tta p2  (Alomone Labs)


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    Alomone Labs tta p2
    Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or <t>TTA-P2</t> (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.
    Tta P2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tta p2/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tta p2 - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "Neuromedin B receptor stimulation of Cav3.2 T-type Ca 2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity"

    Article Title: Neuromedin B receptor stimulation of Cav3.2 T-type Ca 2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity

    Journal: Theranostics

    doi: 10.7150/thno.62255

    Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or TTA-P2 (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.
    Figure Legend Snippet: Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or TTA-P2 (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.

    Techniques Used: Injection, Produced, Expressing, Two Tailed Test

    tta p2  (Alomone Labs)


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    Alomone Labs tta p2
    Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or <t>TTA-P2</t> (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.
    Tta P2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tta p2/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tta p2 - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "Neuromedin B receptor stimulation of Cav3.2 T-type Ca 2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity"

    Article Title: Neuromedin B receptor stimulation of Cav3.2 T-type Ca 2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity

    Journal: Theranostics

    doi: 10.7150/thno.62255

    Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or TTA-P2 (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.
    Figure Legend Snippet: Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or TTA-P2 (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.

    Techniques Used: Injection, Produced, Expressing, Two Tailed Test

    tta p2  (Alomone Labs)


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    Alomone Labs tta p2

    Tta P2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tta p2/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tta p2 - by Bioz Stars, 2023-02
    86/100 stars

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    1) Product Images from "Centrally expressed Cav3.2 T-type calcium channel is critical for the initiation and maintenance of neuropathic pain"

    Article Title: Centrally expressed Cav3.2 T-type calcium channel is critical for the initiation and maintenance of neuropathic pain

    Journal: eLife

    doi: 10.7554/eLife.79018


    Figure Legend Snippet:

    Techniques Used: Expressing, Variant Assay, Sequencing, Plasmid Preparation, Electron Microscopy, Software, In Vivo, In Vitro, Patch Clamp

    tta p2  (Alomone Labs)


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    Alomone Labs tta p2
    Tta P2, 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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    tta p2 3 5 dichloro n 1 2 2 dimethyl tetrahydro pyran 4 ylmethyl 4 fluoropiperidin 4 yl methyl benzamide  (Alomone Labs)


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    Alomone Labs tta p2 3 5 dichloro n 1 2 2 dimethyl tetrahydro pyran 4 ylmethyl 4 fluoropiperidin 4 yl methyl benzamide
    Tta P2 3 5 Dichloro N 1 2 2 Dimethyl Tetrahydro Pyran 4 Ylmethyl 4 Fluoropiperidin 4 Yl Methyl Benzamide, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    tta p2  (Alomone Labs)


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    Alomone Labs tta p2
    Tta P2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tta p2/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    tta p2  (Alomone Labs)


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    Alomone Labs tta p2
    Selective ligands of T-type calcium channels inhibit cholinergic gamma oscillations in rat hippocampal slices. (A) Original traces (left) and power spectra (right) of cholinergic gamma oscillations before (black) and after (purple) application of the selective T-type calcium channel blocker <t>TTA-P2</t> (1 μM). (B) Original traces (left) and power spectra (right) of cholinergic gamma oscillations before (black) and after (red) application of the selective T-type calcium channel enhancer SAK3 (0.1 μM). (C) Normalized power before, during and after bath application (gray) of the selective T-type blocker TTA-P2 (1 μM, purple) and NNC55-0396 (100 μM, orange) compared to control (blue). (D) Effect of the T-type calcium channel blockers TTA-P2 and NNC55-0396 as well as the enhancer SAK3 on the power of hippocampal gamma oscillations compared to time matched and solvent control. Control (light blue): n = 13 slices, N = 9 animals; TTA-P2 (1 μM, purple): n = 14, N = 6, p = 0.005, NNC55-0396 (100 μM, orange): n = 6, N = 2, p = 0.001; DMSO control (dark blue): n = 8, N = 7; SAK3 (0.1 μM, red): n = 10, N = 6, p = 0.020. (E) Effect of the T-type calcium channel blockers TTA-P2 and NNC55-0396 as well as the enhancer SAK3 on the peak frequency of hippocampal gamma oscillations compared to time matched and solvent control. TTA-P2 (1 μM, purple): p = 0.042; NNC55-0396 (100 μM, orange): p = 0.001; SAK3 (0.1 μM, red): p = 0.306. Recording temperature was between 34 and 36°C. Traces were lowpass filtered at 200 Hz and bandstop filtered at 50 Hz. Bars show mean ± SEM. * p < 0.05, ** p < 0.01. ACh, acetylcholine; Phys, physostigmine.
    Tta P2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tta p2/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tta p2 - by Bioz Stars, 2023-02
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    1) Product Images from "Regulation of Hippocampal Gamma Oscillations by Modulation of Intrinsic Neuronal Excitability"

    Article Title: Regulation of Hippocampal Gamma Oscillations by Modulation of Intrinsic Neuronal Excitability

    Journal: Frontiers in Neural Circuits

    doi: 10.3389/fncir.2021.778022

    Selective ligands of T-type calcium channels inhibit cholinergic gamma oscillations in rat hippocampal slices. (A) Original traces (left) and power spectra (right) of cholinergic gamma oscillations before (black) and after (purple) application of the selective T-type calcium channel blocker TTA-P2 (1 μM). (B) Original traces (left) and power spectra (right) of cholinergic gamma oscillations before (black) and after (red) application of the selective T-type calcium channel enhancer SAK3 (0.1 μM). (C) Normalized power before, during and after bath application (gray) of the selective T-type blocker TTA-P2 (1 μM, purple) and NNC55-0396 (100 μM, orange) compared to control (blue). (D) Effect of the T-type calcium channel blockers TTA-P2 and NNC55-0396 as well as the enhancer SAK3 on the power of hippocampal gamma oscillations compared to time matched and solvent control. Control (light blue): n = 13 slices, N = 9 animals; TTA-P2 (1 μM, purple): n = 14, N = 6, p = 0.005, NNC55-0396 (100 μM, orange): n = 6, N = 2, p = 0.001; DMSO control (dark blue): n = 8, N = 7; SAK3 (0.1 μM, red): n = 10, N = 6, p = 0.020. (E) Effect of the T-type calcium channel blockers TTA-P2 and NNC55-0396 as well as the enhancer SAK3 on the peak frequency of hippocampal gamma oscillations compared to time matched and solvent control. TTA-P2 (1 μM, purple): p = 0.042; NNC55-0396 (100 μM, orange): p = 0.001; SAK3 (0.1 μM, red): p = 0.306. Recording temperature was between 34 and 36°C. Traces were lowpass filtered at 200 Hz and bandstop filtered at 50 Hz. Bars show mean ± SEM. * p < 0.05, ** p < 0.01. ACh, acetylcholine; Phys, physostigmine.
    Figure Legend Snippet: Selective ligands of T-type calcium channels inhibit cholinergic gamma oscillations in rat hippocampal slices. (A) Original traces (left) and power spectra (right) of cholinergic gamma oscillations before (black) and after (purple) application of the selective T-type calcium channel blocker TTA-P2 (1 μM). (B) Original traces (left) and power spectra (right) of cholinergic gamma oscillations before (black) and after (red) application of the selective T-type calcium channel enhancer SAK3 (0.1 μM). (C) Normalized power before, during and after bath application (gray) of the selective T-type blocker TTA-P2 (1 μM, purple) and NNC55-0396 (100 μM, orange) compared to control (blue). (D) Effect of the T-type calcium channel blockers TTA-P2 and NNC55-0396 as well as the enhancer SAK3 on the power of hippocampal gamma oscillations compared to time matched and solvent control. Control (light blue): n = 13 slices, N = 9 animals; TTA-P2 (1 μM, purple): n = 14, N = 6, p = 0.005, NNC55-0396 (100 μM, orange): n = 6, N = 2, p = 0.001; DMSO control (dark blue): n = 8, N = 7; SAK3 (0.1 μM, red): n = 10, N = 6, p = 0.020. (E) Effect of the T-type calcium channel blockers TTA-P2 and NNC55-0396 as well as the enhancer SAK3 on the peak frequency of hippocampal gamma oscillations compared to time matched and solvent control. TTA-P2 (1 μM, purple): p = 0.042; NNC55-0396 (100 μM, orange): p = 0.001; SAK3 (0.1 μM, red): p = 0.306. Recording temperature was between 34 and 36°C. Traces were lowpass filtered at 200 Hz and bandstop filtered at 50 Hz. Bars show mean ± SEM. * p < 0.05, ** p < 0.01. ACh, acetylcholine; Phys, physostigmine.

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    tta p2  (Alomone Labs)


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    Alomone Labs tta p2
    Calcium influx through Ca V 1.2 induces PKA-II activity during depolarization. (A) Expression pattern of VGCC α subunits in overnight cultures of rat and mouse DRG determined by RNA-seq . TPM, transcripts per kilobase million. (B) Expression pattern of VGCC α subunits in mouse DRG neuron subgroups determined by single-cell RNA-seq . (C) Time course of pRII intensity in KCl-depolarized rat sensory neurons after pretreatment (10 min) with the NMDA receptor antagonist D-AP5 (10 µM), the Cav3.1-3.3 blocker <t>TTA-P2</t> (1 µM), and a combination of the Cav2.1/2.2 blocker ω-agatoxin IVA (100 nM), ω-conotoxin MVIIC (200 nM), and ω-conotoxin GVIA (1 µM). (D) Inhibitory effect of verapamil (20 or 200 µM, 10-min pretreatment) on the pRII increase induced by KCl depolarization. (E) Dose–response curve showing the effect of verapamil (0–200 µM; IC 50 = 16 µM) on pRII signals induced by KCl depolarization (3 min). (F) Inhibitory effect of diltiazem (100 µM, 10 min) on the KCl-induced pRII increase. (G) Dose–response curve showing the inhibition of KCl-induced pRII signals by diltiazem (0–200 µM; IC 50 = 37 µM). (H) Reinforcing effect of the Ca V 1 agonist (S)-(-)-Bay K 8644 (2 µM, 10 min) on pRII signals induced by a low dose of KCl (10 mM). (I) Dose–response curve showing the reinforcing effect of Bay K 8644 (0–5 µM; EC 50 = 80 nM) on pRII signals induced by KCl (10 mM, 3 min). (J) Chelation of extracellular calcium with EGTA (2.5 mM, 30-min prestimulation) abolished the pRII response to KCl-depolarization. (K) Effect of the cell-permeable calcium chelator BAPTA-AM (100 µM, 60 min) on pRII signals induced by KCl depolarization (compound effect: F 1,28 = 10.9, P < 0.003). Values in C–K represent means ± SEM; n = 3–4 experiments; >2,000 neurons/condition; two-way ANOVA with Bonferroni’s test; § , P < 0.05; §§ , P < 0.01; §§§ , P < 0.001 indicate significance levels between KCl-induced pRII signals in the absence or presence of an agonist/antagonist.
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    1) Product Images from "Depolarization induces nociceptor sensitization by Ca V 1.2-mediated PKA-II activation"

