isradipine  (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
  • 86

    Structured Review

    Alomone Labs isradipine
    LTCCs are required for cocaine- and stress-primed reinstatement of cocaine conditioned place preference, a) Experimental timeline of cocaine conditioned place preference (CPP) acquisition, extinction and cocaine-primed (CPR) or stress-primed (SPR) reinstatement protocol and <t>isradipine</t> treatment, b) Prior to treatment with either vehicle (pre-vehicle) or isradipine (pre-isradipine), all mice acquired (* p
    Isradipine, 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/isradipine/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    isradipine - by Bioz Stars, 2021-12
    86/100 stars

    Images

    1) Product Images from "Cocaine- and stress-primed reinstatement of drug-associated memories elicit differential behavioral and frontostriatal circuit activity patterns via recruitment of L-type Ca2+ channels"

    Article Title: Cocaine- and stress-primed reinstatement of drug-associated memories elicit differential behavioral and frontostriatal circuit activity patterns via recruitment of L-type Ca2+ channels

    Journal: Molecular psychiatry

    doi: 10.1038/s41380-019-0513-2

    LTCCs are required for cocaine- and stress-primed reinstatement of cocaine conditioned place preference, a) Experimental timeline of cocaine conditioned place preference (CPP) acquisition, extinction and cocaine-primed (CPR) or stress-primed (SPR) reinstatement protocol and isradipine treatment, b) Prior to treatment with either vehicle (pre-vehicle) or isradipine (pre-isradipine), all mice acquired (* p
    Figure Legend Snippet: LTCCs are required for cocaine- and stress-primed reinstatement of cocaine conditioned place preference, a) Experimental timeline of cocaine conditioned place preference (CPP) acquisition, extinction and cocaine-primed (CPR) or stress-primed (SPR) reinstatement protocol and isradipine treatment, b) Prior to treatment with either vehicle (pre-vehicle) or isradipine (pre-isradipine), all mice acquired (* p

    Techniques Used: Conditioned Place Preference, SPR Assay, Mouse Assay

    Cocaine- and stress-primed reinstatement recruit the PrL→NAcC projection, a) C57BL/6J mice were injected with a Cre-dependent AAV expressing GCaMP6s into unilateral PrL and a retrograde AAV expressing Cre recombinase was injected into ipsilateral NAcC. An optic fiber was implanted above the PrL, which could be attached to a patch cord to record Ca 2+ signals, b) Representative image of GCaMP6s expressing in the PrL. Optic fiber location is outlined in white. MO, medial orbitofrontal cortex; Cg, cingulate cortex, c) Experimental timeline for fiber photometry recording during cocaine CPP. Ca 2+ imaging was conducted during the baseline test, acquisition test, extinction test, and CPR/SPR. Mice were treated with vehicle or isradipine to block LTCCs prior to CPR/SPR recording, d) Representative fiber photometry trace of a vehicle-treated mouse during CPR showing Ca 2+ transients prior to cocaine-paired entries (red) but not saline-paired entries (blue). Grey, middle CPP chamber, e) The average amplitude (% ΔF/F) of PrL→NAcC fiber photometry signal 5 seconds prior to entry into the cocaine-paired chamber was significantly higher as compared to entries into the saline-paired chamber in vehicle-treated mice (** p
    Figure Legend Snippet: Cocaine- and stress-primed reinstatement recruit the PrL→NAcC projection, a) C57BL/6J mice were injected with a Cre-dependent AAV expressing GCaMP6s into unilateral PrL and a retrograde AAV expressing Cre recombinase was injected into ipsilateral NAcC. An optic fiber was implanted above the PrL, which could be attached to a patch cord to record Ca 2+ signals, b) Representative image of GCaMP6s expressing in the PrL. Optic fiber location is outlined in white. MO, medial orbitofrontal cortex; Cg, cingulate cortex, c) Experimental timeline for fiber photometry recording during cocaine CPP. Ca 2+ imaging was conducted during the baseline test, acquisition test, extinction test, and CPR/SPR. Mice were treated with vehicle or isradipine to block LTCCs prior to CPR/SPR recording, d) Representative fiber photometry trace of a vehicle-treated mouse during CPR showing Ca 2+ transients prior to cocaine-paired entries (red) but not saline-paired entries (blue). Grey, middle CPP chamber, e) The average amplitude (% ΔF/F) of PrL→NAcC fiber photometry signal 5 seconds prior to entry into the cocaine-paired chamber was significantly higher as compared to entries into the saline-paired chamber in vehicle-treated mice (** p

    Techniques Used: Mouse Assay, Injection, Expressing, Imaging, SPR Assay, Blocking Assay

    2) Product Images from "CaMKII inactivation by extracellular Ca2+ depletion in dorsal root ganglion neurons"

    Article Title: CaMKII inactivation by extracellular Ca2+ depletion in dorsal root ganglion neurons

    Journal: Cell calcium

    doi: 10.1016/j.ceca.2006.01.005

    Activation of CaMKII is independent of VGCC-mediated Ca 2+ influx. Pre-incubation with either the L-type channel blockers isradipine or SR 33805 ( n = 6) at 10 μM failed to block CaMKII activation. Additionally, the Na + /Ca 2+ -exchanger inhibitor KB-R7943 at 10 μM ( n = 6) also did not affect activation of CaMKII by Ca 2+ O -stimulation. Basal phosphorylation at 286/287 Thr in 0 Ca 2+ was 12 ± 1% of stimulation by 1.8 Ca 2+ O . Neither compound significantly affected Ca 2+ -stimulation ( n = 6) suggesting that changes in [Ca 2+ ] O act at a site independent of VGCC.
    Figure Legend Snippet: Activation of CaMKII is independent of VGCC-mediated Ca 2+ influx. Pre-incubation with either the L-type channel blockers isradipine or SR 33805 ( n = 6) at 10 μM failed to block CaMKII activation. Additionally, the Na + /Ca 2+ -exchanger inhibitor KB-R7943 at 10 μM ( n = 6) also did not affect activation of CaMKII by Ca 2+ O -stimulation. Basal phosphorylation at 286/287 Thr in 0 Ca 2+ was 12 ± 1% of stimulation by 1.8 Ca 2+ O . Neither compound significantly affected Ca 2+ -stimulation ( n = 6) suggesting that changes in [Ca 2+ ] O act at a site independent of VGCC.

    Techniques Used: Activation Assay, Incubation, Blocking Assay, Activated Clotting Time Assay

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86
    Alomone Labs isradipine
    LTCCs are required for cocaine- and stress-primed reinstatement of cocaine conditioned place preference, a) Experimental timeline of cocaine conditioned place preference (CPP) acquisition, extinction and cocaine-primed (CPR) or stress-primed (SPR) reinstatement protocol and <t>isradipine</t> treatment, b) Prior to treatment with either vehicle (pre-vehicle) or isradipine (pre-isradipine), all mice acquired (* p
    Isradipine, 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/isradipine/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    isradipine - by Bioz Stars, 2021-12
    86/100 stars
      Buy from Supplier

    94
    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: 94/100, 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 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    nnc 55 0396 dihydrochloride - by Bioz Stars, 2021-12
    94/100 stars
      Buy from Supplier

    Image Search Results


    LTCCs are required for cocaine- and stress-primed reinstatement of cocaine conditioned place preference, a) Experimental timeline of cocaine conditioned place preference (CPP) acquisition, extinction and cocaine-primed (CPR) or stress-primed (SPR) reinstatement protocol and isradipine treatment, b) Prior to treatment with either vehicle (pre-vehicle) or isradipine (pre-isradipine), all mice acquired (* p

    Journal: Molecular psychiatry

    Article Title: Cocaine- and stress-primed reinstatement of drug-associated memories elicit differential behavioral and frontostriatal circuit activity patterns via recruitment of L-type Ca2+ channels

    doi: 10.1038/s41380-019-0513-2

    Figure Lengend Snippet: LTCCs are required for cocaine- and stress-primed reinstatement of cocaine conditioned place preference, a) Experimental timeline of cocaine conditioned place preference (CPP) acquisition, extinction and cocaine-primed (CPR) or stress-primed (SPR) reinstatement protocol and isradipine treatment, b) Prior to treatment with either vehicle (pre-vehicle) or isradipine (pre-isradipine), all mice acquired (* p

    Article Snippet: Isradipine (Alomone Labs) was dissolved in saline (16% ethanol) at a concentration of 0.12 mg/ml to be injected i.p. at 0.01 ml/g body weight for a final dosage of 1.2 mg/kg.

    Techniques: Conditioned Place Preference, SPR Assay, Mouse Assay

    Cocaine- and stress-primed reinstatement recruit the PrL→NAcC projection, a) C57BL/6J mice were injected with a Cre-dependent AAV expressing GCaMP6s into unilateral PrL and a retrograde AAV expressing Cre recombinase was injected into ipsilateral NAcC. An optic fiber was implanted above the PrL, which could be attached to a patch cord to record Ca 2+ signals, b) Representative image of GCaMP6s expressing in the PrL. Optic fiber location is outlined in white. MO, medial orbitofrontal cortex; Cg, cingulate cortex, c) Experimental timeline for fiber photometry recording during cocaine CPP. Ca 2+ imaging was conducted during the baseline test, acquisition test, extinction test, and CPR/SPR. Mice were treated with vehicle or isradipine to block LTCCs prior to CPR/SPR recording, d) Representative fiber photometry trace of a vehicle-treated mouse during CPR showing Ca 2+ transients prior to cocaine-paired entries (red) but not saline-paired entries (blue). Grey, middle CPP chamber, e) The average amplitude (% ΔF/F) of PrL→NAcC fiber photometry signal 5 seconds prior to entry into the cocaine-paired chamber was significantly higher as compared to entries into the saline-paired chamber in vehicle-treated mice (** p

    Journal: Molecular psychiatry

    Article Title: Cocaine- and stress-primed reinstatement of drug-associated memories elicit differential behavioral and frontostriatal circuit activity patterns via recruitment of L-type Ca2+ channels

    doi: 10.1038/s41380-019-0513-2

    Figure Lengend Snippet: Cocaine- and stress-primed reinstatement recruit the PrL→NAcC projection, a) C57BL/6J mice were injected with a Cre-dependent AAV expressing GCaMP6s into unilateral PrL and a retrograde AAV expressing Cre recombinase was injected into ipsilateral NAcC. An optic fiber was implanted above the PrL, which could be attached to a patch cord to record Ca 2+ signals, b) Representative image of GCaMP6s expressing in the PrL. Optic fiber location is outlined in white. MO, medial orbitofrontal cortex; Cg, cingulate cortex, c) Experimental timeline for fiber photometry recording during cocaine CPP. Ca 2+ imaging was conducted during the baseline test, acquisition test, extinction test, and CPR/SPR. Mice were treated with vehicle or isradipine to block LTCCs prior to CPR/SPR recording, d) Representative fiber photometry trace of a vehicle-treated mouse during CPR showing Ca 2+ transients prior to cocaine-paired entries (red) but not saline-paired entries (blue). Grey, middle CPP chamber, e) The average amplitude (% ΔF/F) of PrL→NAcC fiber photometry signal 5 seconds prior to entry into the cocaine-paired chamber was significantly higher as compared to entries into the saline-paired chamber in vehicle-treated mice (** p

    Article Snippet: Isradipine (Alomone Labs) was dissolved in saline (16% ethanol) at a concentration of 0.12 mg/ml to be injected i.p. at 0.01 ml/g body weight for a final dosage of 1.2 mg/kg.

    Techniques: Mouse Assay, Injection, Expressing, Imaging, SPR Assay, Blocking Assay

    Activation of CaMKII is independent of VGCC-mediated Ca 2+ influx. Pre-incubation with either the L-type channel blockers isradipine or SR 33805 ( n = 6) at 10 μM failed to block CaMKII activation. Additionally, the Na + /Ca 2+ -exchanger inhibitor KB-R7943 at 10 μM ( n = 6) also did not affect activation of CaMKII by Ca 2+ O -stimulation. Basal phosphorylation at 286/287 Thr in 0 Ca 2+ was 12 ± 1% of stimulation by 1.8 Ca 2+ O . Neither compound significantly affected Ca 2+ -stimulation ( n = 6) suggesting that changes in [Ca 2+ ] O act at a site independent of VGCC.

    Journal: Cell calcium

    Article Title: CaMKII inactivation by extracellular Ca2+ depletion in dorsal root ganglion neurons

    doi: 10.1016/j.ceca.2006.01.005

    Figure Lengend Snippet: Activation of CaMKII is independent of VGCC-mediated Ca 2+ influx. Pre-incubation with either the L-type channel blockers isradipine or SR 33805 ( n = 6) at 10 μM failed to block CaMKII activation. Additionally, the Na + /Ca 2+ -exchanger inhibitor KB-R7943 at 10 μM ( n = 6) also did not affect activation of CaMKII by Ca 2+ O -stimulation. Basal phosphorylation at 286/287 Thr in 0 Ca 2+ was 12 ± 1% of stimulation by 1.8 Ca 2+ O . Neither compound significantly affected Ca 2+ -stimulation ( n = 6) suggesting that changes in [Ca 2+ ] O act at a site independent of VGCC.

    Article Snippet: The following drugs were used: isradipine (Alomone Labs, Jerusalem, Israel), flunarizine, ionomycin, ω-agatoxin-IVA, and ω-conotoxin-GVIA (EMD Biosciences Inc., San Diego, CA), Fluo-4/AM and Indo-1/AM (Molecular Probes, Eugene OR), caffeine, EGTA, gadolinium chloride, lanthanum chloride, nickel chloride, and nifedipine (Sigma, St. Louis, MO), KB-R7943, MRS 1845, Ruthenium Red (RR), SK & F 96365, and SR 33805 (Tocris Cookson, Ellisville, MO).

    Techniques: Activation Assay, Incubation, Blocking Assay, Activated Clotting Time Assay

    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).

    Techniques:

    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).

    Techniques: