nifedipine  (Abcam)

 
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    Name:
    Nifedipine
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    ab120135
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    Structured Review

    Abcam nifedipine
    Effect of extracellular Ca 2+ removal, <t>nifedipine,</t> CPA, and ryanodine on PMA-induced airway SMC twitching. Line scans from airway wall regions obtained from phase-contrast images (similar to that presented in Fig. 1 ) showing airway SMC twitching induced by 10 µM PMA (added 30 min before the recordings started) and their sensitivity to: (A) Ca 2+ -free sHBSS, (B) 10 µM nifedipine, (C) 10 µM CPA, or (D) 25 µM ryanodine. PMA-induced SMC twitching was inhibited by removal of extracellular Ca 2+ , nifedipine, CPA, and ryanodine. Each line scan is representative of three experiments in lung slices from two mice.

    https://www.bioz.com/result/nifedipine/product/Abcam
    Average 94 stars, based on 3 article reviews
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    nifedipine - by Bioz Stars, 2021-01
    94/100 stars

    Images

    1) Product Images from "Ca2+ oscillations, Ca2+ sensitization, and contraction activated by protein kinase C in small airway smooth muscle"

    Article Title: Ca2+ oscillations, Ca2+ sensitization, and contraction activated by protein kinase C in small airway smooth muscle

    Journal: The Journal of General Physiology

    doi: 10.1085/jgp.201210876

    Effect of extracellular Ca 2+ removal, nifedipine, CPA, and ryanodine on PMA-induced airway SMC twitching. Line scans from airway wall regions obtained from phase-contrast images (similar to that presented in Fig. 1 ) showing airway SMC twitching induced by 10 µM PMA (added 30 min before the recordings started) and their sensitivity to: (A) Ca 2+ -free sHBSS, (B) 10 µM nifedipine, (C) 10 µM CPA, or (D) 25 µM ryanodine. PMA-induced SMC twitching was inhibited by removal of extracellular Ca 2+ , nifedipine, CPA, and ryanodine. Each line scan is representative of three experiments in lung slices from two mice.
    Figure Legend Snippet: Effect of extracellular Ca 2+ removal, nifedipine, CPA, and ryanodine on PMA-induced airway SMC twitching. Line scans from airway wall regions obtained from phase-contrast images (similar to that presented in Fig. 1 ) showing airway SMC twitching induced by 10 µM PMA (added 30 min before the recordings started) and their sensitivity to: (A) Ca 2+ -free sHBSS, (B) 10 µM nifedipine, (C) 10 µM CPA, or (D) 25 µM ryanodine. PMA-induced SMC twitching was inhibited by removal of extracellular Ca 2+ , nifedipine, CPA, and ryanodine. Each line scan is representative of three experiments in lung slices from two mice.

    Techniques Used: Mouse Assay

    Effect of extracellular Ca 2+ removal, nifedipine, CPA, and ryanodine on PMA-induced Ca 2+ oscillations. Ca 2+ oscillations in single airway SMCs induced by 10 µM PMA (added 30 min before the recording started) and its inhibition by: (A) superfusion with Ca 2+ -free sHBSS, (B) 10 µM nifedipine, (C) 10 µM CPA, or (D) 25 µM ryanodine. Each trace is representative of four experiments in lung slices from three mice.
    Figure Legend Snippet: Effect of extracellular Ca 2+ removal, nifedipine, CPA, and ryanodine on PMA-induced Ca 2+ oscillations. Ca 2+ oscillations in single airway SMCs induced by 10 µM PMA (added 30 min before the recording started) and its inhibition by: (A) superfusion with Ca 2+ -free sHBSS, (B) 10 µM nifedipine, (C) 10 µM CPA, or (D) 25 µM ryanodine. Each trace is representative of four experiments in lung slices from three mice.

    Techniques Used: Inhibition, Mouse Assay

    2) Product Images from "Allopregnanolone Modulates GABAAR-Dependent CaMKIIδ3 and BDNF to Protect SH-SY5Y Cells Against 6-OHDA-Induced Damage"

    Article Title: Allopregnanolone Modulates GABAAR-Dependent CaMKIIδ3 and BDNF to Protect SH-SY5Y Cells Against 6-OHDA-Induced Damage

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00569

    A schematic diagram of timeline in the treatment of SH-SY5Y cells. It showed the time points of EGTA or Nifedipine, Bic, APα, BrdU, 6-OHDA administrations. SH-SY5Y cells sampling was used for the morphological and molecular biological studies. APα, allopregnanolone; 6-OHDA, 6-hydroxydopamine.
    Figure Legend Snippet: A schematic diagram of timeline in the treatment of SH-SY5Y cells. It showed the time points of EGTA or Nifedipine, Bic, APα, BrdU, 6-OHDA administrations. SH-SY5Y cells sampling was used for the morphological and molecular biological studies. APα, allopregnanolone; 6-OHDA, 6-hydroxydopamine.

    Techniques Used: Sampling

    Action of intracellular Ca 2+ and VGLCC in the effect of APα on the expression levels of CaMKIIδ3, CaM, and BDNF in 6-OHDA-treated SH-SY5Y cells. (A) Measurement of cytosolic Ca 2+ concentration levels in various groups of SH-SY5Y cells. (B,E) Representative Western blot bands for CaMKIIδ3 (52 kD), CaM (17 kD) and BDNF (15 kD) expressions were shown in the cytosolic or nuclear fraction of SH-SY5Y cells. GAPDH (36 kD) and Histone H3 (17 kD) bands showed as loading controls. Lane 1–7: the control; EGTA (Nifedipine)+control; DMSO+6-OHDA; EGTA (Nifedipine)+6-OHDA; the most optimal concentration of APα+6-OHDA; Bic+the most optimal concentration of APα+6-OHDA and EGTA (Nifedipine)+Bic+the most optimal concentration of APα+6-OHDA. C: cytosolic fraction; N: nuclear fraction. (C,D,F–I) Quantification of the relative protein levels was shown for CaMKIIδ3 (C,F,G) , CaM (D,H) and BDNF (I) in the cytosolic or nuclear fraction of SH-SY5Y cells. ** p
    Figure Legend Snippet: Action of intracellular Ca 2+ and VGLCC in the effect of APα on the expression levels of CaMKIIδ3, CaM, and BDNF in 6-OHDA-treated SH-SY5Y cells. (A) Measurement of cytosolic Ca 2+ concentration levels in various groups of SH-SY5Y cells. (B,E) Representative Western blot bands for CaMKIIδ3 (52 kD), CaM (17 kD) and BDNF (15 kD) expressions were shown in the cytosolic or nuclear fraction of SH-SY5Y cells. GAPDH (36 kD) and Histone H3 (17 kD) bands showed as loading controls. Lane 1–7: the control; EGTA (Nifedipine)+control; DMSO+6-OHDA; EGTA (Nifedipine)+6-OHDA; the most optimal concentration of APα+6-OHDA; Bic+the most optimal concentration of APα+6-OHDA and EGTA (Nifedipine)+Bic+the most optimal concentration of APα+6-OHDA. C: cytosolic fraction; N: nuclear fraction. (C,D,F–I) Quantification of the relative protein levels was shown for CaMKIIδ3 (C,F,G) , CaM (D,H) and BDNF (I) in the cytosolic or nuclear fraction of SH-SY5Y cells. ** p

    Techniques Used: Expressing, Chick Chorioallantoic Membrane Assay, Concentration Assay, Western Blot

    3) Product Images from "Adenosine A1 Receptor-Mediated Attenuation of Reciprocal Dendro-Dendritic Inhibition in the Mouse Olfactory Bulb"

    Article Title: Adenosine A1 Receptor-Mediated Attenuation of Reciprocal Dendro-Dendritic Inhibition in the Mouse Olfactory Bulb

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2017.00435

    Adenosine inhibits N-type and P/Q-type calcium currents. (A) Effect of the L-type calcium channel blocker nifedipine (Nif, 10 μM) on calcium currents. (B) IV relationship of nifedipine-sensitive calcium currents (green graph). (C) Effect of the N-type calcium channel blocker conotoxin GVIA (CTX, 100 nM) on calcium currents. (D) IV relationship of CTX-sensitive calcium currents (yellow graph). (E) P/Q-type calcium currents were isolated by blocking N-type and L-type calcium currents with CTX + Nif. (F) IV relationship of isolated P/Q-type calcium currents (red graph). (G) Adenosine strongly reduces calcium currents in the presence of Nif. (H) In the presence of CTX and (I) CTX plus Nif, adenosine only weakly reduces calcium currents. (J) Effect of adenosine on calcium currents in the absence of calcium channel blockers (Ctrl) and in the presence of Nif, CTX and CTX plus Nif. Incubation with CTX as well as CTX plus Nif significantly reduced the adenosine-mediated attenuation on calcium currents, while Nif alone had no effect on the adenosine-mediated attenuation. n.s., not significant. ∗∗∗ p
    Figure Legend Snippet: Adenosine inhibits N-type and P/Q-type calcium currents. (A) Effect of the L-type calcium channel blocker nifedipine (Nif, 10 μM) on calcium currents. (B) IV relationship of nifedipine-sensitive calcium currents (green graph). (C) Effect of the N-type calcium channel blocker conotoxin GVIA (CTX, 100 nM) on calcium currents. (D) IV relationship of CTX-sensitive calcium currents (yellow graph). (E) P/Q-type calcium currents were isolated by blocking N-type and L-type calcium currents with CTX + Nif. (F) IV relationship of isolated P/Q-type calcium currents (red graph). (G) Adenosine strongly reduces calcium currents in the presence of Nif. (H) In the presence of CTX and (I) CTX plus Nif, adenosine only weakly reduces calcium currents. (J) Effect of adenosine on calcium currents in the absence of calcium channel blockers (Ctrl) and in the presence of Nif, CTX and CTX plus Nif. Incubation with CTX as well as CTX plus Nif significantly reduced the adenosine-mediated attenuation on calcium currents, while Nif alone had no effect on the adenosine-mediated attenuation. n.s., not significant. ∗∗∗ p

    Techniques Used: Isolation, Blocking Assay, Incubation

    4) Product Images from "Regulation of Ca2+ channels by SNAP-25 via recruitment of syntaxin-1 from plasma membrane clusters"

    Article Title: Regulation of Ca2+ channels by SNAP-25 via recruitment of syntaxin-1 from plasma membrane clusters

    Journal: Molecular Biology of the Cell

    doi: 10.1091/mbc.E16-03-0184

    SNAP-25 WT and KO cells show similar relative expression of calcium channel subtypes. (A) Representative traces from a single-KO adrenal chromaffin cell during sequential additive application of calcium channel blockers. Bottom to top: nifedipine (L type, 3 μM), ω-conotoxin (N type, 1 μM), agatoxin (P/Q type, 1 μM), SNX482 (R type, 300 nM), Ni 2+ (T type, 40 μM). (B) Sequential application of blockers did not reveal large differences in the fraction of calcium channel subtypes between SNAP-25 WT and KO cells. N = 3, n = 10–13.
    Figure Legend Snippet: SNAP-25 WT and KO cells show similar relative expression of calcium channel subtypes. (A) Representative traces from a single-KO adrenal chromaffin cell during sequential additive application of calcium channel blockers. Bottom to top: nifedipine (L type, 3 μM), ω-conotoxin (N type, 1 μM), agatoxin (P/Q type, 1 μM), SNX482 (R type, 300 nM), Ni 2+ (T type, 40 μM). (B) Sequential application of blockers did not reveal large differences in the fraction of calcium channel subtypes between SNAP-25 WT and KO cells. N = 3, n = 10–13.

    Techniques Used: Expressing

    5) Product Images from "Direct conversion of mouse fibroblasts to GABAergic neurons with combined medium without the introduction of transcription factors or miRNAs"

    Article Title: Direct conversion of mouse fibroblasts to GABAergic neurons with combined medium without the introduction of transcription factors or miRNAs

    Journal: Cell Cycle

    doi: 10.1080/15384101.2015.1060382

    Characterization of the neuron-like cells derived from MEFs. ( A ) Immunostaining of the neuron-like cells at 1–3 weeks post-induction with synapsin and Tuj-1 antibodies. scale bar, 50 μm. ( B ) Functional characterization of the L-type Calcium channel. The panels show typical calcium imagines response observed in neuron-like cells at 2–3 weeks post-induction. 1F/F0 represents the ratio of fluorescence intensity of cells for 0s and an indicated time. Bay-K (10 μM) in the presence or absence of nifedipine (5 μM) was added at the marked time point. ( C ) The represent figures of calcium imaging of the induced neurons or MEFs with or without nifedipine following in the treatment with BayK. The total number of cells analyzed in each experiment was 40–50 cells, represent results were present. scale bar, 20 μm.
    Figure Legend Snippet: Characterization of the neuron-like cells derived from MEFs. ( A ) Immunostaining of the neuron-like cells at 1–3 weeks post-induction with synapsin and Tuj-1 antibodies. scale bar, 50 μm. ( B ) Functional characterization of the L-type Calcium channel. The panels show typical calcium imagines response observed in neuron-like cells at 2–3 weeks post-induction. 1F/F0 represents the ratio of fluorescence intensity of cells for 0s and an indicated time. Bay-K (10 μM) in the presence or absence of nifedipine (5 μM) was added at the marked time point. ( C ) The represent figures of calcium imaging of the induced neurons or MEFs with or without nifedipine following in the treatment with BayK. The total number of cells analyzed in each experiment was 40–50 cells, represent results were present. scale bar, 20 μm.

    Techniques Used: Derivative Assay, Immunostaining, Functional Assay, Fluorescence, Imaging

    6) Product Images from "AT1-receptor response to non-saturating Ang-II concentrations is amplified by calcium channel blockers"

    Article Title: AT1-receptor response to non-saturating Ang-II concentrations is amplified by calcium channel blockers

    Journal: BMC Cardiovascular Disorders

    doi: 10.1186/s12872-017-0562-x

    Ca V 1.2 regulates AT 1 R signaling in rat aortic smooth muscle cells and ventricular cardiomyocytes. ( a ) Representative [Ca 2+ ] i traces of Oregon Green Bapta 1 loaded rat aortic smooth muscle cells treated with two minutes of 1 nM AngII at times indicated by arrows. Smooth muscle cells were co-treated from 15 min after first AngII exposure throughout the experiment with vehicle (upper), 0.2 μM nifedipine (middle) and 0.9 μM verapamil (lower). (b ) Relative change between first and second response to AngII stimulation for vehicle (open bar), 0.2 μM nifedipine (dark grey bar) and 0.9 μM verapamil (light grey bar). Peaks are calculated as signal above baseline. n = 6 - 7 individual experiments, *: p ≤ 0.05 compared to vehicle. ( c ) Representative [Ca 2+ ] i traces of Oregon Green Bapta 1 loaded rat ventricular myocytes treated with two minutes of 1 nM AngII at times indicated by arrows. Myocytes were co-treated from 15 min after first AngII exposure throughout the experiment with vehicle (upper), 0.2 μM nifedipine (middle) and 0.9 μM verapamil (lower). ( d ) Relative change between first and second response to AngII stimulation for vehicle (open bar), 0.2 μM nifedipine (dark grey bar) and 0.9 μM verapamil (light grey bar). Peaks are calculated as signal above baseline. n = 6 - 10 individual experiments, *: p ≤ 0.05 compared to vehicle, #: p ≤ 0.05 compared to nifedipine
    Figure Legend Snippet: Ca V 1.2 regulates AT 1 R signaling in rat aortic smooth muscle cells and ventricular cardiomyocytes. ( a ) Representative [Ca 2+ ] i traces of Oregon Green Bapta 1 loaded rat aortic smooth muscle cells treated with two minutes of 1 nM AngII at times indicated by arrows. Smooth muscle cells were co-treated from 15 min after first AngII exposure throughout the experiment with vehicle (upper), 0.2 μM nifedipine (middle) and 0.9 μM verapamil (lower). (b ) Relative change between first and second response to AngII stimulation for vehicle (open bar), 0.2 μM nifedipine (dark grey bar) and 0.9 μM verapamil (light grey bar). Peaks are calculated as signal above baseline. n = 6 - 7 individual experiments, *: p ≤ 0.05 compared to vehicle. ( c ) Representative [Ca 2+ ] i traces of Oregon Green Bapta 1 loaded rat ventricular myocytes treated with two minutes of 1 nM AngII at times indicated by arrows. Myocytes were co-treated from 15 min after first AngII exposure throughout the experiment with vehicle (upper), 0.2 μM nifedipine (middle) and 0.9 μM verapamil (lower). ( d ) Relative change between first and second response to AngII stimulation for vehicle (open bar), 0.2 μM nifedipine (dark grey bar) and 0.9 μM verapamil (light grey bar). Peaks are calculated as signal above baseline. n = 6 - 10 individual experiments, *: p ≤ 0.05 compared to vehicle, #: p ≤ 0.05 compared to nifedipine

    Techniques Used:

    Ca V 1.2 inhibition up-regulates physiological AT 1 R signaling. a Gel image shows a typical RT-PCR of HEK mRNA using primers for Ca V 1.1(left), Ca V 1.2 (center) and Ca V 1.4 (right). As a negative control, each reaction was done omitting the cDNA. Expected band size is, for Ca V 1.1564 bp, Ca V 1.2621 bp and Ca V 1.4501 bp. Gene Ruler 1 kb DNA ladder was used as a size marker. b Quantification of peak [Ca 2+ ] i response to 1 nM AngII exposure alone or in presence of 1 μM or 100 μM nifedipine in Fura Red loaded HEK cells. n = 4 - 6 experiments. **: p ≤ 0.01 compared to 1 nM AngII exposure alone. c Quantification of peak [Ca 2+ ] i response to 1 nM AngII exposure alone or in presence of 2 μM verapamil in Fura Red loaded HEK cells. n = 10 experiments. *: p ≤ 0.05 compared to 1 nM AngII exposure alone. d Representative [Ca 2+ ] i traces from Fura Red loaded HEK cells treated with repeated 1 nM AngII for two minutes at times indicated by the arrows in the presence of 100 μM nifedipine. e Quantification of peak [Ca 2+ ] i response to repeated 1 nM AngII treatment as shown in D. Peaks are calculated as peak signal above baseline. Open bars show 1 nM AngII alone and grey bars show 1 nM AngII in presence of 100 μM nifedipine. n = 4 - 6 experiments. **: p ≤ 0.01 compared to vehicle
    Figure Legend Snippet: Ca V 1.2 inhibition up-regulates physiological AT 1 R signaling. a Gel image shows a typical RT-PCR of HEK mRNA using primers for Ca V 1.1(left), Ca V 1.2 (center) and Ca V 1.4 (right). As a negative control, each reaction was done omitting the cDNA. Expected band size is, for Ca V 1.1564 bp, Ca V 1.2621 bp and Ca V 1.4501 bp. Gene Ruler 1 kb DNA ladder was used as a size marker. b Quantification of peak [Ca 2+ ] i response to 1 nM AngII exposure alone or in presence of 1 μM or 100 μM nifedipine in Fura Red loaded HEK cells. n = 4 - 6 experiments. **: p ≤ 0.01 compared to 1 nM AngII exposure alone. c Quantification of peak [Ca 2+ ] i response to 1 nM AngII exposure alone or in presence of 2 μM verapamil in Fura Red loaded HEK cells. n = 10 experiments. *: p ≤ 0.05 compared to 1 nM AngII exposure alone. d Representative [Ca 2+ ] i traces from Fura Red loaded HEK cells treated with repeated 1 nM AngII for two minutes at times indicated by the arrows in the presence of 100 μM nifedipine. e Quantification of peak [Ca 2+ ] i response to repeated 1 nM AngII treatment as shown in D. Peaks are calculated as peak signal above baseline. Open bars show 1 nM AngII alone and grey bars show 1 nM AngII in presence of 100 μM nifedipine. n = 4 - 6 experiments. **: p ≤ 0.01 compared to vehicle

    Techniques Used: Inhibition, Reverse Transcription Polymerase Chain Reaction, Negative Control, Marker

    G-protein activation is not affected by nifedipine. a The cartoon show the principle of the FRET based assay for detection of G-protein activity. Activity is detected as a decreased FRET signal (increased FRET ratio) when Gαq dissociate from the βγ complex. b Representative FRET ratio traces of HEK cells expressing pGβ-2A-YFP-Gγ2 in response to 2 min exposure to (at arrow) 1 nM AngII in absence (left) or presence of 100 μM nifedipine (right). c Quantification of peak FRET ratio, in response to 1 nM Ang II alone (open bar) and in presence of nifedipine (grey bar) in HEK cells. n = 9 - 11 experiments
    Figure Legend Snippet: G-protein activation is not affected by nifedipine. a The cartoon show the principle of the FRET based assay for detection of G-protein activity. Activity is detected as a decreased FRET signal (increased FRET ratio) when Gαq dissociate from the βγ complex. b Representative FRET ratio traces of HEK cells expressing pGβ-2A-YFP-Gγ2 in response to 2 min exposure to (at arrow) 1 nM AngII in absence (left) or presence of 100 μM nifedipine (right). c Quantification of peak FRET ratio, in response to 1 nM Ang II alone (open bar) and in presence of nifedipine (grey bar) in HEK cells. n = 9 - 11 experiments

    Techniques Used: Activation Assay, Activity Assay, Expressing

    7) Product Images from "Adenosine A1 Receptor-Mediated Attenuation of Reciprocal Dendro-Dendritic Inhibition in the Mouse Olfactory Bulb"

    Article Title: Adenosine A1 Receptor-Mediated Attenuation of Reciprocal Dendro-Dendritic Inhibition in the Mouse Olfactory Bulb

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2017.00435

    Adenosine inhibits N-type and P/Q-type calcium currents. (A) Effect of the L-type calcium channel blocker nifedipine (Nif, 10 μM) on calcium currents. (B) IV relationship of nifedipine-sensitive calcium currents (green graph). (C) Effect of the N-type calcium channel blocker conotoxin GVIA (CTX, 100 nM) on calcium currents. (D) IV relationship of CTX-sensitive calcium currents (yellow graph). (E) P/Q-type calcium currents were isolated by blocking N-type and L-type calcium currents with CTX + Nif. (F) IV relationship of isolated P/Q-type calcium currents (red graph). (G) Adenosine strongly reduces calcium currents in the presence of Nif. (H) In the presence of CTX and (I) CTX plus Nif, adenosine only weakly reduces calcium currents. (J) Effect of adenosine on calcium currents in the absence of calcium channel blockers (Ctrl) and in the presence of Nif, CTX and CTX plus Nif. Incubation with CTX as well as CTX plus Nif significantly reduced the adenosine-mediated attenuation on calcium currents, while Nif alone had no effect on the adenosine-mediated attenuation. n.s., not significant. ∗∗∗ p
    Figure Legend Snippet: Adenosine inhibits N-type and P/Q-type calcium currents. (A) Effect of the L-type calcium channel blocker nifedipine (Nif, 10 μM) on calcium currents. (B) IV relationship of nifedipine-sensitive calcium currents (green graph). (C) Effect of the N-type calcium channel blocker conotoxin GVIA (CTX, 100 nM) on calcium currents. (D) IV relationship of CTX-sensitive calcium currents (yellow graph). (E) P/Q-type calcium currents were isolated by blocking N-type and L-type calcium currents with CTX + Nif. (F) IV relationship of isolated P/Q-type calcium currents (red graph). (G) Adenosine strongly reduces calcium currents in the presence of Nif. (H) In the presence of CTX and (I) CTX plus Nif, adenosine only weakly reduces calcium currents. (J) Effect of adenosine on calcium currents in the absence of calcium channel blockers (Ctrl) and in the presence of Nif, CTX and CTX plus Nif. Incubation with CTX as well as CTX plus Nif significantly reduced the adenosine-mediated attenuation on calcium currents, while Nif alone had no effect on the adenosine-mediated attenuation. n.s., not significant. ∗∗∗ p

    Techniques Used: Isolation, Blocking Assay, Incubation

    Related Articles

    Modification:

    Article Title: Allopregnanolone Modulates GABAAR-Dependent CaMKIIδ3 and BDNF to Protect SH-SY5Y Cells Against 6-OHDA-Induced Damage
    Article Snippet: .. Chemicals and Reagents In this study, all reagents, materials, and chemicals were analytical grade and highest purity, including human neuroblastoma SH-SY5Y cell lines (SCSP-5014, Chinese Academy of Sciences, China); Dulbecco’s modified Eagle’s medium (DMEM, 11965092), Neurobasal (21103049), B27 (17504044), fetal bovine serum (FBS), glutamax (35050061), trypsin-EDTA (25300062) and sodium pyruvate (11360070; Gibco Invitrogen, MA, USA); APα (3653) and Bic (485494; Tocris, USA); Nifedipine (ab120135, Abcam, Burlingame, CA, USA); RA (R2500) and 6-OHDA (H4381; Sigma-Aldrich, St. Louis, MI, USA); penicillin and streptomycin (Solarbio, Beijing, China); bovine serum albumin (BSA) and BrdU (Bio-Sharp, China); DMSO (ST038), EGTA (ST068), phenylmethanesulfonyl fluoride (PMSF, ST506), TritonX-100, cytosolic and nuclear extraction kit (P0028; Beyotime, China). ..

    Activation Assay:

    Article Title: AT1-receptor response to non-saturating Ang-II concentrations is amplified by calcium channel blockers
    Article Snippet: .. Nifedipine effects on bradykinin activation of bradykinin B2 receptors were evaluated through comparing signaling strength with or without pretreatment of 100 μM nifedipine on 100 nM bradykinin (Abcam) treatment. ..

    other:

    Article Title: Adenosine A1 Receptor-Mediated Attenuation of Reciprocal Dendro-Dendritic Inhibition in the Mouse Olfactory Bulb
    Article Snippet: Drugs Adenosine was purchased from Sigma–Aldrich (Munich, Germany); 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo-[f]-quinoxaline-7-sulfonamide (NBQX), D -(-)-2-amino-5-phosphonopentanic acid (D-APV), gabazine hydrobromide (GBZ), tetrodotoxin citrate (TTX), nifedipine (Nif) and cyclothiazide (CTZ) from Abcam (Cambridge, United Kingdom); Conotoxin GVIA (CTX) and Naspm trihydrochloride from Alomone labs (Jerusalem, Israel).

    Article Title: Adenosine A1 Receptor-Mediated Attenuation of Reciprocal Dendro-Dendritic Inhibition in the Mouse Olfactory Bulb
    Article Snippet: Adenosine was purchased from Sigma–Aldrich (Munich, Germany); 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo-[f]-quinoxaline-7-sulfonamide (NBQX), D -(-)-2-amino-5-phosphonopentanic acid (D-APV), gabazine hydrobromide (GBZ), tetrodotoxin citrate (TTX), nifedipine (Nif) and cyclothiazide (CTZ) from Abcam (Cambridge, United Kingdom); Conotoxin GVIA (CTX) and Naspm trihydrochloride from Alomone labs (Jerusalem, Israel).

    Article Title: Ca2+ oscillations, Ca2+ sensitization, and contraction activated by protein kinase C in small airway smooth muscle
    Article Snippet: GF-109203X and cyclopiazonic acid (CPA) were from Enzo Life Sciences, whereas Y-27632, nifedipine, and ryanodine were from Abcam.

    Imaging:

    Article Title: Direct conversion of mouse fibroblasts to GABAergic neurons with combined medium without the introduction of transcription factors or miRNAs
    Article Snippet: .. To better observe Ca2+ influx, 10 μm BayK (BayK8644, Stemgent), a specific L-type calcium channel activator was applied for 10 s on the cells and then repeatedly wash with EM for 10 min. Next, 5 μm nifedipine (Abcam), a specifi L-type calcium channel blocker, was used to block Ca2+ influx before the addition of Bay-K. For calcium imaging in Ca2+ -free extracellular medium, cells were treated for 1 min with Ca2+ -free medium containing 1 mM EGTA without CaCl2 before the Calcium imaging experiments. ..

    Blocking Assay:

    Article Title: Direct conversion of mouse fibroblasts to GABAergic neurons with combined medium without the introduction of transcription factors or miRNAs
    Article Snippet: .. To better observe Ca2+ influx, 10 μm BayK (BayK8644, Stemgent), a specific L-type calcium channel activator was applied for 10 s on the cells and then repeatedly wash with EM for 10 min. Next, 5 μm nifedipine (Abcam), a specifi L-type calcium channel blocker, was used to block Ca2+ influx before the addition of Bay-K. For calcium imaging in Ca2+ -free extracellular medium, cells were treated for 1 min with Ca2+ -free medium containing 1 mM EGTA without CaCl2 before the Calcium imaging experiments. ..

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    Abcam nifedipine
    Effect of extracellular Ca 2+ removal, <t>nifedipine,</t> CPA, and ryanodine on PMA-induced airway SMC twitching. Line scans from airway wall regions obtained from phase-contrast images (similar to that presented in Fig. 1 ) showing airway SMC twitching induced by 10 µM PMA (added 30 min before the recordings started) and their sensitivity to: (A) Ca 2+ -free sHBSS, (B) 10 µM nifedipine, (C) 10 µM CPA, or (D) 25 µM ryanodine. PMA-induced SMC twitching was inhibited by removal of extracellular Ca 2+ , nifedipine, CPA, and ryanodine. Each line scan is representative of three experiments in lung slices from two mice.
    Nifedipine, supplied by Abcam, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nifedipine/product/Abcam
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    Effect of extracellular Ca 2+ removal, nifedipine, CPA, and ryanodine on PMA-induced airway SMC twitching. Line scans from airway wall regions obtained from phase-contrast images (similar to that presented in Fig. 1 ) showing airway SMC twitching induced by 10 µM PMA (added 30 min before the recordings started) and their sensitivity to: (A) Ca 2+ -free sHBSS, (B) 10 µM nifedipine, (C) 10 µM CPA, or (D) 25 µM ryanodine. PMA-induced SMC twitching was inhibited by removal of extracellular Ca 2+ , nifedipine, CPA, and ryanodine. Each line scan is representative of three experiments in lung slices from two mice.

    Journal: The Journal of General Physiology

    Article Title: Ca2+ oscillations, Ca2+ sensitization, and contraction activated by protein kinase C in small airway smooth muscle

    doi: 10.1085/jgp.201210876

    Figure Lengend Snippet: Effect of extracellular Ca 2+ removal, nifedipine, CPA, and ryanodine on PMA-induced airway SMC twitching. Line scans from airway wall regions obtained from phase-contrast images (similar to that presented in Fig. 1 ) showing airway SMC twitching induced by 10 µM PMA (added 30 min before the recordings started) and their sensitivity to: (A) Ca 2+ -free sHBSS, (B) 10 µM nifedipine, (C) 10 µM CPA, or (D) 25 µM ryanodine. PMA-induced SMC twitching was inhibited by removal of extracellular Ca 2+ , nifedipine, CPA, and ryanodine. Each line scan is representative of three experiments in lung slices from two mice.

    Article Snippet: GF-109203X and cyclopiazonic acid (CPA) were from Enzo Life Sciences, whereas Y-27632, nifedipine, and ryanodine were from Abcam.

    Techniques: Mouse Assay

    Effect of extracellular Ca 2+ removal, nifedipine, CPA, and ryanodine on PMA-induced Ca 2+ oscillations. Ca 2+ oscillations in single airway SMCs induced by 10 µM PMA (added 30 min before the recording started) and its inhibition by: (A) superfusion with Ca 2+ -free sHBSS, (B) 10 µM nifedipine, (C) 10 µM CPA, or (D) 25 µM ryanodine. Each trace is representative of four experiments in lung slices from three mice.

    Journal: The Journal of General Physiology

    Article Title: Ca2+ oscillations, Ca2+ sensitization, and contraction activated by protein kinase C in small airway smooth muscle

    doi: 10.1085/jgp.201210876

    Figure Lengend Snippet: Effect of extracellular Ca 2+ removal, nifedipine, CPA, and ryanodine on PMA-induced Ca 2+ oscillations. Ca 2+ oscillations in single airway SMCs induced by 10 µM PMA (added 30 min before the recording started) and its inhibition by: (A) superfusion with Ca 2+ -free sHBSS, (B) 10 µM nifedipine, (C) 10 µM CPA, or (D) 25 µM ryanodine. Each trace is representative of four experiments in lung slices from three mice.

    Article Snippet: GF-109203X and cyclopiazonic acid (CPA) were from Enzo Life Sciences, whereas Y-27632, nifedipine, and ryanodine were from Abcam.

    Techniques: Inhibition, Mouse Assay

    Ca V 1.2 regulates AT 1 R signaling in rat aortic smooth muscle cells and ventricular cardiomyocytes. ( a ) Representative [Ca 2+ ] i traces of Oregon Green Bapta 1 loaded rat aortic smooth muscle cells treated with two minutes of 1 nM AngII at times indicated by arrows. Smooth muscle cells were co-treated from 15 min after first AngII exposure throughout the experiment with vehicle (upper), 0.2 μM nifedipine (middle) and 0.9 μM verapamil (lower). (b ) Relative change between first and second response to AngII stimulation for vehicle (open bar), 0.2 μM nifedipine (dark grey bar) and 0.9 μM verapamil (light grey bar). Peaks are calculated as signal above baseline. n = 6 - 7 individual experiments, *: p ≤ 0.05 compared to vehicle. ( c ) Representative [Ca 2+ ] i traces of Oregon Green Bapta 1 loaded rat ventricular myocytes treated with two minutes of 1 nM AngII at times indicated by arrows. Myocytes were co-treated from 15 min after first AngII exposure throughout the experiment with vehicle (upper), 0.2 μM nifedipine (middle) and 0.9 μM verapamil (lower). ( d ) Relative change between first and second response to AngII stimulation for vehicle (open bar), 0.2 μM nifedipine (dark grey bar) and 0.9 μM verapamil (light grey bar). Peaks are calculated as signal above baseline. n = 6 - 10 individual experiments, *: p ≤ 0.05 compared to vehicle, #: p ≤ 0.05 compared to nifedipine

    Journal: BMC Cardiovascular Disorders

    Article Title: AT1-receptor response to non-saturating Ang-II concentrations is amplified by calcium channel blockers

    doi: 10.1186/s12872-017-0562-x

    Figure Lengend Snippet: Ca V 1.2 regulates AT 1 R signaling in rat aortic smooth muscle cells and ventricular cardiomyocytes. ( a ) Representative [Ca 2+ ] i traces of Oregon Green Bapta 1 loaded rat aortic smooth muscle cells treated with two minutes of 1 nM AngII at times indicated by arrows. Smooth muscle cells were co-treated from 15 min after first AngII exposure throughout the experiment with vehicle (upper), 0.2 μM nifedipine (middle) and 0.9 μM verapamil (lower). (b ) Relative change between first and second response to AngII stimulation for vehicle (open bar), 0.2 μM nifedipine (dark grey bar) and 0.9 μM verapamil (light grey bar). Peaks are calculated as signal above baseline. n = 6 - 7 individual experiments, *: p ≤ 0.05 compared to vehicle. ( c ) Representative [Ca 2+ ] i traces of Oregon Green Bapta 1 loaded rat ventricular myocytes treated with two minutes of 1 nM AngII at times indicated by arrows. Myocytes were co-treated from 15 min after first AngII exposure throughout the experiment with vehicle (upper), 0.2 μM nifedipine (middle) and 0.9 μM verapamil (lower). ( d ) Relative change between first and second response to AngII stimulation for vehicle (open bar), 0.2 μM nifedipine (dark grey bar) and 0.9 μM verapamil (light grey bar). Peaks are calculated as signal above baseline. n = 6 - 10 individual experiments, *: p ≤ 0.05 compared to vehicle, #: p ≤ 0.05 compared to nifedipine

    Article Snippet: Nifedipine effects on bradykinin activation of bradykinin B2 receptors were evaluated through comparing signaling strength with or without pretreatment of 100 μM nifedipine on 100 nM bradykinin (Abcam) treatment.

    Techniques:

    Ca V 1.2 inhibition up-regulates physiological AT 1 R signaling. a Gel image shows a typical RT-PCR of HEK mRNA using primers for Ca V 1.1(left), Ca V 1.2 (center) and Ca V 1.4 (right). As a negative control, each reaction was done omitting the cDNA. Expected band size is, for Ca V 1.1564 bp, Ca V 1.2621 bp and Ca V 1.4501 bp. Gene Ruler 1 kb DNA ladder was used as a size marker. b Quantification of peak [Ca 2+ ] i response to 1 nM AngII exposure alone or in presence of 1 μM or 100 μM nifedipine in Fura Red loaded HEK cells. n = 4 - 6 experiments. **: p ≤ 0.01 compared to 1 nM AngII exposure alone. c Quantification of peak [Ca 2+ ] i response to 1 nM AngII exposure alone or in presence of 2 μM verapamil in Fura Red loaded HEK cells. n = 10 experiments. *: p ≤ 0.05 compared to 1 nM AngII exposure alone. d Representative [Ca 2+ ] i traces from Fura Red loaded HEK cells treated with repeated 1 nM AngII for two minutes at times indicated by the arrows in the presence of 100 μM nifedipine. e Quantification of peak [Ca 2+ ] i response to repeated 1 nM AngII treatment as shown in D. Peaks are calculated as peak signal above baseline. Open bars show 1 nM AngII alone and grey bars show 1 nM AngII in presence of 100 μM nifedipine. n = 4 - 6 experiments. **: p ≤ 0.01 compared to vehicle

    Journal: BMC Cardiovascular Disorders

    Article Title: AT1-receptor response to non-saturating Ang-II concentrations is amplified by calcium channel blockers

    doi: 10.1186/s12872-017-0562-x

    Figure Lengend Snippet: Ca V 1.2 inhibition up-regulates physiological AT 1 R signaling. a Gel image shows a typical RT-PCR of HEK mRNA using primers for Ca V 1.1(left), Ca V 1.2 (center) and Ca V 1.4 (right). As a negative control, each reaction was done omitting the cDNA. Expected band size is, for Ca V 1.1564 bp, Ca V 1.2621 bp and Ca V 1.4501 bp. Gene Ruler 1 kb DNA ladder was used as a size marker. b Quantification of peak [Ca 2+ ] i response to 1 nM AngII exposure alone or in presence of 1 μM or 100 μM nifedipine in Fura Red loaded HEK cells. n = 4 - 6 experiments. **: p ≤ 0.01 compared to 1 nM AngII exposure alone. c Quantification of peak [Ca 2+ ] i response to 1 nM AngII exposure alone or in presence of 2 μM verapamil in Fura Red loaded HEK cells. n = 10 experiments. *: p ≤ 0.05 compared to 1 nM AngII exposure alone. d Representative [Ca 2+ ] i traces from Fura Red loaded HEK cells treated with repeated 1 nM AngII for two minutes at times indicated by the arrows in the presence of 100 μM nifedipine. e Quantification of peak [Ca 2+ ] i response to repeated 1 nM AngII treatment as shown in D. Peaks are calculated as peak signal above baseline. Open bars show 1 nM AngII alone and grey bars show 1 nM AngII in presence of 100 μM nifedipine. n = 4 - 6 experiments. **: p ≤ 0.01 compared to vehicle

    Article Snippet: Nifedipine effects on bradykinin activation of bradykinin B2 receptors were evaluated through comparing signaling strength with or without pretreatment of 100 μM nifedipine on 100 nM bradykinin (Abcam) treatment.

    Techniques: Inhibition, Reverse Transcription Polymerase Chain Reaction, Negative Control, Marker

    G-protein activation is not affected by nifedipine. a The cartoon show the principle of the FRET based assay for detection of G-protein activity. Activity is detected as a decreased FRET signal (increased FRET ratio) when Gαq dissociate from the βγ complex. b Representative FRET ratio traces of HEK cells expressing pGβ-2A-YFP-Gγ2 in response to 2 min exposure to (at arrow) 1 nM AngII in absence (left) or presence of 100 μM nifedipine (right). c Quantification of peak FRET ratio, in response to 1 nM Ang II alone (open bar) and in presence of nifedipine (grey bar) in HEK cells. n = 9 - 11 experiments

    Journal: BMC Cardiovascular Disorders

    Article Title: AT1-receptor response to non-saturating Ang-II concentrations is amplified by calcium channel blockers

    doi: 10.1186/s12872-017-0562-x

    Figure Lengend Snippet: G-protein activation is not affected by nifedipine. a The cartoon show the principle of the FRET based assay for detection of G-protein activity. Activity is detected as a decreased FRET signal (increased FRET ratio) when Gαq dissociate from the βγ complex. b Representative FRET ratio traces of HEK cells expressing pGβ-2A-YFP-Gγ2 in response to 2 min exposure to (at arrow) 1 nM AngII in absence (left) or presence of 100 μM nifedipine (right). c Quantification of peak FRET ratio, in response to 1 nM Ang II alone (open bar) and in presence of nifedipine (grey bar) in HEK cells. n = 9 - 11 experiments

    Article Snippet: Nifedipine effects on bradykinin activation of bradykinin B2 receptors were evaluated through comparing signaling strength with or without pretreatment of 100 μM nifedipine on 100 nM bradykinin (Abcam) treatment.

    Techniques: Activation Assay, Activity Assay, Expressing

    A schematic diagram of timeline in the treatment of SH-SY5Y cells. It showed the time points of EGTA or Nifedipine, Bic, APα, BrdU, 6-OHDA administrations. SH-SY5Y cells sampling was used for the morphological and molecular biological studies. APα, allopregnanolone; 6-OHDA, 6-hydroxydopamine.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Allopregnanolone Modulates GABAAR-Dependent CaMKIIδ3 and BDNF to Protect SH-SY5Y Cells Against 6-OHDA-Induced Damage

    doi: 10.3389/fncel.2019.00569

    Figure Lengend Snippet: A schematic diagram of timeline in the treatment of SH-SY5Y cells. It showed the time points of EGTA or Nifedipine, Bic, APα, BrdU, 6-OHDA administrations. SH-SY5Y cells sampling was used for the morphological and molecular biological studies. APα, allopregnanolone; 6-OHDA, 6-hydroxydopamine.

    Article Snippet: Chemicals and Reagents In this study, all reagents, materials, and chemicals were analytical grade and highest purity, including human neuroblastoma SH-SY5Y cell lines (SCSP-5014, Chinese Academy of Sciences, China); Dulbecco’s modified Eagle’s medium (DMEM, 11965092), Neurobasal (21103049), B27 (17504044), fetal bovine serum (FBS), glutamax (35050061), trypsin-EDTA (25300062) and sodium pyruvate (11360070; Gibco Invitrogen, MA, USA); APα (3653) and Bic (485494; Tocris, USA); Nifedipine (ab120135, Abcam, Burlingame, CA, USA); RA (R2500) and 6-OHDA (H4381; Sigma-Aldrich, St. Louis, MI, USA); penicillin and streptomycin (Solarbio, Beijing, China); bovine serum albumin (BSA) and BrdU (Bio-Sharp, China); DMSO (ST038), EGTA (ST068), phenylmethanesulfonyl fluoride (PMSF, ST506), TritonX-100, cytosolic and nuclear extraction kit (P0028; Beyotime, China).

    Techniques: Sampling

    Action of intracellular Ca 2+ and VGLCC in the effect of APα on the expression levels of CaMKIIδ3, CaM, and BDNF in 6-OHDA-treated SH-SY5Y cells. (A) Measurement of cytosolic Ca 2+ concentration levels in various groups of SH-SY5Y cells. (B,E) Representative Western blot bands for CaMKIIδ3 (52 kD), CaM (17 kD) and BDNF (15 kD) expressions were shown in the cytosolic or nuclear fraction of SH-SY5Y cells. GAPDH (36 kD) and Histone H3 (17 kD) bands showed as loading controls. Lane 1–7: the control; EGTA (Nifedipine)+control; DMSO+6-OHDA; EGTA (Nifedipine)+6-OHDA; the most optimal concentration of APα+6-OHDA; Bic+the most optimal concentration of APα+6-OHDA and EGTA (Nifedipine)+Bic+the most optimal concentration of APα+6-OHDA. C: cytosolic fraction; N: nuclear fraction. (C,D,F–I) Quantification of the relative protein levels was shown for CaMKIIδ3 (C,F,G) , CaM (D,H) and BDNF (I) in the cytosolic or nuclear fraction of SH-SY5Y cells. ** p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Allopregnanolone Modulates GABAAR-Dependent CaMKIIδ3 and BDNF to Protect SH-SY5Y Cells Against 6-OHDA-Induced Damage

    doi: 10.3389/fncel.2019.00569

    Figure Lengend Snippet: Action of intracellular Ca 2+ and VGLCC in the effect of APα on the expression levels of CaMKIIδ3, CaM, and BDNF in 6-OHDA-treated SH-SY5Y cells. (A) Measurement of cytosolic Ca 2+ concentration levels in various groups of SH-SY5Y cells. (B,E) Representative Western blot bands for CaMKIIδ3 (52 kD), CaM (17 kD) and BDNF (15 kD) expressions were shown in the cytosolic or nuclear fraction of SH-SY5Y cells. GAPDH (36 kD) and Histone H3 (17 kD) bands showed as loading controls. Lane 1–7: the control; EGTA (Nifedipine)+control; DMSO+6-OHDA; EGTA (Nifedipine)+6-OHDA; the most optimal concentration of APα+6-OHDA; Bic+the most optimal concentration of APα+6-OHDA and EGTA (Nifedipine)+Bic+the most optimal concentration of APα+6-OHDA. C: cytosolic fraction; N: nuclear fraction. (C,D,F–I) Quantification of the relative protein levels was shown for CaMKIIδ3 (C,F,G) , CaM (D,H) and BDNF (I) in the cytosolic or nuclear fraction of SH-SY5Y cells. ** p

    Article Snippet: Chemicals and Reagents In this study, all reagents, materials, and chemicals were analytical grade and highest purity, including human neuroblastoma SH-SY5Y cell lines (SCSP-5014, Chinese Academy of Sciences, China); Dulbecco’s modified Eagle’s medium (DMEM, 11965092), Neurobasal (21103049), B27 (17504044), fetal bovine serum (FBS), glutamax (35050061), trypsin-EDTA (25300062) and sodium pyruvate (11360070; Gibco Invitrogen, MA, USA); APα (3653) and Bic (485494; Tocris, USA); Nifedipine (ab120135, Abcam, Burlingame, CA, USA); RA (R2500) and 6-OHDA (H4381; Sigma-Aldrich, St. Louis, MI, USA); penicillin and streptomycin (Solarbio, Beijing, China); bovine serum albumin (BSA) and BrdU (Bio-Sharp, China); DMSO (ST038), EGTA (ST068), phenylmethanesulfonyl fluoride (PMSF, ST506), TritonX-100, cytosolic and nuclear extraction kit (P0028; Beyotime, China).

    Techniques: Expressing, Chick Chorioallantoic Membrane Assay, Concentration Assay, Western Blot

    Adenosine inhibits N-type and P/Q-type calcium currents. (A) Effect of the L-type calcium channel blocker nifedipine (Nif, 10 μM) on calcium currents. (B) IV relationship of nifedipine-sensitive calcium currents (green graph). (C) Effect of the N-type calcium channel blocker conotoxin GVIA (CTX, 100 nM) on calcium currents. (D) IV relationship of CTX-sensitive calcium currents (yellow graph). (E) P/Q-type calcium currents were isolated by blocking N-type and L-type calcium currents with CTX + Nif. (F) IV relationship of isolated P/Q-type calcium currents (red graph). (G) Adenosine strongly reduces calcium currents in the presence of Nif. (H) In the presence of CTX and (I) CTX plus Nif, adenosine only weakly reduces calcium currents. (J) Effect of adenosine on calcium currents in the absence of calcium channel blockers (Ctrl) and in the presence of Nif, CTX and CTX plus Nif. Incubation with CTX as well as CTX plus Nif significantly reduced the adenosine-mediated attenuation on calcium currents, while Nif alone had no effect on the adenosine-mediated attenuation. n.s., not significant. ∗∗∗ p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Adenosine A1 Receptor-Mediated Attenuation of Reciprocal Dendro-Dendritic Inhibition in the Mouse Olfactory Bulb

    doi: 10.3389/fncel.2017.00435

    Figure Lengend Snippet: Adenosine inhibits N-type and P/Q-type calcium currents. (A) Effect of the L-type calcium channel blocker nifedipine (Nif, 10 μM) on calcium currents. (B) IV relationship of nifedipine-sensitive calcium currents (green graph). (C) Effect of the N-type calcium channel blocker conotoxin GVIA (CTX, 100 nM) on calcium currents. (D) IV relationship of CTX-sensitive calcium currents (yellow graph). (E) P/Q-type calcium currents were isolated by blocking N-type and L-type calcium currents with CTX + Nif. (F) IV relationship of isolated P/Q-type calcium currents (red graph). (G) Adenosine strongly reduces calcium currents in the presence of Nif. (H) In the presence of CTX and (I) CTX plus Nif, adenosine only weakly reduces calcium currents. (J) Effect of adenosine on calcium currents in the absence of calcium channel blockers (Ctrl) and in the presence of Nif, CTX and CTX plus Nif. Incubation with CTX as well as CTX plus Nif significantly reduced the adenosine-mediated attenuation on calcium currents, while Nif alone had no effect on the adenosine-mediated attenuation. n.s., not significant. ∗∗∗ p

    Article Snippet: Adenosine was purchased from Sigma–Aldrich (Munich, Germany); 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo-[f]-quinoxaline-7-sulfonamide (NBQX), D -(-)-2-amino-5-phosphonopentanic acid (D-APV), gabazine hydrobromide (GBZ), tetrodotoxin citrate (TTX), nifedipine (Nif) and cyclothiazide (CTZ) from Abcam (Cambridge, United Kingdom); Conotoxin GVIA (CTX) and Naspm trihydrochloride from Alomone labs (Jerusalem, Israel).

    Techniques: Isolation, Blocking Assay, Incubation