    Article Title: Depolarization induces nociceptor sensitization by Ca V 1.2-mediated PKA-II activation

    Journal: The Journal of Cell Biology

    doi: 10.1083/jcb.202002083

    Calcium influx through Ca V 1.2 induces PKA-II activity during depolarization. (A) Expression pattern of VGCC α subunits in overnight cultures of rat and mouse DRG determined by RNA-seq . TPM, transcripts per kilobase million. (B) Expression pattern of VGCC α subunits in mouse DRG neuron subgroups determined by single-cell RNA-seq . (C) Time course of pRII intensity in KCl-depolarized rat sensory neurons after pretreatment (10 min) with the NMDA receptor antagonist D-AP5 (10 µM), the Cav3.1-3.3 blocker TTA-P2 (1 µM), and a combination of the Cav2.1/2.2 blocker ω-agatoxin IVA (100 nM), ω-conotoxin MVIIC (200 nM), and ω-conotoxin GVIA (1 µM). (D) Inhibitory effect of verapamil (20 or 200 µM, 10-min pretreatment) on the pRII increase induced by KCl depolarization. (E) Dose–response curve showing the effect of verapamil (0–200 µM; IC 50 = 16 µM) on pRII signals induced by KCl depolarization (3 min). (F) Inhibitory effect of diltiazem (100 µM, 10 min) on the KCl-induced pRII increase. (G) Dose–response curve showing the inhibition of KCl-induced pRII signals by diltiazem (0–200 µM; IC 50 = 37 µM). (H) Reinforcing effect of the Ca V 1 agonist (S)-(-)-Bay K 8644 (2 µM, 10 min) on pRII signals induced by a low dose of KCl (10 mM). (I) Dose–response curve showing the reinforcing effect of Bay K 8644 (0–5 µM; EC 50 = 80 nM) on pRII signals induced by KCl (10 mM, 3 min). (J) Chelation of extracellular calcium with EGTA (2.5 mM, 30-min prestimulation) abolished the pRII response to KCl-depolarization. (K) Effect of the cell-permeable calcium chelator BAPTA-AM (100 µM, 60 min) on pRII signals induced by KCl depolarization (compound effect: F 1,28 = 10.9, P < 0.003). Values in C–K represent means ± SEM; n = 3–4 experiments; >2,000 neurons/condition; two-way ANOVA with Bonferroni’s test; § , P < 0.05; §§ , P < 0.01; §§§ , P < 0.001 indicate significance levels between KCl-induced pRII signals in the absence or presence of an agonist/antagonist.
    Figure Legend Snippet: Calcium influx through Ca V 1.2 induces PKA-II activity during depolarization. (A) Expression pattern of VGCC α subunits in overnight cultures of rat and mouse DRG determined by RNA-seq . TPM, transcripts per kilobase million. (B) Expression pattern of VGCC α subunits in mouse DRG neuron subgroups determined by single-cell RNA-seq . (C) Time course of pRII intensity in KCl-depolarized rat sensory neurons after pretreatment (10 min) with the NMDA receptor antagonist D-AP5 (10 µM), the Cav3.1-3.3 blocker TTA-P2 (1 µM), and a combination of the Cav2.1/2.2 blocker ω-agatoxin IVA (100 nM), ω-conotoxin MVIIC (200 nM), and ω-conotoxin GVIA (1 µM). (D) Inhibitory effect of verapamil (20 or 200 µM, 10-min pretreatment) on the pRII increase induced by KCl depolarization. (E) Dose–response curve showing the effect of verapamil (0–200 µM; IC 50 = 16 µM) on pRII signals induced by KCl depolarization (3 min). (F) Inhibitory effect of diltiazem (100 µM, 10 min) on the KCl-induced pRII increase. (G) Dose–response curve showing the inhibition of KCl-induced pRII signals by diltiazem (0–200 µM; IC 50 = 37 µM). (H) Reinforcing effect of the Ca V 1 agonist (S)-(-)-Bay K 8644 (2 µM, 10 min) on pRII signals induced by a low dose of KCl (10 mM). (I) Dose–response curve showing the reinforcing effect of Bay K 8644 (0–5 µM; EC 50 = 80 nM) on pRII signals induced by KCl (10 mM, 3 min). (J) Chelation of extracellular calcium with EGTA (2.5 mM, 30-min prestimulation) abolished the pRII response to KCl-depolarization. (K) Effect of the cell-permeable calcium chelator BAPTA-AM (100 µM, 60 min) on pRII signals induced by KCl depolarization (compound effect: F 1,28 = 10.9, P < 0.003). Values in C–K represent means ± SEM; n = 3–4 experiments; >2,000 neurons/condition; two-way ANOVA with Bonferroni’s test; § , P < 0.05; §§ , P < 0.01; §§§ , P < 0.001 indicate significance levels between KCl-induced pRII signals in the absence or presence of an agonist/antagonist.

