tta a2  (Alomone Labs)


Bioz Verified Symbol Alomone Labs is a verified supplier
Bioz Manufacturer Symbol Alomone Labs manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 93
      Buy from Supplier

    Structured Review

    Alomone Labs tta a2
    Effect of T-type Ca 2+ channel blockers and genetic deletion of Ca v 3.2 on CPA-induced bladder pain-like nociceptive behavior ( A , D , G , J ), referred hyperalgesia ( B , E , H , K ) and bladder swelling ( C , F , I , L ) in mice. ( A – F ) In ddY mice, 6-prenylnaringenin (6-PNG), a hop-derived T-type Ca 2+ channel blocker, or KTt-45, a derivative of 6-PNG, at 10 and 30 mg/kg was administered i.p. 3 h 15 min after i.p. CPA at 400 mg/kg. ( G – I ) In C57BL/6 mice, <t>TTA-A2</t> at 1 mg/kg was administered i.p. 3 h after the CPA treatment. ( J – L ) CPA at 400 mg/kg was administered i.p. to wild-type (WT) and Ca v 3.2-knockout mice (KO) of a C57BL/6J background. Nociceptive behaviors were counted for 30 min starting 3.5 h after CPA treatment, followed immediately by evaluation of referred hyperalgesia/allodynia and then measurement of wet tissue weight of the excised bladder. V, vehicle. Data show the mean with S.E.M. for 6–8 (A–C), 5 (D–F), 5–6 (G–I) or 6 (J–L) mice. * p
    Tta A2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tta a2/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tta a2 - by Bioz Stars, 2022-01
    93/100 stars

    Images

    1) Product Images from "Cystitis-Related Bladder Pain Involves ATP-Dependent HMGB1 Release from Macrophages and Its Downstream H2S/Cav3.2 Signaling in Mice"

    Article Title: Cystitis-Related Bladder Pain Involves ATP-Dependent HMGB1 Release from Macrophages and Its Downstream H2S/Cav3.2 Signaling in Mice

    Journal: Cells

    doi: 10.3390/cells9081748

    Effect of T-type Ca 2+ channel blockers and genetic deletion of Ca v 3.2 on CPA-induced bladder pain-like nociceptive behavior ( A , D , G , J ), referred hyperalgesia ( B , E , H , K ) and bladder swelling ( C , F , I , L ) in mice. ( A – F ) In ddY mice, 6-prenylnaringenin (6-PNG), a hop-derived T-type Ca 2+ channel blocker, or KTt-45, a derivative of 6-PNG, at 10 and 30 mg/kg was administered i.p. 3 h 15 min after i.p. CPA at 400 mg/kg. ( G – I ) In C57BL/6 mice, TTA-A2 at 1 mg/kg was administered i.p. 3 h after the CPA treatment. ( J – L ) CPA at 400 mg/kg was administered i.p. to wild-type (WT) and Ca v 3.2-knockout mice (KO) of a C57BL/6J background. Nociceptive behaviors were counted for 30 min starting 3.5 h after CPA treatment, followed immediately by evaluation of referred hyperalgesia/allodynia and then measurement of wet tissue weight of the excised bladder. V, vehicle. Data show the mean with S.E.M. for 6–8 (A–C), 5 (D–F), 5–6 (G–I) or 6 (J–L) mice. * p
    Figure Legend Snippet: Effect of T-type Ca 2+ channel blockers and genetic deletion of Ca v 3.2 on CPA-induced bladder pain-like nociceptive behavior ( A , D , G , J ), referred hyperalgesia ( B , E , H , K ) and bladder swelling ( C , F , I , L ) in mice. ( A – F ) In ddY mice, 6-prenylnaringenin (6-PNG), a hop-derived T-type Ca 2+ channel blocker, or KTt-45, a derivative of 6-PNG, at 10 and 30 mg/kg was administered i.p. 3 h 15 min after i.p. CPA at 400 mg/kg. ( G – I ) In C57BL/6 mice, TTA-A2 at 1 mg/kg was administered i.p. 3 h after the CPA treatment. ( J – L ) CPA at 400 mg/kg was administered i.p. to wild-type (WT) and Ca v 3.2-knockout mice (KO) of a C57BL/6J background. Nociceptive behaviors were counted for 30 min starting 3.5 h after CPA treatment, followed immediately by evaluation of referred hyperalgesia/allodynia and then measurement of wet tissue weight of the excised bladder. V, vehicle. Data show the mean with S.E.M. for 6–8 (A–C), 5 (D–F), 5–6 (G–I) or 6 (J–L) mice. * p

