nnc 55 0396 dihydrochloride  (Alomone Labs)


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    Alomone Labs nnc 55 0396 dihydrochloride
    Effects of Cd ++ , NNC 55-0396, isradipine and NPS 2143 on RD.  (Aa)  Current protocol applied to evoke voltage changes shown in  (b,c)  (compare Figure   1Aa ).  (b)  RD was not evoked in the presence of Ca ++  (1 mM) and the absence of Cd ++  in the bath in response to 200-ms current pulses from −20 pA to +160 pA.  (c)  RD evoked by a threshold 200-ms current pulse to 0 pA in the bath presence of Ca ++  (1 mM) and Cd ++  (50 μM).  (d)  Absence of the RD in the bath in the presence of only Ca ++  (Ca ++ , 1 mM). RD could be evoked in the bath in the presence of Ca ++  (1 mM) together with Cd ++  (50 μM, Ca ++  + Cd ++ ).  (Ba)  Current protocol applied to evoke voltage changes shown in  (b,c)  (compare Figure   1Aa ).  (b)  RD was not evoked in the presence of Ca ++  (0.1 mM) in the bath in response to 200-ms current pulses from −20 pA to +160 pA.  (c)  RD evoked by a threshold 200-ms current pulse to 0 pA in the presence of Ca ++  (0.1 mM) together with the T-type Ca ++  channel blocker NNC 55-0396 (50 μM) in the bath.  (d)  The RD duration in the presence of only 0.1 mM of Ca ++  (Ca ++ ) or Ca ++  (0.1 mM) together with the T-type channel blocker NNC 55-0396 (50 μM) ( d , Ca ++  + NNC 55-0396) in the extracellular solution.  (e)  The RD duration in the presence of only Ca ++  (Ca ++ , 0.1 mM) or Ca ++  (0.1 mM) together with the L-type channel blocker isradipine (10 μM; Ca ++  + isradipine) in the extracellular solution.  (Ca)  Current protocol applied to evoke voltage changes shown in  (b,c)  (compare Figure   1Aa ).  (b)  RD was not evoked in the presence of only Ca ++  (0.1 mM) in the bath in response to 200-ms current pulses from −20 pA to +160 pA.  (c)  RD was evoked in response to a 200-ms threshold current pulse to 0 pA in the presence of Ca ++  (0.1 mM) together with calcium sensing receptor (CaSR) blocker (NPS 2143, 3 μM) in the bath.  (d)  The RD was not evoked in the presence of only 0.1 mM of Ca ++  (Ca ++ ). RD duration in the bath presence Ca ++  (0.1 mM) together with NPS 2143 (3 μM) (Ca ++  + NPS 2143).
    Nnc 55 0396 Dihydrochloride, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Ionic Mechanism Underlying Rebound Depolarization in Medial Prefrontal Cortex Pyramidal Neurons"

    Article Title: Ionic Mechanism Underlying Rebound Depolarization in Medial Prefrontal Cortex Pyramidal Neurons

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2018.00093

    Effects of Cd ++ , NNC 55-0396, isradipine and NPS 2143 on RD.  (Aa)  Current protocol applied to evoke voltage changes shown in  (b,c)  (compare Figure   1Aa ).  (b)  RD was not evoked in the presence of Ca ++  (1 mM) and the absence of Cd ++  in the bath in response to 200-ms current pulses from −20 pA to +160 pA.  (c)  RD evoked by a threshold 200-ms current pulse to 0 pA in the bath presence of Ca ++  (1 mM) and Cd ++  (50 μM).  (d)  Absence of the RD in the bath in the presence of only Ca ++  (Ca ++ , 1 mM). RD could be evoked in the bath in the presence of Ca ++  (1 mM) together with Cd ++  (50 μM, Ca ++  + Cd ++ ).  (Ba)  Current protocol applied to evoke voltage changes shown in  (b,c)  (compare Figure   1Aa ).  (b)  RD was not evoked in the presence of Ca ++  (0.1 mM) in the bath in response to 200-ms current pulses from −20 pA to +160 pA.  (c)  RD evoked by a threshold 200-ms current pulse to 0 pA in the presence of Ca ++  (0.1 mM) together with the T-type Ca ++  channel blocker NNC 55-0396 (50 μM) in the bath.  (d)  The RD duration in the presence of only 0.1 mM of Ca ++  (Ca ++ ) or Ca ++  (0.1 mM) together with the T-type channel blocker NNC 55-0396 (50 μM) ( d , Ca ++  + NNC 55-0396) in the extracellular solution.  (e)  The RD duration in the presence of only Ca ++  (Ca ++ , 0.1 mM) or Ca ++  (0.1 mM) together with the L-type channel blocker isradipine (10 μM; Ca ++  + isradipine) in the extracellular solution.  (Ca)  Current protocol applied to evoke voltage changes shown in  (b,c)  (compare Figure   1Aa ).  (b)  RD was not evoked in the presence of only Ca ++  (0.1 mM) in the bath in response to 200-ms current pulses from −20 pA to +160 pA.  (c)  RD was evoked in response to a 200-ms threshold current pulse to 0 pA in the presence of Ca ++  (0.1 mM) together with calcium sensing receptor (CaSR) blocker (NPS 2143, 3 μM) in the bath.  (d)  The RD was not evoked in the presence of only 0.1 mM of Ca ++  (Ca ++ ). RD duration in the bath presence Ca ++  (0.1 mM) together with NPS 2143 (3 μM) (Ca ++  + NPS 2143).
    Figure Legend Snippet: Effects of Cd ++ , NNC 55-0396, isradipine and NPS 2143 on RD. (Aa) Current protocol applied to evoke voltage changes shown in (b,c) (compare Figure 1Aa ). (b) RD was not evoked in the presence of Ca ++ (1 mM) and the absence of Cd ++ in the bath in response to 200-ms current pulses from −20 pA to +160 pA. (c) RD evoked by a threshold 200-ms current pulse to 0 pA in the bath presence of Ca ++ (1 mM) and Cd ++ (50 μM). (d) Absence of the RD in the bath in the presence of only Ca ++ (Ca ++ , 1 mM). RD could be evoked in the bath in the presence of Ca ++ (1 mM) together with Cd ++ (50 μM, Ca ++ + Cd ++ ). (Ba) Current protocol applied to evoke voltage changes shown in (b,c) (compare Figure 1Aa ). (b) RD was not evoked in the presence of Ca ++ (0.1 mM) in the bath in response to 200-ms current pulses from −20 pA to +160 pA. (c) RD evoked by a threshold 200-ms current pulse to 0 pA in the presence of Ca ++ (0.1 mM) together with the T-type Ca ++ channel blocker NNC 55-0396 (50 μM) in the bath. (d) The RD duration in the presence of only 0.1 mM of Ca ++ (Ca ++ ) or Ca ++ (0.1 mM) together with the T-type channel blocker NNC 55-0396 (50 μM) ( d , Ca ++ + NNC 55-0396) in the extracellular solution. (e) The RD duration in the presence of only Ca ++ (Ca ++ , 0.1 mM) or Ca ++ (0.1 mM) together with the L-type channel blocker isradipine (10 μM; Ca ++ + isradipine) in the extracellular solution. (Ca) Current protocol applied to evoke voltage changes shown in (b,c) (compare Figure 1Aa ). (b) RD was not evoked in the presence of only Ca ++ (0.1 mM) in the bath in response to 200-ms current pulses from −20 pA to +160 pA. (c) RD was evoked in response to a 200-ms threshold current pulse to 0 pA in the presence of Ca ++ (0.1 mM) together with calcium sensing receptor (CaSR) blocker (NPS 2143, 3 μM) in the bath. (d) The RD was not evoked in the presence of only 0.1 mM of Ca ++ (Ca ++ ). RD duration in the bath presence Ca ++ (0.1 mM) together with NPS 2143 (3 μM) (Ca ++ + NPS 2143).

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    Alomone Labs nnc 55 0396 dihydrochloride
    Effects of Cd ++ , NNC 55-0396, isradipine and NPS 2143 on RD.  (Aa)  Current protocol applied to evoke voltage changes shown in  (b,c)  (compare Figure   1Aa ).  (b)  RD was not evoked in the presence of Ca ++  (1 mM) and the absence of Cd ++  in the bath in response to 200-ms current pulses from −20 pA to +160 pA.  (c)  RD evoked by a threshold 200-ms current pulse to 0 pA in the bath presence of Ca ++  (1 mM) and Cd ++  (50 μM).  (d)  Absence of the RD in the bath in the presence of only Ca ++  (Ca ++ , 1 mM). RD could be evoked in the bath in the presence of Ca ++  (1 mM) together with Cd ++  (50 μM, Ca ++  + Cd ++ ).  (Ba)  Current protocol applied to evoke voltage changes shown in  (b,c)  (compare Figure   1Aa ).  (b)  RD was not evoked in the presence of Ca ++  (0.1 mM) in the bath in response to 200-ms current pulses from −20 pA to +160 pA.  (c)  RD evoked by a threshold 200-ms current pulse to 0 pA in the presence of Ca ++  (0.1 mM) together with the T-type Ca ++  channel blocker NNC 55-0396 (50 μM) in the bath.  (d)  The RD duration in the presence of only 0.1 mM of Ca ++  (Ca ++ ) or Ca ++  (0.1 mM) together with the T-type channel blocker NNC 55-0396 (50 μM) ( d , Ca ++  + NNC 55-0396) in the extracellular solution.  (e)  The RD duration in the presence of only Ca ++  (Ca ++ , 0.1 mM) or Ca ++  (0.1 mM) together with the L-type channel blocker isradipine (10 μM; Ca ++  + isradipine) in the extracellular solution.  (Ca)  Current protocol applied to evoke voltage changes shown in  (b,c)  (compare Figure   1Aa ).  (b)  RD was not evoked in the presence of only Ca ++  (0.1 mM) in the bath in response to 200-ms current pulses from −20 pA to +160 pA.  (c)  RD was evoked in response to a 200-ms threshold current pulse to 0 pA in the presence of Ca ++  (0.1 mM) together with calcium sensing receptor (CaSR) blocker (NPS 2143, 3 μM) in the bath.  (d)  The RD was not evoked in the presence of only 0.1 mM of Ca ++  (Ca ++ ). RD duration in the bath presence Ca ++  (0.1 mM) together with NPS 2143 (3 μM) (Ca ++  + NPS 2143).
    Nnc 55 0396 Dihydrochloride, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nnc 55 0396 dihydrochloride/product/Alomone Labs
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    nnc 55 0396 dihydrochloride - by Bioz Stars, 2022-01
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    Effects of Cd ++ , NNC 55-0396, isradipine and NPS 2143 on RD.  (Aa)  Current protocol applied to evoke voltage changes shown in  (b,c)  (compare Figure   1Aa ).  (b)  RD was not evoked in the presence of Ca ++  (1 mM) and the absence of Cd ++  in the bath in response to 200-ms current pulses from −20 pA to +160 pA.  (c)  RD evoked by a threshold 200-ms current pulse to 0 pA in the bath presence of Ca ++  (1 mM) and Cd ++  (50 μM).  (d)  Absence of the RD in the bath in the presence of only Ca ++  (Ca ++ , 1 mM). RD could be evoked in the bath in the presence of Ca ++  (1 mM) together with Cd ++  (50 μM, Ca ++  + Cd ++ ).  (Ba)  Current protocol applied to evoke voltage changes shown in  (b,c)  (compare Figure   1Aa ).  (b)  RD was not evoked in the presence of Ca ++  (0.1 mM) in the bath in response to 200-ms current pulses from −20 pA to +160 pA.  (c)  RD evoked by a threshold 200-ms current pulse to 0 pA in the presence of Ca ++  (0.1 mM) together with the T-type Ca ++  channel blocker NNC 55-0396 (50 μM) in the bath.  (d)  The RD duration in the presence of only 0.1 mM of Ca ++  (Ca ++ ) or Ca ++  (0.1 mM) together with the T-type channel blocker NNC 55-0396 (50 μM) ( d , Ca ++  + NNC 55-0396) in the extracellular solution.  (e)  The RD duration in the presence of only Ca ++  (Ca ++ , 0.1 mM) or Ca ++  (0.1 mM) together with the L-type channel blocker isradipine (10 μM; Ca ++  + isradipine) in the extracellular solution.  (Ca)  Current protocol applied to evoke voltage changes shown in  (b,c)  (compare Figure   1Aa ).  (b)  RD was not evoked in the presence of only Ca ++  (0.1 mM) in the bath in response to 200-ms current pulses from −20 pA to +160 pA.  (c)  RD was evoked in response to a 200-ms threshold current pulse to 0 pA in the presence of Ca ++  (0.1 mM) together with calcium sensing receptor (CaSR) blocker (NPS 2143, 3 μM) in the bath.  (d)  The RD was not evoked in the presence of only 0.1 mM of Ca ++  (Ca ++ ). RD duration in the bath presence Ca ++  (0.1 mM) together with NPS 2143 (3 μM) (Ca ++  + NPS 2143).

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Ionic Mechanism Underlying Rebound Depolarization in Medial Prefrontal Cortex Pyramidal Neurons

    doi: 10.3389/fncel.2018.00093

    Figure Lengend Snippet: Effects of Cd ++ , NNC 55-0396, isradipine and NPS 2143 on RD. (Aa) Current protocol applied to evoke voltage changes shown in (b,c) (compare Figure 1Aa ). (b) RD was not evoked in the presence of Ca ++ (1 mM) and the absence of Cd ++ in the bath in response to 200-ms current pulses from −20 pA to +160 pA. (c) RD evoked by a threshold 200-ms current pulse to 0 pA in the bath presence of Ca ++ (1 mM) and Cd ++ (50 μM). (d) Absence of the RD in the bath in the presence of only Ca ++ (Ca ++ , 1 mM). RD could be evoked in the bath in the presence of Ca ++ (1 mM) together with Cd ++ (50 μM, Ca ++ + Cd ++ ). (Ba) Current protocol applied to evoke voltage changes shown in (b,c) (compare Figure 1Aa ). (b) RD was not evoked in the presence of Ca ++ (0.1 mM) in the bath in response to 200-ms current pulses from −20 pA to +160 pA. (c) RD evoked by a threshold 200-ms current pulse to 0 pA in the presence of Ca ++ (0.1 mM) together with the T-type Ca ++ channel blocker NNC 55-0396 (50 μM) in the bath. (d) The RD duration in the presence of only 0.1 mM of Ca ++ (Ca ++ ) or Ca ++ (0.1 mM) together with the T-type channel blocker NNC 55-0396 (50 μM) ( d , Ca ++ + NNC 55-0396) in the extracellular solution. (e) The RD duration in the presence of only Ca ++ (Ca ++ , 0.1 mM) or Ca ++ (0.1 mM) together with the L-type channel blocker isradipine (10 μM; Ca ++ + isradipine) in the extracellular solution. (Ca) Current protocol applied to evoke voltage changes shown in (b,c) (compare Figure 1Aa ). (b) RD was not evoked in the presence of only Ca ++ (0.1 mM) in the bath in response to 200-ms current pulses from −20 pA to +160 pA. (c) RD was evoked in response to a 200-ms threshold current pulse to 0 pA in the presence of Ca ++ (0.1 mM) together with calcium sensing receptor (CaSR) blocker (NPS 2143, 3 μM) in the bath. (d) The RD was not evoked in the presence of only 0.1 mM of Ca ++ (Ca ++ ). RD duration in the bath presence Ca ++ (0.1 mM) together with NPS 2143 (3 μM) (Ca ++ + NPS 2143).

    Article Snippet: ZD 7288, isradipine, phorbol 12-myristate 13-acetate (PMA), and DNQX were purchased from Hello Bio (Bristol, UK); BAPTA, Cd++ and 4α-phorbol 12-myristate 13-acetate (4α-PMA) were purchased from Sigma-Aldrich (St. Louis, MO, USA); TTX was purchased from Latoxan (Valence, France); NNC 55-0396 dihydrochloride (NNC 55-0396), DL-AP5, and anti-Nav1.9 antibody were purchased from Alomone Labs (Jerusalem, Israel); Aβ1–42 was purchased from Abcam (Cambridge, UK); and normal IgG was purchased from Santa Cruz Biotechnology (Heidelberg, Germany).

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    Chemical structures of compounds  1  (Z160/NP118809),  2  (MONIRO‐1) and  3  (NNC 55‐0396) relevant to this study.

    Journal: British Journal of Pharmacology

    Article Title: Inhibition of human N‐ and T‐type calcium channels by an ortho‐phenoxyanilide derivative, MONIRO‐1) Inhibition of human N‐ and T‐type calcium channels by an ortho‐phenoxyanilide derivative, MONIRO‐1

    doi: 10.1111/bph.13910

    Figure Lengend Snippet: Chemical structures of compounds 1 (Z160/NP118809), 2 (MONIRO‐1) and 3 (NNC 55‐0396) relevant to this study.

    Article Snippet: Control compound NNC 55–0396 dihydrochloride was provided by Alomone Labs (Jerusalem, Israel).

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