    Techniques Used: Activity Assay, Expressing, RNA Sequencing Assay, Inhibition

    dimethyl tetrahydro pyran 4 ylmethyl 4 fluoro piperidin 4 ylmethyl benzamide tta p2  (Alomone Labs)


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    Alomone Labs dimethyl tetrahydro pyran 4 ylmethyl 4 fluoro piperidin 4 ylmethyl benzamide tta p2
    Dimethyl Tetrahydro Pyran 4 Ylmethyl 4 Fluoro Piperidin 4 Ylmethyl Benzamide Tta P2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    t type calcium channel blocker tta p2  (Alomone Labs)


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    Alomone Labs t type calcium channel blocker tta p2
    IL-6 treatment increases T-type calcium currents, and eFT508 pretreatment prevents this upregulation. A: representative traces of inward T-type calcium currents evoked from a holding potential of −90 mV and stepping from −60 mV to 0 mV in 5-mV increments. B: representative traces from all treatment groups, from a holding potential of −90 mV and test potential of 0 mV, showing that IL-6 treatment increases the amplitude of T-type currents. C: current-voltage (I-V) curves of the calcium current density (pA/pF). *P < 0.05, post hoc Dunnett’s test following 2-way ANOVA. Vehicle vs. IL-6 at −10 mV: mean difference 1.434 [95% confidence interval (95CI) 0.33, 2.54]; at −5 mV: 1.3 [95CI 0.19, 2.41]; at 0 mV: 1.8 [95CI 0.68, 2.91]. D: I-V curves of the current amplitudes used to obtain the density in C. *P < 0.05, post hoc Dunnett’s test following 2-way ANOVA. Vehicle vs. IL-6 at −15 mV: mean difference 32.59 [95% confidence interval (95CI) 5.06, 60.12]; at −10 mV: 44.17 [95CI 16.64, 71.7]; at −5 mV: 41.96 [95CI 14.44, 69.49]; at 0 mV: 52.81 [25.28, 80.34]. Inset shows the activation curve G/Gmax. The curve was obtained by fitting the conductances (G) of the amplitudes from D and estimated reversal potential (Erev) of 60 mV to the equation G/Gmax = 1/{1 + exp[(V50 − V)/slope]}, where V50 is the voltage at which current is half-maximal and V is the step voltage. E: average amplitudes of a subset of cells from D showing the effect of application of <t>TTA-P2</t> on T-type calcium currents. TTA-P2 application depresses the amplitude of T-type currents. Data are shown for the vehicle, IL-6, and eFT508+IL-6 groups. *P < 0.05, main effect of treatment, repeated measures ANOVA. Number of cells: vehicle, 10 from 5 mice; IL-6, 11 from 6 mice; eFT508+IL-6, 8 from 2 mice; eFT508, 7 from 3 mice.
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    1) Product Images from "IL-6 induced upregulation of T-type Ca 2+ currents and sensitization of DRG nociceptors is attenuated by MNK inhibition"

    Article Title: IL-6 induced upregulation of T-type Ca 2+ currents and sensitization of DRG nociceptors is attenuated by MNK inhibition

    Journal: Journal of Neurophysiology

    doi: 10.1152/jn.00188.2020

    IL-6 treatment increases T-type calcium currents, and eFT508 pretreatment prevents this upregulation. A: representative traces of inward T-type calcium currents evoked from a holding potential of −90 mV and stepping from −60 mV to 0 mV in 5-mV increments. B: representative traces from all treatment groups, from a holding potential of −90 mV and test potential of 0 mV, showing that IL-6 treatment increases the amplitude of T-type currents. C: current-voltage (I-V) curves of the calcium current density (pA/pF). *P < 0.05, post hoc Dunnett’s test following 2-way ANOVA. Vehicle vs. IL-6 at −10 mV: mean difference 1.434 [95% confidence interval (95CI) 0.33, 2.54]; at −5 mV: 1.3 [95CI 0.19, 2.41]; at 0 mV: 1.8 [95CI 0.68, 2.91]. D: I-V curves of the current amplitudes used to obtain the density in C. *P < 0.05, post hoc Dunnett’s test following 2-way ANOVA. Vehicle vs. IL-6 at −15 mV: mean difference 32.59 [95% confidence interval (95CI) 5.06, 60.12]; at −10 mV: 44.17 [95CI 16.64, 71.7]; at −5 mV: 41.96 [95CI 14.44, 69.49]; at 0 mV: 52.81 [25.28, 80.34]. Inset shows the activation curve G/Gmax. The curve was obtained by fitting the conductances (G) of the amplitudes from D and estimated reversal potential (Erev) of 60 mV to the equation G/Gmax = 1/{1 + exp[(V50 − V)/slope]}, where V50 is the voltage at which current is half-maximal and V is the step voltage. E: average amplitudes of a subset of cells from D showing the effect of application of TTA-P2 on T-type calcium currents. TTA-P2 application depresses the amplitude of T-type currents. Data are shown for the vehicle, IL-6, and eFT508+IL-6 groups. *P < 0.05, main effect of treatment, repeated measures ANOVA. Number of cells: vehicle, 10 from 5 mice; IL-6, 11 from 6 mice; eFT508+IL-6, 8 from 2 mice; eFT508, 7 from 3 mice.
    Figure Legend Snippet: IL-6 treatment increases T-type calcium currents, and eFT508 pretreatment prevents this upregulation. A: representative traces of inward T-type calcium currents evoked from a holding potential of −90 mV and stepping from −60 mV to 0 mV in 5-mV increments. B: representative traces from all treatment groups, from a holding potential of −90 mV and test potential of 0 mV, showing that IL-6 treatment increases the amplitude of T-type currents. C: current-voltage (I-V) curves of the calcium current density (pA/pF). *P < 0.05, post hoc Dunnett’s test following 2-way ANOVA. Vehicle vs. IL-6 at −10 mV: mean difference 1.434 [95% confidence interval (95CI) 0.33, 2.54]; at −5 mV: 1.3 [95CI 0.19, 2.41]; at 0 mV: 1.8 [95CI 0.68, 2.91]. D: I-V curves of the current amplitudes used to obtain the density in C. *P < 0.05, post hoc Dunnett’s test following 2-way ANOVA. Vehicle vs. IL-6 at −15 mV: mean difference 32.59 [95% confidence interval (95CI) 5.06, 60.12]; at −10 mV: 44.17 [95CI 16.64, 71.7]; at −5 mV: 41.96 [95CI 14.44, 69.49]; at 0 mV: 52.81 [25.28, 80.34]. Inset shows the activation curve G/Gmax. The curve was obtained by fitting the conductances (G) of the amplitudes from D and estimated reversal potential (Erev) of 60 mV to the equation G/Gmax = 1/{1 + exp[(V50 − V)/slope]}, where V50 is the voltage at which current is half-maximal and V is the step voltage. E: average amplitudes of a subset of cells from D showing the effect of application of TTA-P2 on T-type calcium currents. TTA-P2 application depresses the amplitude of T-type currents. Data are shown for the vehicle, IL-6, and eFT508+IL-6 groups. *P < 0.05, main effect of treatment, repeated measures ANOVA. Number of cells: vehicle, 10 from 5 mice; IL-6, 11 from 6 mice; eFT508+IL-6, 8 from 2 mice; eFT508, 7 from 3 mice.

    Techniques Used: Activation Assay

    T-type calcium channel antagonist TTA-P2 modifies IL-6-induced changes in membrane properties of dorsal root ganglion (DRG) neurons. A: TTA-P2 does not alter the number of action potentials (AP) in IL-6-treated cells in response to ramp currents. B: following 1 h of IL-6 treatment, the latency to the first spike is decreased, and this is reversed following the application of TTA-P2 at 100-pA and 300-pA ramp intensities. Inset shows representative traces from the same cell before and after TTA-P2 application indicating increased latency at 100 pA. *P < 0.05, post hoc Bonferroni correction following 2-way ANOVA. Mean difference at 100 pA: −170.3 [95% confidence interval (95CI) −224.9, −115.6]; at 300 pA: −64.07 [95CI −118.7, −9.41]. C, left: the rheobase to evoke an action potential is increased following TTA-P2 application. Right, representative traces from the same IL-6-treated cell before and after TTA-P2 application in response to a 5-s step protocol. The current required to evoke an action potential increases from 220 pA to 250 pA after TTA-P2 application. *P < 0.05, paired t test. Mean difference: 31.67 [95CI 17.63, 45.7]. Number of cells: 13 from 3 mice.
    Figure Legend Snippet: T-type calcium channel antagonist TTA-P2 modifies IL-6-induced changes in membrane properties of dorsal root ganglion (DRG) neurons. A: TTA-P2 does not alter the number of action potentials (AP) in IL-6-treated cells in response to ramp currents. B: following 1 h of IL-6 treatment, the latency to the first spike is decreased, and this is reversed following the application of TTA-P2 at 100-pA and 300-pA ramp intensities. Inset shows representative traces from the same cell before and after TTA-P2 application indicating increased latency at 100 pA. *P < 0.05, post hoc Bonferroni correction following 2-way ANOVA. Mean difference at 100 pA: −170.3 [95% confidence interval (95CI) −224.9, −115.6]; at 300 pA: −64.07 [95CI −118.7, −9.41]. C, left: the rheobase to evoke an action potential is increased following TTA-P2 application. Right, representative traces from the same IL-6-treated cell before and after TTA-P2 application in response to a 5-s step protocol. The current required to evoke an action potential increases from 220 pA to 250 pA after TTA-P2 application. *P < 0.05, paired t test. Mean difference: 31.67 [95CI 17.63, 45.7]. Number of cells: 13 from 3 mice.

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    Alomone Labs tta p2
    Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or <t>TTA-P2</t> (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.
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    Alomone Labs tta p2 3 5 dichloro n 1 2 2 dimethyl tetrahydro pyran 4 ylmethyl 4 fluoropiperidin 4 yl methyl benzamide
    Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or <t>TTA-P2</t> (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.
    Tta P2 3 5 Dichloro N 1 2 2 Dimethyl Tetrahydro Pyran 4 Ylmethyl 4 Fluoropiperidin 4 Yl Methyl Benzamide, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Alomone Labs dimethyl tetrahydro pyran 4 ylmethyl 4 fluoro piperidin 4 ylmethyl benzamide tta p2
    Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or <t>TTA-P2</t> (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.
    Dimethyl Tetrahydro Pyran 4 Ylmethyl 4 Fluoro Piperidin 4 Ylmethyl Benzamide Tta P2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    Alomone Labs t type calcium channel blocker tta p2
    IL-6 treatment increases T-type calcium currents, and eFT508 pretreatment prevents this upregulation. A: representative traces of inward T-type calcium currents evoked from a holding potential of −90 mV and stepping from −60 mV to 0 mV in 5-mV increments. B: representative traces from all treatment groups, from a holding potential of −90 mV and test potential of 0 mV, showing that IL-6 treatment increases the amplitude of T-type currents. C: current-voltage (I-V) curves of the calcium current density (pA/pF). *P < 0.05, post hoc Dunnett’s test following 2-way ANOVA. Vehicle vs. IL-6 at −10 mV: mean difference 1.434 [95% confidence interval (95CI) 0.33, 2.54]; at −5 mV: 1.3 [95CI 0.19, 2.41]; at 0 mV: 1.8 [95CI 0.68, 2.91]. D: I-V curves of the current amplitudes used to obtain the density in C. *P < 0.05, post hoc Dunnett’s test following 2-way ANOVA. Vehicle vs. IL-6 at −15 mV: mean difference 32.59 [95% confidence interval (95CI) 5.06, 60.12]; at −10 mV: 44.17 [95CI 16.64, 71.7]; at −5 mV: 41.96 [95CI 14.44, 69.49]; at 0 mV: 52.81 [25.28, 80.34]. Inset shows the activation curve G/Gmax. The curve was obtained by fitting the conductances (G) of the amplitudes from D and estimated reversal potential (Erev) of 60 mV to the equation G/Gmax = 1/{1 + exp[(V50 − V)/slope]}, where V50 is the voltage at which current is half-maximal and V is the step voltage. E: average amplitudes of a subset of cells from D showing the effect of application of <t>TTA-P2</t> on T-type calcium currents. TTA-P2 application depresses the amplitude of T-type currents. Data are shown for the vehicle, IL-6, and eFT508+IL-6 groups. *P < 0.05, main effect of treatment, repeated measures ANOVA. Number of cells: vehicle, 10 from 5 mice; IL-6, 11 from 6 mice; eFT508+IL-6, 8 from 2 mice; eFT508, 7 from 3 mice.
    T Type Calcium Channel Blocker Tta P2, 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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    Image Search Results


    Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or TTA-P2 (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.

    Journal: Theranostics

    Article Title: Neuromedin B receptor stimulation of Cav3.2 T-type Ca 2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity

    doi: 10.7150/thno.62255

    Figure Lengend Snippet: Involvement of peripheral NmbR in mechanical pain hypersensitivity. A, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces mechanical hypersensitivity ( n = 6 - 8 mice per group). * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. BL, baseline. B, the total contact time assessed by orofacial operant test was significantly decreased 1 h after intra-TG injection of 1 nmol Nmb, compared to vehicle group. * p < 0.05 versus vehicle, one-way ANOVA followed by Bonferroni post hoc test. C, pretreatment of BIM23042 (5 nmol), KT-5720 (2 nmol), Z941 (2 nmol) or TTA-P2 (1 nmol) significantly attenuates 1 nmol Nmb-induced mechanical hypersensitivity ( n = 8 - 10 mice per group). * p < 0.05 versus vehicle at 1 h, + p < 0.05 versus Z941 + vehicle, # p < 0.05 versus TTA-P2 + vehicle, one-way ANOVA followed by Bonferroni post hoc test. D, intra-TG injection of 1 nmol or 5 nmol of Nmb significantly induces heat hypersensitivity. * p < 0.05 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. E, intra-TG administration of BIM23042 (5 nmol) prevented 1 nmol Nmb-induced heat hypersensitivity (n = 6 - 8 mice per group). * p < 0.05 versus vehicle at 1 h, one-way ANOVA followed by Bonferroni post hoc test. F, rofecoxib (1 mg/kg administrated subcutaneously) reduced the mechanical allodynia produced by CFA. Behavioral analysis was performed at 2 d after CFA injection, and the effect of rofecoxib was assessed at 1 h after administration (n = 7 - 9 mice per group). ** p < 0.01 versus basline (BL) in vehicle group, ## p < 0.01 versus basline (BL) in rofecoxib group, ++ p < 0.01 versus vehicle at 1 h. G, intra-TG injection of BIM23042 (5 nmol) 2 d after CFA injection significantly suppresses the mechanical hypersensitivity in CFA-treated group ( n = 7 - 9 mice per group). * p < 0.05 and ** p < 0.01 versus vehicle, two-way ANOVA followed by Bonferroni post hoc test. H-I, intra-TG administration of Cav3.2 siRNA resulted in a significant decrease of Cav3.2 protein abundance in mouse TGs ( H ), while the expression level of Cav3.1 or Cav3.3 ( I ) remained unchanged. The blots shown are representative of three independent experiments. # p < 0.05 versus NC-siRNA, two-tailed t test. J, siRNA knock-down of Cav3.2 attenuates the BIM23042-induced alleviation of mechanical allodynia in CFA-treated mice ( n = 8 - 10 mice per group). * p < 0.01 and ** p < 0.01 versus NC-siRNA in CFA-treated mice; ++ p < 0.01 versus CFA 2 d; # p < 0.05 versus 0 h point in NC-siRNA-treated mice, two-way ANOVA followed by Bonferroni post hoc test. The black arrow indicates the intra-TG injection of 5 nmol BIM23042.

    Article Snippet: Stock solutions of phorbol 12-myristate 13-acetate (PMA), BIM23042 (Tocris Bioscience), rofecoxib, U73122, compound C, TTA-P2 (Alomone Labs), Z941 (kindly provided by Dr Terrance P. Snutch, University of British Columbia, Canada), KT-5720, and nifedipine were prepared in dimethyl sulfoxide (DMSO).

    Techniques: Injection, Produced, Expressing, Two Tailed Test

    IL-6 treatment increases T-type calcium currents, and eFT508 pretreatment prevents this upregulation. A: representative traces of inward T-type calcium currents evoked from a holding potential of −90 mV and stepping from −60 mV to 0 mV in 5-mV increments. B: representative traces from all treatment groups, from a holding potential of −90 mV and test potential of 0 mV, showing that IL-6 treatment increases the amplitude of T-type currents. C: current-voltage (I-V) curves of the calcium current density (pA/pF). *P < 0.05, post hoc Dunnett’s test following 2-way ANOVA. Vehicle vs. IL-6 at −10 mV: mean difference 1.434 [95% confidence interval (95CI) 0.33, 2.54]; at −5 mV: 1.3 [95CI 0.19, 2.41]; at 0 mV: 1.8 [95CI 0.68, 2.91]. D: I-V curves of the current amplitudes used to obtain the density in C. *P < 0.05, post hoc Dunnett’s test following 2-way ANOVA. Vehicle vs. IL-6 at −15 mV: mean difference 32.59 [95% confidence interval (95CI) 5.06, 60.12]; at −10 mV: 44.17 [95CI 16.64, 71.7]; at −5 mV: 41.96 [95CI 14.44, 69.49]; at 0 mV: 52.81 [25.28, 80.34]. Inset shows the activation curve G/Gmax. The curve was obtained by fitting the conductances (G) of the amplitudes from D and estimated reversal potential (Erev) of 60 mV to the equation G/Gmax = 1/{1 + exp[(V50 − V)/slope]}, where V50 is the voltage at which current is half-maximal and V is the step voltage. E: average amplitudes of a subset of cells from D showing the effect of application of TTA-P2 on T-type calcium currents. TTA-P2 application depresses the amplitude of T-type currents. Data are shown for the vehicle, IL-6, and eFT508+IL-6 groups. *P < 0.05, main effect of treatment, repeated measures ANOVA. Number of cells: vehicle, 10 from 5 mice; IL-6, 11 from 6 mice; eFT508+IL-6, 8 from 2 mice; eFT508, 7 from 3 mice.

    Journal: Journal of Neurophysiology

    Article Title: IL-6 induced upregulation of T-type Ca 2+ currents and sensitization of DRG nociceptors is attenuated by MNK inhibition

    doi: 10.1152/jn.00188.2020

    Figure Lengend Snippet: IL-6 treatment increases T-type calcium currents, and eFT508 pretreatment prevents this upregulation. A: representative traces of inward T-type calcium currents evoked from a holding potential of −90 mV and stepping from −60 mV to 0 mV in 5-mV increments. B: representative traces from all treatment groups, from a holding potential of −90 mV and test potential of 0 mV, showing that IL-6 treatment increases the amplitude of T-type currents. C: current-voltage (I-V) curves of the calcium current density (pA/pF). *P < 0.05, post hoc Dunnett’s test following 2-way ANOVA. Vehicle vs. IL-6 at −10 mV: mean difference 1.434 [95% confidence interval (95CI) 0.33, 2.54]; at −5 mV: 1.3 [95CI 0.19, 2.41]; at 0 mV: 1.8 [95CI 0.68, 2.91]. D: I-V curves of the current amplitudes used to obtain the density in C. *P < 0.05, post hoc Dunnett’s test following 2-way ANOVA. Vehicle vs. IL-6 at −15 mV: mean difference 32.59 [95% confidence interval (95CI) 5.06, 60.12]; at −10 mV: 44.17 [95CI 16.64, 71.7]; at −5 mV: 41.96 [95CI 14.44, 69.49]; at 0 mV: 52.81 [25.28, 80.34]. Inset shows the activation curve G/Gmax. The curve was obtained by fitting the conductances (G) of the amplitudes from D and estimated reversal potential (Erev) of 60 mV to the equation G/Gmax = 1/{1 + exp[(V50 − V)/slope]}, where V50 is the voltage at which current is half-maximal and V is the step voltage. E: average amplitudes of a subset of cells from D showing the effect of application of TTA-P2 on T-type calcium currents. TTA-P2 application depresses the amplitude of T-type currents. Data are shown for the vehicle, IL-6, and eFT508+IL-6 groups. *P < 0.05, main effect of treatment, repeated measures ANOVA. Number of cells: vehicle, 10 from 5 mice; IL-6, 11 from 6 mice; eFT508+IL-6, 8 from 2 mice; eFT508, 7 from 3 mice.

    Article Snippet: The specific T-type calcium channel blocker TTA-P2 was purchased from Alomone Laboratories, diluted to a stock concentration of 25 mM in DMSO, and dissolved in external solution to a working concentration of 2 µM.

    Techniques: Activation Assay

    T-type calcium channel antagonist TTA-P2 modifies IL-6-induced changes in membrane properties of dorsal root ganglion (DRG) neurons. A: TTA-P2 does not alter the number of action potentials (AP) in IL-6-treated cells in response to ramp currents. B: following 1 h of IL-6 treatment, the latency to the first spike is decreased, and this is reversed following the application of TTA-P2 at 100-pA and 300-pA ramp intensities. Inset shows representative traces from the same cell before and after TTA-P2 application indicating increased latency at 100 pA. *P < 0.05, post hoc Bonferroni correction following 2-way ANOVA. Mean difference at 100 pA: −170.3 [95% confidence interval (95CI) −224.9, −115.6]; at 300 pA: −64.07 [95CI −118.7, −9.41]. C, left: the rheobase to evoke an action potential is increased following TTA-P2 application. Right, representative traces from the same IL-6-treated cell before and after TTA-P2 application in response to a 5-s step protocol. The current required to evoke an action potential increases from 220 pA to 250 pA after TTA-P2 application. *P < 0.05, paired t test. Mean difference: 31.67 [95CI 17.63, 45.7]. Number of cells: 13 from 3 mice.

    Journal: Journal of Neurophysiology

    Article Title: IL-6 induced upregulation of T-type Ca 2+ currents and sensitization of DRG nociceptors is attenuated by MNK inhibition

    doi: 10.1152/jn.00188.2020

    Figure Lengend Snippet: T-type calcium channel antagonist TTA-P2 modifies IL-6-induced changes in membrane properties of dorsal root ganglion (DRG) neurons. A: TTA-P2 does not alter the number of action potentials (AP) in IL-6-treated cells in response to ramp currents. B: following 1 h of IL-6 treatment, the latency to the first spike is decreased, and this is reversed following the application of TTA-P2 at 100-pA and 300-pA ramp intensities. Inset shows representative traces from the same cell before and after TTA-P2 application indicating increased latency at 100 pA. *P < 0.05, post hoc Bonferroni correction following 2-way ANOVA. Mean difference at 100 pA: −170.3 [95% confidence interval (95CI) −224.9, −115.6]; at 300 pA: −64.07 [95CI −118.7, −9.41]. C, left: the rheobase to evoke an action potential is increased following TTA-P2 application. Right, representative traces from the same IL-6-treated cell before and after TTA-P2 application in response to a 5-s step protocol. The current required to evoke an action potential increases from 220 pA to 250 pA after TTA-P2 application. *P < 0.05, paired t test. Mean difference: 31.67 [95CI 17.63, 45.7]. Number of cells: 13 from 3 mice.

    Article Snippet: The specific T-type calcium channel blocker TTA-P2 was purchased from Alomone Laboratories, diluted to a stock concentration of 25 mM in DMSO, and dissolved in external solution to a working concentration of 2 µM.

    Techniques: