† P <0.001. (h) Antioxidant gene expression L4/5 DRG was determined after 3 days of treatment (n=3 males, n=3 females). Relative to ipsilateral vehicle: * P <0.05, ** P <0.01; relative to contralateral vehicle: # P <0.05; relative to contralateral 1c : † P <0.05; †† P <0.01, ††† P <0.001. ( i ) Naive male (n=3) and female (n = 3) mice were orally treated with 1c (350 µmol/kg), diroximel fumarate (350 µmol/kg), or vehicle daily for 10 days. Blood was collected by cardiac puncture and leukocytes were manually counted. Relative to vehicle: * P <0.05. Individual replicates are presented in spaghetti plots or grey dots.

    Article Snippet: Average scores for each mouse were obtained from three stimulations at intervals of at least 3 min. Spontaneous pain was tested using a conditioning paradigm with retigabine (#R-100; Alomone Laboratory, Jerusalem, Israel) as the conditioned stimulus to briefly relieve pain, as previously described , , .

    Techniques: Expressing