    Techniques Used: Mouse Assay, Derivative Assay, Knock-Out

    2) Product Images from "T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice"

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0206986

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p
    Figure Legend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Techniques Used:

    3) Product Images from "T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice"

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0206986

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p
    Figure Legend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Techniques Used:

    4) Product Images from "T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice"

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0206986

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p
    Figure Legend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Techniques Used:

    5) Product Images from "Ca2+ signaling driving pacemaker activity in submucosal interstitial cells of Cajal in the colon"

    Article Title: Ca2+ signaling driving pacemaker activity in submucosal interstitial cells of Cajal in the colon

    Journal: bioRxiv

    doi: 10.1101/2020.10.26.355404

    Effects of T-type Ca 2+ channel antagonists, TTA-A2 and Z-944 on ICC-SM Ca 2+ transients. A B Occurrence maps showing ICC-SM network active firing sites. Sites were individually color-coded and plotted under control A and in the presence of TTA-A2 (10 μM) B conditions. Plots of Ca 2+ transient particle activity of ICC-SM in control conditions and in the presence of TTA-A2 showing PTCL area (blue) and PTCL count (green) under control conditions C and in the presence of TTA-A2 D . Summary graphs of average percentage change of PTCL area E , PTCL count F and the number of Ca 2+ firing sites was reduced by TTA-A2 G ( n = 7). H I Active firing sites were individually color-coded and plotted as an occurrence maps in the ICC-SM network under control H and Z-944 (1 μM) I conditions. Plots of Ca 2+ transient particle activity of ICC-SM in control conditions and in the presence of Z-944 showing PTCL area (blue) and PTCL count (green) under control conditions J and in the presence of Z-944 K . Summary graphs of average percentage change of PTCL area L , PTCL count M and the number of Ca 2+ firing sites was reduced by Z-944 N ( n = 5). Significance determined using unpaired t-test, ** = P
    Figure Legend Snippet: Effects of T-type Ca 2+ channel antagonists, TTA-A2 and Z-944 on ICC-SM Ca 2+ transients. A B Occurrence maps showing ICC-SM network active firing sites. Sites were individually color-coded and plotted under control A and in the presence of TTA-A2 (10 μM) B conditions. Plots of Ca 2+ transient particle activity of ICC-SM in control conditions and in the presence of TTA-A2 showing PTCL area (blue) and PTCL count (green) under control conditions C and in the presence of TTA-A2 D . Summary graphs of average percentage change of PTCL area E , PTCL count F and the number of Ca 2+ firing sites was reduced by TTA-A2 G ( n = 7). H I Active firing sites were individually color-coded and plotted as an occurrence maps in the ICC-SM network under control H and Z-944 (1 μM) I conditions. Plots of Ca 2+ transient particle activity of ICC-SM in control conditions and in the presence of Z-944 showing PTCL area (blue) and PTCL count (green) under control conditions J and in the presence of Z-944 K . Summary graphs of average percentage change of PTCL area L , PTCL count M and the number of Ca 2+ firing sites was reduced by Z-944 N ( n = 5). Significance determined using unpaired t-test, ** = P

    Techniques Used: Immunocytochemistry, Activity Assay

    6) Product Images from "T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice"

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0206986

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p
    Figure Legend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Techniques Used:

    7) Product Images from "Clustering of Ca2+ transients in interstitial cells of Cajal defines slow wave duration"

    Article Title: Clustering of Ca2+ transients in interstitial cells of Cajal defines slow wave duration

    Journal: The Journal of General Physiology

    doi: 10.1085/jgp.201711771

    The effect of TTA-A2 on Ca 2+ transients in ICC-MY. (A) Representative heat map showing the summated PTCLs recording of ICC-MY in control and TTA-A2 (1 µM). (B) Occurrence map of individually color-coded Ca 2+ firing sites in the ICC-MY network in control and TTA-A2 conditions. (C) Traces of PTCL activity of the ICC-MY network in control conditions and in the presence of TTA-A2 showing PTCL area (dark blue) and PTCL count (brown). (D) Histogram showing the probability (%) that an individual Ca 2+ firing site in the ICC-MY cell somata will fire during a CTC cycle in control conditions (black bars) and TTA-A2 (1 µM; red bars; n = 5, FOV = 6). (E) Histogram showing the probability (%) that an individual Ca 2+ firing site in the ICC-MY cell processes will fire during a CTC cycle in control conditions (black bars) and TTA-A2 (1 µM; red bars; n = 5, FOV = 6). (F) The number of firing sites in the cell soma was reduced from 3.5 ± 0.6 in control to 0.3 ± 0.25 in TTA-A2 (1 µM; P = 0.006, n = 5, FOV = 6). (G) In the presence of TTA-A2 (1 µM), the PTCL area/frame in the cell somata was 0.07 ± 0.069 µm 2 compared with 11.4 ± 3.3 µm 2 in control (P = 0.0197, n = 5, FOV = 6). (H) The PTCL count/frame in the cell somata was reduced from 0.3 ± 0.03 in control to 0.005 ± 0.0039 in TTA-A2 (1 µM; P = 0.0007 n = 5, FOV = 6). (I) In the cell processes, the number of Ca 2+ firing sites per FOV was reduced from 56.5 ± 7.4 in control to 8.7 ± 6.9 in TTA-A2 (1 µM; P = 0.0001, n = 5, FOV = 6). (J) The PTCL area/frame in the cell processes was reduced from 27.4 ± 4.8 µm 2 in control to 0.7 ± 0.59 µm 2 in the presence of TTA-A2 (1 µM; P = 0.0016 n = 5, FOV = 6). (K) In the cell processes, PTCL count/frame was reduced from 0.87 ± 0.15 in control to 0.05 ± 0.04 in TTA-A2 (1 µM; P = 0.0014 n = 5, FOV = 6). *, P
    Figure Legend Snippet: The effect of TTA-A2 on Ca 2+ transients in ICC-MY. (A) Representative heat map showing the summated PTCLs recording of ICC-MY in control and TTA-A2 (1 µM). (B) Occurrence map of individually color-coded Ca 2+ firing sites in the ICC-MY network in control and TTA-A2 conditions. (C) Traces of PTCL activity of the ICC-MY network in control conditions and in the presence of TTA-A2 showing PTCL area (dark blue) and PTCL count (brown). (D) Histogram showing the probability (%) that an individual Ca 2+ firing site in the ICC-MY cell somata will fire during a CTC cycle in control conditions (black bars) and TTA-A2 (1 µM; red bars; n = 5, FOV = 6). (E) Histogram showing the probability (%) that an individual Ca 2+ firing site in the ICC-MY cell processes will fire during a CTC cycle in control conditions (black bars) and TTA-A2 (1 µM; red bars; n = 5, FOV = 6). (F) The number of firing sites in the cell soma was reduced from 3.5 ± 0.6 in control to 0.3 ± 0.25 in TTA-A2 (1 µM; P = 0.006, n = 5, FOV = 6). (G) In the presence of TTA-A2 (1 µM), the PTCL area/frame in the cell somata was 0.07 ± 0.069 µm 2 compared with 11.4 ± 3.3 µm 2 in control (P = 0.0197, n = 5, FOV = 6). (H) The PTCL count/frame in the cell somata was reduced from 0.3 ± 0.03 in control to 0.005 ± 0.0039 in TTA-A2 (1 µM; P = 0.0007 n = 5, FOV = 6). (I) In the cell processes, the number of Ca 2+ firing sites per FOV was reduced from 56.5 ± 7.4 in control to 8.7 ± 6.9 in TTA-A2 (1 µM; P = 0.0001, n = 5, FOV = 6). (J) The PTCL area/frame in the cell processes was reduced from 27.4 ± 4.8 µm 2 in control to 0.7 ± 0.59 µm 2 in the presence of TTA-A2 (1 µM; P = 0.0016 n = 5, FOV = 6). (K) In the cell processes, PTCL count/frame was reduced from 0.87 ± 0.15 in control to 0.05 ± 0.04 in TTA-A2 (1 µM; P = 0.0014 n = 5, FOV = 6). *, P

    Techniques Used: Immunocytochemistry, Activity Assay

    8) Product Images from "T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice"

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0206986

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p
    Figure Legend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Techniques Used:

    9) Product Images from "T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice"

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0206986

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p
    Figure Legend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Techniques Used:

    10) Product Images from "T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice"

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0206986

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p
    Figure Legend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Techniques Used:

    11) Product Images from "T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice"

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0206986

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p
    Figure Legend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Techniques Used:

    12) Product Images from "T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice"

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0206986

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p
    Figure Legend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Techniques Used:

    13) Product Images from "Ca2+ signaling driving pacemaker activity in submucosal interstitial cells of Cajal in the murine colon"

    Article Title: Ca2+ signaling driving pacemaker activity in submucosal interstitial cells of Cajal in the murine colon

    Journal: eLife

    doi: 10.7554/eLife.64099

    Effects of T-type Ca 2+ channel antagonists, TTA-A2 and Z-944 on submucosal interstitial cells of Cajal (ICC-SM) Ca 2+ transients. A and B Occurrence maps showing ICC-SM network active firing sites. Sites were individually color coded and plotted under control A and in the presence of TTA-A2 (10 μM) ( B ) conditions. Plots of Ca 2+ transient particle activity of ICC-SM in control conditions and in the presence of TTA-A2 showing PTCL area (blue) and PTCL count (green) under control conditions C and in the presence of TTA-A2 D . Summary graphs of average percentage change of PTCL area E , PTCL count F and the number of Ca 2+ -firing sites was reduced by TTA-A2 G ( n = 7). H and I Active firing sites were individually color coded and plotted as an occurrence maps in the ICC-SM network under control H and Z-944 (1 μM) ( I ) conditions. Plots of Ca 2+ transient particle activity of ICC-SM in control conditions and in the presence of Z-944 showing PTCL area (blue) and PTCL count (green) under control conditions J and in the presence of Z-944 K . Summary graphs of average percentage change of PTCL area L , PTCL count M and the number of Ca 2+ -firing sites was reduced by Z-944 N ( n = 5). Significance determined using unpaired t-test, ** = p
    Figure Legend Snippet: Effects of T-type Ca 2+ channel antagonists, TTA-A2 and Z-944 on submucosal interstitial cells of Cajal (ICC-SM) Ca 2+ transients. A and B Occurrence maps showing ICC-SM network active firing sites. Sites were individually color coded and plotted under control A and in the presence of TTA-A2 (10 μM) ( B ) conditions. Plots of Ca 2+ transient particle activity of ICC-SM in control conditions and in the presence of TTA-A2 showing PTCL area (blue) and PTCL count (green) under control conditions C and in the presence of TTA-A2 D . Summary graphs of average percentage change of PTCL area E , PTCL count F and the number of Ca 2+ -firing sites was reduced by TTA-A2 G ( n = 7). H and I Active firing sites were individually color coded and plotted as an occurrence maps in the ICC-SM network under control H and Z-944 (1 μM) ( I ) conditions. Plots of Ca 2+ transient particle activity of ICC-SM in control conditions and in the presence of Z-944 showing PTCL area (blue) and PTCL count (green) under control conditions J and in the presence of Z-944 K . Summary graphs of average percentage change of PTCL area L , PTCL count M and the number of Ca 2+ -firing sites was reduced by Z-944 N ( n = 5). Significance determined using unpaired t-test, ** = p

    Techniques Used: Immunocytochemistry, Activity Assay

    14) Product Images from "T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice"

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0206986

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p
    Figure Legend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Techniques Used:

    15) Product Images from "T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice"

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0206986

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p
    Figure Legend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Techniques Used:

    16) Product Images from "T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice"

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0206986

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p
    Figure Legend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Techniques Used:

    17) Product Images from "Cell-Type Specific Distribution of T-Type Calcium Currents in Lamina II Neurons of the Rat Spinal Cord"

    Article Title: Cell-Type Specific Distribution of T-Type Calcium Currents in Lamina II Neurons of the Rat Spinal Cord

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2018.00370

    Pharmacological properties of T-type current in SG neurons. (A) Representative traces of T-type current in control, with 0.2 mM NiCl 2 , after washout of NiCl 2 , and the superimposed traces. In this figure, all the T-type current was activated every 10 s by a 200-ms voltage step to −50 mV from a holding potential of −110 mV for 500 ms (inset). (B) Time course of a representative experiment during application of NiCl 2 that shown in panel (A) . The amplitude of T-type current is depicted over time. (C) Summary of the blockade of T-type current by NiCl 2 . (D) Representative traces of T-type current in control, with 40 μM TTA-A2, after washout of TTA-A2, and the superimposed traces. (E) Time course of a representative experiment during application of TTA-A2 that shown in panel (D) . The amplitude of T-type current is depicted over time. (F) Summary of the blockade of T-type current by TTA-A2. (G,H) Concentration-response relationship for NiCl 2 and TTA-A2. Concentration-response curve was fitted with the Hill equation as follows: y = I max /(1 + IC 50 /x), in which I max represents the maximal current amplitude, IC 50 is the half-maximal inhibitory concentration, and x is the concentration. * P
    Figure Legend Snippet: Pharmacological properties of T-type current in SG neurons. (A) Representative traces of T-type current in control, with 0.2 mM NiCl 2 , after washout of NiCl 2 , and the superimposed traces. In this figure, all the T-type current was activated every 10 s by a 200-ms voltage step to −50 mV from a holding potential of −110 mV for 500 ms (inset). (B) Time course of a representative experiment during application of NiCl 2 that shown in panel (A) . The amplitude of T-type current is depicted over time. (C) Summary of the blockade of T-type current by NiCl 2 . (D) Representative traces of T-type current in control, with 40 μM TTA-A2, after washout of TTA-A2, and the superimposed traces. (E) Time course of a representative experiment during application of TTA-A2 that shown in panel (D) . The amplitude of T-type current is depicted over time. (F) Summary of the blockade of T-type current by TTA-A2. (G,H) Concentration-response relationship for NiCl 2 and TTA-A2. Concentration-response curve was fitted with the Hill equation as follows: y = I max /(1 + IC 50 /x), in which I max represents the maximal current amplitude, IC 50 is the half-maximal inhibitory concentration, and x is the concentration. * P

    Techniques Used: Mass Spectrometry, Concentration Assay

    Isolation of T-type current in substantia gelatinosa (SG) neurons from the rat transverse spinal cord slices. (A) Representative families of current traces in control (Aa) , with 0.5 μM tetrodotoxin (TTX; Ab ), 1 mM NiCl 2 (Ac) , and that of the digital subtraction of (Ab–Ad) . The inset shows the voltage-clamp protocol. (B) Plots of T-type current density against the test potentials in various groups showing in Aa , Ab , and Ad ( n = 19 cells in four rats). (C) Representative families of current traces in control (Ca) , with 0.5 μM TTX (Cb) , 40 μM TTA-A2 (Cc) , and that of the digital subtraction of (Cb–Cd) . (D) Plots of T-type current density against the membrane potentials in various groups showing in Ca , Cb and Cd ( n = 7 cells in three rats).
    Figure Legend Snippet: Isolation of T-type current in substantia gelatinosa (SG) neurons from the rat transverse spinal cord slices. (A) Representative families of current traces in control (Aa) , with 0.5 μM tetrodotoxin (TTX; Ab ), 1 mM NiCl 2 (Ac) , and that of the digital subtraction of (Ab–Ad) . The inset shows the voltage-clamp protocol. (B) Plots of T-type current density against the test potentials in various groups showing in Aa , Ab , and Ad ( n = 19 cells in four rats). (C) Representative families of current traces in control (Ca) , with 0.5 μM TTX (Cb) , 40 μM TTA-A2 (Cc) , and that of the digital subtraction of (Cb–Cd) . (D) Plots of T-type current density against the membrane potentials in various groups showing in Ca , Cb and Cd ( n = 7 cells in three rats).

    Techniques Used: Isolation

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • tta p2  (Alomone Labs)
    93
    Alomone Labs tta p2
    The selective T-type calcium channel inhibitor, <t>TTA-P2,</t> blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).
    Tta P2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tta p2/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tta p2 - by Bioz Stars, 2022-01
    93/100 stars
    		  Buy from Supplier
    tta a2  (Alomone Labs)
    93
    Alomone Labs tta a2
    Effect of T-type Ca 2+ channel blockers and genetic deletion of Ca v 3.2 on CPA-induced bladder pain-like nociceptive behavior ( A , D , G , J ), referred hyperalgesia ( B , E , H , K ) and bladder swelling ( C , F , I , L ) in mice. ( A – F ) In ddY mice, 6-prenylnaringenin (6-PNG), a hop-derived T-type Ca 2+ channel blocker, or KTt-45, a derivative of 6-PNG, at 10 and 30 mg/kg was administered i.p. 3 h 15 min after i.p. CPA at 400 mg/kg. ( G – I ) In C57BL/6 mice, <t>TTA-A2</t> at 1 mg/kg was administered i.p. 3 h after the CPA treatment. ( J – L ) CPA at 400 mg/kg was administered i.p. to wild-type (WT) and Ca v 3.2-knockout mice (KO) of a C57BL/6J background. Nociceptive behaviors were counted for 30 min starting 3.5 h after CPA treatment, followed immediately by evaluation of referred hyperalgesia/allodynia and then measurement of wet tissue weight of the excised bladder. V, vehicle. Data show the mean with S.E.M. for 6–8 (A–C), 5 (D–F), 5–6 (G–I) or 6 (J–L) mice. * p
    Tta A2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tta a2/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tta a2 - by Bioz Stars, 2022-01
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).

    Journal: Neuroscience

    Article Title: Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro

    doi: 10.1016/j.neuroscience.2017.04.002

    Figure Lengend Snippet: The selective T-type calcium channel inhibitor, TTA-P2, blocked low-threshold spikes/currents in BF vGluT2+ neurons A. In current clamp, a representative vGluT2+ neuron showed rebound spikes following 1 s hyperpolarizing current injections (-180 or -300 pA). The neuron was initially held at ∼-70 mV. B. The same neuron shown in A was incubated with 500 nM TTX to block sodium-dependent action potentials. A hyperpolarizing current injection induced a low-threshold spike (control: black trace) which was blocked by TTA-P2 (red trace). C. In voltage clamp and in the presence of TTX, a representative vGluT2+ neuron showed an inward current at the removal of a 1s voltage step to -125 mV (control: black trace). TTA-P2 also blocked this rebound inward current (red trace). D. I-V plot with the voltage steps shown on the x-axis and the amplitude of rebound inward currents shown on the y-axis. Data were plotted as mean± SEM (n=6).

    Article Snippet: TTA-P2 is a potent and selective blocker of T-type calcium channels in rat sensory neurons and a novel antinociceptive agent.

    Techniques: Incubation, Blocking Assay, Injection

    T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Journal: The Journal of Neuroscience

    Article Title: Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels

    doi: 10.1523/JNEUROSCI.0117-17.2017

    Figure Lengend Snippet: T-type Ca 2+ channels contribute to rebound spike timing. A , Rebound spikes (top) and rebound Ca 2+ (bottom) before (black) and after (red) TTA-P2 application. Scale bars: top, 20 mV, 100 ms; bottom, 0.05 dG / Gs , 100 ms. B , Time course of TTA-P2 application

    Article Snippet: Comparing TTA-P2 application to time-matched no-drug control experiments, we found that TTA-P2 significantly increased the duration of the rebound delay 6–8 min after application (control, 103 ± 2.3% n = 6 cells from 4 mice; TTA-P2, 138 ± 13.6%, n = 7 cells from 4 mice; Mann–Whitney U test, p = 0.0023), and substantially reduced the rebound dendritic Ca2+ signal (control, 86 ± 8.9%; TTA-P2, 49 ± 7.9%; Mann–Whitney U test, p = 0.014; A–C ).

    Techniques:

    Effect of T-type Ca 2+ channel blockers and genetic deletion of Ca v 3.2 on CPA-induced bladder pain-like nociceptive behavior ( A , D , G , J ), referred hyperalgesia ( B , E , H , K ) and bladder swelling ( C , F , I , L ) in mice. ( A – F ) In ddY mice, 6-prenylnaringenin (6-PNG), a hop-derived T-type Ca 2+ channel blocker, or KTt-45, a derivative of 6-PNG, at 10 and 30 mg/kg was administered i.p. 3 h 15 min after i.p. CPA at 400 mg/kg. ( G – I ) In C57BL/6 mice, TTA-A2 at 1 mg/kg was administered i.p. 3 h after the CPA treatment. ( J – L ) CPA at 400 mg/kg was administered i.p. to wild-type (WT) and Ca v 3.2-knockout mice (KO) of a C57BL/6J background. Nociceptive behaviors were counted for 30 min starting 3.5 h after CPA treatment, followed immediately by evaluation of referred hyperalgesia/allodynia and then measurement of wet tissue weight of the excised bladder. V, vehicle. Data show the mean with S.E.M. for 6–8 (A–C), 5 (D–F), 5–6 (G–I) or 6 (J–L) mice. * p

    Journal: Cells

    Article Title: Cystitis-Related Bladder Pain Involves ATP-Dependent HMGB1 Release from Macrophages and Its Downstream H2S/Cav3.2 Signaling in Mice

    doi: 10.3390/cells9081748

    Figure Lengend Snippet: Effect of T-type Ca 2+ channel blockers and genetic deletion of Ca v 3.2 on CPA-induced bladder pain-like nociceptive behavior ( A , D , G , J ), referred hyperalgesia ( B , E , H , K ) and bladder swelling ( C , F , I , L ) in mice. ( A – F ) In ddY mice, 6-prenylnaringenin (6-PNG), a hop-derived T-type Ca 2+ channel blocker, or KTt-45, a derivative of 6-PNG, at 10 and 30 mg/kg was administered i.p. 3 h 15 min after i.p. CPA at 400 mg/kg. ( G – I ) In C57BL/6 mice, TTA-A2 at 1 mg/kg was administered i.p. 3 h after the CPA treatment. ( J – L ) CPA at 400 mg/kg was administered i.p. to wild-type (WT) and Ca v 3.2-knockout mice (KO) of a C57BL/6J background. Nociceptive behaviors were counted for 30 min starting 3.5 h after CPA treatment, followed immediately by evaluation of referred hyperalgesia/allodynia and then measurement of wet tissue weight of the excised bladder. V, vehicle. Data show the mean with S.E.M. for 6–8 (A–C), 5 (D–F), 5–6 (G–I) or 6 (J–L) mice. * p

    Article Snippet: TTA-A2 was obtained from Alomone Labs. (Jerusalem, Israel), and A438079, 5-BDBD and AZ 10606120 were from Tocris Bioscience (Bristol, UK). (2R/S)-6-Prenylnaringenin (6-PNG) and KTt-45 [6-(3-ethylpent-2-enyl)-5,7-dihydroxy-2-(2-hydroxyphenyl)chroman-4-one] were synthesized in-house, as reported previously [ ].

    Techniques: Mouse Assay, Derivative Assay, Knock-Out

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Journal: PLoS ONE

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    doi: 10.1371/journal.pone.0206986

    Figure Lengend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Article Snippet: While T-type calcium channel inhibitor NNC 55–0396 (1 μM) significantly inhibited SAK3-promoted hippocampal DA and 5-HT releases, the same dose of TTA-A2 (1 μM) failed to inhibit SAK3 effect completely.

    Techniques: