nifedipine  (Tocris)

 
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  • 99
    Name:
    Nifedipine
    Description:
    CaV1 x blocker
    Catalog Number:
    1075
    Price:
    None
    Purity:
    ≥98% (HPLC)
    Category:
    CaV1 x Channel L type Blockers CaV1 x Channels L type Voltage gated Calcium Channels CaV Calcium Channels Ion Channels Pharmacology
    Formula:
    1,4-Dihydro-2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridinedicarboxylic acid dimethyl ester
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    Structured Review

    Tocris nifedipine
    Nifedipine
    CaV1 x blocker
    https://www.bioz.com/result/nifedipine/product/Tocris
    Average 99 stars, based on 36 article reviews
    Price from $9.99 to $1999.99
    nifedipine - by Bioz Stars, 2020-09
    99/100 stars

    Images

    1) Product Images from "Intrinsic neuronal activity during migration controls the recruitment of specific interneuron subtypes in the postnatal mouse olfactory bulb"

    Article Title: Intrinsic neuronal activity during migration controls the recruitment of specific interneuron subtypes in the postnatal mouse olfactory bulb

    Journal: bioRxiv

    doi: 10.1101/2020.07.28.224568

    Spontaneous neuronal calcium activity in GC-P and PGN-P in the RMS, RMS-OB and deep GCL. A. Schematic representation of an olfactory bulb sagittal slice. B. Ai14/GCaMP6s P0 animals received lateral or medial electroporation of a Cre mRNAs. C. Calcium activity was recorded on acute brain slices between 6 and 10 dpe. Red and green cells represent medial and lateral cells migrating in the RMS, RMS-OB or in the deep GCL. D.F.H. Raster plot of calcium activity of GC-P (left) and PGN-P (right) recorded in the RMS (D), RMS OB (F) and deep GCL (H). E.G.I. Percentage of active cells, frequency and mean amplitude for GC-P and PGN-P in the RMS (E), RMS-OB (G) and in the deep GCL (I). Cells were defined as active if they showed at least one detectable calcium transient. The calcium activity of GC-P greatly increased upon arrival in the RMS-OB and the deep GCL, in contrast with PGN-P activity. N = 6 slices per condition. Error bars are SEM. J. Left: Raster plot of calcium activity of GC-P in the deep GCL in control and calcium-free medium (No Calcium + 2mM EGTA). Right: The percentage of active cells is highly decreased in calcium free medium. K. Left: Raster plot of calcium activity of GC-P in the deep GCL in control condition and nifedipine (10 μM) supplemented medium. Right: The percentage of active after incubation with the L-Type Voltage Gated Calcium Channels antagonist Nifedipine at 10 μM is highly decreased.
    Figure Legend Snippet: Spontaneous neuronal calcium activity in GC-P and PGN-P in the RMS, RMS-OB and deep GCL. A. Schematic representation of an olfactory bulb sagittal slice. B. Ai14/GCaMP6s P0 animals received lateral or medial electroporation of a Cre mRNAs. C. Calcium activity was recorded on acute brain slices between 6 and 10 dpe. Red and green cells represent medial and lateral cells migrating in the RMS, RMS-OB or in the deep GCL. D.F.H. Raster plot of calcium activity of GC-P (left) and PGN-P (right) recorded in the RMS (D), RMS OB (F) and deep GCL (H). E.G.I. Percentage of active cells, frequency and mean amplitude for GC-P and PGN-P in the RMS (E), RMS-OB (G) and in the deep GCL (I). Cells were defined as active if they showed at least one detectable calcium transient. The calcium activity of GC-P greatly increased upon arrival in the RMS-OB and the deep GCL, in contrast with PGN-P activity. N = 6 slices per condition. Error bars are SEM. J. Left: Raster plot of calcium activity of GC-P in the deep GCL in control and calcium-free medium (No Calcium + 2mM EGTA). Right: The percentage of active cells is highly decreased in calcium free medium. K. Left: Raster plot of calcium activity of GC-P in the deep GCL in control condition and nifedipine (10 μM) supplemented medium. Right: The percentage of active after incubation with the L-Type Voltage Gated Calcium Channels antagonist Nifedipine at 10 μM is highly decreased.

    Techniques Used: Activity Assay, Electroporation, Incubation

    Spontaneous neuronal calcium activity in GC-P in the deep GCL is not affected by classical antagonists. Incubation with a calcium free medium decrease the frequency of calcium transients. (A) The L-type voltage-dependent calcium channel blocker nifedipine decrease the frequency of calcium transients. (B) The NMDA receptors antagonist D-APV (C), AMPA/Kainate receptors antagonist NBQX (D), metabotropic glutamate receptor 5 antagonist MPEP (E), GABAA receptors antagonist Bicuculline (F) and glycine receptor antagonist strychnine (G) do no modify the percentage of active cells or the amplitude of calcium transient.
    Figure Legend Snippet: Spontaneous neuronal calcium activity in GC-P in the deep GCL is not affected by classical antagonists. Incubation with a calcium free medium decrease the frequency of calcium transients. (A) The L-type voltage-dependent calcium channel blocker nifedipine decrease the frequency of calcium transients. (B) The NMDA receptors antagonist D-APV (C), AMPA/Kainate receptors antagonist NBQX (D), metabotropic glutamate receptor 5 antagonist MPEP (E), GABAA receptors antagonist Bicuculline (F) and glycine receptor antagonist strychnine (G) do no modify the percentage of active cells or the amplitude of calcium transient.

    Techniques Used: Activity Assay, Incubation

    2) Product Images from "Myosin II ATPase Activity Mediates the Long-Term Potentiation-Induced Exodus of Stable F-Actin Bound by Drebrin A from Dendritic Spines"

    Article Title: Myosin II ATPase Activity Mediates the Long-Term Potentiation-Induced Exodus of Stable F-Actin Bound by Drebrin A from Dendritic Spines

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0085367

    Effects of various inhibitors of Ca 2+ entry on DA-actin distribution. Neurons (21 DIV) were incubated in normal medium containing 50 µM APV (A), 20 mM EGTA (B), 20 µM nifedipine (C), or 1 µM thapsigargin (D) for 30 min. The neurons were then stimulated with 100 µM glutamate for an additional 10 min. F-actin images indicate that spines kept their structure during the experiment although their shapes were changed. Scale bars, 5 µm. ( A ) APV pretreatment significantly increased both the drebrin and actin SDRs (n = 30 cells; p
    Figure Legend Snippet: Effects of various inhibitors of Ca 2+ entry on DA-actin distribution. Neurons (21 DIV) were incubated in normal medium containing 50 µM APV (A), 20 mM EGTA (B), 20 µM nifedipine (C), or 1 µM thapsigargin (D) for 30 min. The neurons were then stimulated with 100 µM glutamate for an additional 10 min. F-actin images indicate that spines kept their structure during the experiment although their shapes were changed. Scale bars, 5 µm. ( A ) APV pretreatment significantly increased both the drebrin and actin SDRs (n = 30 cells; p

    Techniques Used: Incubation

    3) Product Images from "Role of Phosphatidylinositol 3-Kinase (PI3K), Mitogen-Activated Protein Kinase (MAPK), and Protein Kinase C (PKC) in Calcium Signaling Pathways Linked to the α1-Adrenoceptor in Resistance Arteries"

    Article Title: Role of Phosphatidylinositol 3-Kinase (PI3K), Mitogen-Activated Protein Kinase (MAPK), and Protein Kinase C (PKC) in Calcium Signaling Pathways Linked to the α1-Adrenoceptor in Resistance Arteries

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2019.00055

    α 1 -Adrenoceptor-elicited vasoconstriction in resistance arteries is mostly due to Ca 2+ entry through voltage-dependent L-type channels. (A,B) Average inhibitory effects of the selective L-type Ca 2+ channel blocker nifedipine (0.3 μM) (A) or the inhibitor of the Orai1–mediated Ca 2+ entry Pyr6 (3 μM) alone or in combination with the SERCA inhibitor CPA (10 μM) (B ) on the CaCl 2 concentration-response curves (CRCs) in endothelium-denuded mesenteric resistance arteries kept in nominally Ca 2+ -free medium and stimulated with 10 μM PE. (C,D ) Summarized data showing the effects of SR Ca 2+ store depletion by SERCA inhibition with CPA (10 μM) alone or CPA plus nifedipine (0.3 μM) on the changes in [Ca 2+ ] i (C) and contraction (D) in response to 10 μM PE in resistance arteries kept in a nominally Ca 2+ -free medium (0 mM Ca 2+ , open bar) after Ca 2+ readmission (1 mM CaCl 2 , closed bar). Results are expressed as a percentage of control maximal responses (A,B) or the KPSS responses (C,D) . Values are means ± SEM of n = 6 arteries (one from each animal). ∗ P
    Figure Legend Snippet: α 1 -Adrenoceptor-elicited vasoconstriction in resistance arteries is mostly due to Ca 2+ entry through voltage-dependent L-type channels. (A,B) Average inhibitory effects of the selective L-type Ca 2+ channel blocker nifedipine (0.3 μM) (A) or the inhibitor of the Orai1–mediated Ca 2+ entry Pyr6 (3 μM) alone or in combination with the SERCA inhibitor CPA (10 μM) (B ) on the CaCl 2 concentration-response curves (CRCs) in endothelium-denuded mesenteric resistance arteries kept in nominally Ca 2+ -free medium and stimulated with 10 μM PE. (C,D ) Summarized data showing the effects of SR Ca 2+ store depletion by SERCA inhibition with CPA (10 μM) alone or CPA plus nifedipine (0.3 μM) on the changes in [Ca 2+ ] i (C) and contraction (D) in response to 10 μM PE in resistance arteries kept in a nominally Ca 2+ -free medium (0 mM Ca 2+ , open bar) after Ca 2+ readmission (1 mM CaCl 2 , closed bar). Results are expressed as a percentage of control maximal responses (A,B) or the KPSS responses (C,D) . Values are means ± SEM of n = 6 arteries (one from each animal). ∗ P

    Techniques Used: Concentration Assay, Inhibition

    4) Product Images from "Mechanisms of GABAB receptor enhancement of extrasynaptic GABAA receptor currents in cerebellar granule cells"

    Article Title: Mechanisms of GABAB receptor enhancement of extrasynaptic GABAA receptor currents in cerebellar granule cells

    Journal: Scientific Reports

    doi: 10.1038/s41598-019-53087-4

    Intracellular calcium dependent enhancement of GABA A Rs. ( A ) Representative uncaging current traces (left) and average current amplitudes (right) in control ACSF (black), in the presence of the EGTA-AM (red) and following the addition of CGP55845 (green). ( B ) Representative uncaging current traces (left) and average current amplitudes (right) in control ACSF (black) and in the presence of CGP55845 (red) when high (10 mM) EGTA is included in the internal solution. ( C ) Representative uncaging current traces (left) and average current amplitudes (right) in 0 calcium ACSF (black) and following application of CGP55845 (red). ( D ) Representative uncaging current traces (left) and average current amplitudes (right) in the presence of nifedipine (black), and following addition of CGP55845 (red). ( E ) Representative uncaging current traces (left) and average current amplitudes (right) in the presence of dantrolene (black) and following addition of CGP55845 (red). Data from individual cells are plotted as connected gray markers. (**) indicates p-value ≤ 0.01, (***) indicates p-value ≤ 0.001, ns indicates p-value > 0.05 .
    Figure Legend Snippet: Intracellular calcium dependent enhancement of GABA A Rs. ( A ) Representative uncaging current traces (left) and average current amplitudes (right) in control ACSF (black), in the presence of the EGTA-AM (red) and following the addition of CGP55845 (green). ( B ) Representative uncaging current traces (left) and average current amplitudes (right) in control ACSF (black) and in the presence of CGP55845 (red) when high (10 mM) EGTA is included in the internal solution. ( C ) Representative uncaging current traces (left) and average current amplitudes (right) in 0 calcium ACSF (black) and following application of CGP55845 (red). ( D ) Representative uncaging current traces (left) and average current amplitudes (right) in the presence of nifedipine (black), and following addition of CGP55845 (red). ( E ) Representative uncaging current traces (left) and average current amplitudes (right) in the presence of dantrolene (black) and following addition of CGP55845 (red). Data from individual cells are plotted as connected gray markers. (**) indicates p-value ≤ 0.01, (***) indicates p-value ≤ 0.001, ns indicates p-value > 0.05 .

    Techniques Used:

    5) Product Images from "Mechanisms of NMDA Receptor- and Voltage-Gated L-Type Calcium Channel-Dependent Hippocampal LTP Critically Rely on Proteolysis That Is Mediated by Distinct Metalloproteinases"

    Article Title: Mechanisms of NMDA Receptor- and Voltage-Gated L-Type Calcium Channel-Dependent Hippocampal LTP Critically Rely on Proteolysis That Is Mediated by Distinct Metalloproteinases

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.2170-16.2016

    nmdaLTP and vdccLTP show distinct profiles of sensitivity to MMP blockade. A , LTP in the CA3-CA1 pathway was induced by 200 Hz HFS (white). Two components that depend on the activation of NMDARs (nmdaLTP in the presence of 100 μ m nifedipine, red)
    Figure Legend Snippet: nmdaLTP and vdccLTP show distinct profiles of sensitivity to MMP blockade. A , LTP in the CA3-CA1 pathway was induced by 200 Hz HFS (white). Two components that depend on the activation of NMDARs (nmdaLTP in the presence of 100 μ m nifedipine, red)

    Techniques Used: Activation Assay

    LTP that is dependent on L-type calcium channels is impaired in MMP-3-deficient slices. A , In WT slices, 200 Hz tetanus that was delivered in the presence of 100 μ m nifedipine induced nmdaLTP, which was similar to nmdaLTP in MMP-3 KO slices (CTR:
    Figure Legend Snippet: LTP that is dependent on L-type calcium channels is impaired in MMP-3-deficient slices. A , In WT slices, 200 Hz tetanus that was delivered in the presence of 100 μ m nifedipine induced nmdaLTP, which was similar to nmdaLTP in MMP-3 KO slices (CTR:

    Techniques Used:

    6) Product Images from "NMDA receptors in mouse anterior piriform cortex initialize early odor preference learning and L-type calcium channels engage for long-term memory"

    Article Title: NMDA receptors in mouse anterior piriform cortex initialize early odor preference learning and L-type calcium channels engage for long-term memory

    Journal: Scientific Reports

    doi: 10.1038/srep35256

    Lateral olfactory tract (LOT) stimulation activates LTCCs. ( a1–a3 ) Somatic calcium transients in the anterior piriform pyramidal cells by LOT stimulations are dependent on postsynaptic AMPARs and NMDARs. (a1 ) Example images of population calcium imaging evoked by a single LOT stimulation in control, D-APV and D-APV+ NBQX conditions. Images were constructed by averaging 4–6 frames of evoked calcium responses (ΔF/F) from 5 stimulus trials. Example calcium transient traces from 4 cells are shown on the right. ( a2 ) Peak calcium transients (ΔF/F%) averaged from a population of cells (yellow circles, regions of interest) on the same slice. ( a3 ). Normalized calcium changes (to control) during D-APV and D-APV+ NBQX applications from 4 slices (n = 80 cells). ( b1–b3 ) Blockade of LTCCs reduce somatic calcium transients in pyramidal cells. ( b1 ) Example images of population calcium imaging in control, nifedipine (Nif) and Nif washout conditions. ( b2 ). Peak calcium transients averaged from a population of cells on the same slice. ( b3 ) Normalized calcium changes during Nif and Nif washout from 4 slices (n = 110 cells). **p
    Figure Legend Snippet: Lateral olfactory tract (LOT) stimulation activates LTCCs. ( a1–a3 ) Somatic calcium transients in the anterior piriform pyramidal cells by LOT stimulations are dependent on postsynaptic AMPARs and NMDARs. (a1 ) Example images of population calcium imaging evoked by a single LOT stimulation in control, D-APV and D-APV+ NBQX conditions. Images were constructed by averaging 4–6 frames of evoked calcium responses (ΔF/F) from 5 stimulus trials. Example calcium transient traces from 4 cells are shown on the right. ( a2 ) Peak calcium transients (ΔF/F%) averaged from a population of cells (yellow circles, regions of interest) on the same slice. ( a3 ). Normalized calcium changes (to control) during D-APV and D-APV+ NBQX applications from 4 slices (n = 80 cells). ( b1–b3 ) Blockade of LTCCs reduce somatic calcium transients in pyramidal cells. ( b1 ) Example images of population calcium imaging in control, nifedipine (Nif) and Nif washout conditions. ( b2 ). Peak calcium transients averaged from a population of cells on the same slice. ( b3 ) Normalized calcium changes during Nif and Nif washout from 4 slices (n = 110 cells). **p

    Techniques Used: Imaging, Construct

    LTCC activation is subsequent to NMDAR activation. ( a1–a5 ) Nifedipine does not further reduce calcium transients in the presence of NMDAR blockade by D-APV. ( a1 ) Example images of population calcium imaging in control, D-APV and D-APV + Nif conditions. Example calcium transient traces from 4 cells are shown on the right. ( a2 ) Peak calcium transients (ΔF/F%) to a single LOT stimulation, averaged from a population of cells (yellow circles) on the same slice. ( a3 ) Normalized calcium changes (to control) to a single LOT stimulation during D-APV and D-APV + Nif applications from 3 slices (n = 55 cells). ( a4 ) Peak calcium transients to 4 LOT stimulations at 100 Hz. ( a5 ) Normalized calcium changes to 4 LOT stimulations from 3 slices (n = 70 cells). ( b1–b3 ) Application of BayK-8644 increased somatic calcium transients in the presence of D-APV. ( b1 ) Example images of population calcium imaging in control, D-APV and D-APV + BayK-8644 conditions. ( b2 ) Peak calcium transients averaged from a population of cells on the same slice. ( b3 ) Normalized calcium changes during D-APV and D-APV + BayK-8644 from 5 slices (n = 125 cells). **p
    Figure Legend Snippet: LTCC activation is subsequent to NMDAR activation. ( a1–a5 ) Nifedipine does not further reduce calcium transients in the presence of NMDAR blockade by D-APV. ( a1 ) Example images of population calcium imaging in control, D-APV and D-APV + Nif conditions. Example calcium transient traces from 4 cells are shown on the right. ( a2 ) Peak calcium transients (ΔF/F%) to a single LOT stimulation, averaged from a population of cells (yellow circles) on the same slice. ( a3 ) Normalized calcium changes (to control) to a single LOT stimulation during D-APV and D-APV + Nif applications from 3 slices (n = 55 cells). ( a4 ) Peak calcium transients to 4 LOT stimulations at 100 Hz. ( a5 ) Normalized calcium changes to 4 LOT stimulations from 3 slices (n = 70 cells). ( b1–b3 ) Application of BayK-8644 increased somatic calcium transients in the presence of D-APV. ( b1 ) Example images of population calcium imaging in control, D-APV and D-APV + BayK-8644 conditions. ( b2 ) Peak calcium transients averaged from a population of cells on the same slice. ( b3 ) Normalized calcium changes during D-APV and D-APV + BayK-8644 from 5 slices (n = 125 cells). **p

    Techniques Used: Activation Assay, Imaging

    7) Product Images from "Two Distinct Mechanisms Mediate Potentiating Effects of Depolarization on Synaptic Transmission"

    Article Title: Two Distinct Mechanisms Mediate Potentiating Effects of Depolarization on Synaptic Transmission

    Journal: Journal of Neurophysiology

    doi: 10.1152/jn.00418.2009

    Inhibitory effects of nifedipine on calcium fluorescence in B21, and on B21–B8 synaptic transmission. A1 : changes in calcium fluorescence induced by subthreshold depolarizing pulses were significantly reduced by nifedipine (10 μM, bath
    Figure Legend Snippet: Inhibitory effects of nifedipine on calcium fluorescence in B21, and on B21–B8 synaptic transmission. A1 : changes in calcium fluorescence induced by subthreshold depolarizing pulses were significantly reduced by nifedipine (10 μM, bath

    Techniques Used: Fluorescence, Transmission Assay

    8) Product Images from "Ionic currents in intimal cultured synoviocytes from the rabbit"

    Article Title: Ionic currents in intimal cultured synoviocytes from the rabbit

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00028.2010

    A and B : family of currents (evoked by the same protocol as that described in Fig. 4 ) before ( A ) and in the presence of nifedipine ( B ). The transient inward current was blocked, indicating that it was an L-type calcium current. C : summary of 6 such experiments. Mean inward current (■) peaked at 0 mV and reversed at +23 mV. In the presence of nifedipine, inward current was abolished, leaving only the outward current carried by Cs + . D and E : effects of the calcium channel agonist FPL-64176. The control inward currents ( D ) were greatly enhanced by 300 nM FPL 64176 (FPL; E ). This was accompanied by somewhat slower activation kinetics and by very much slower inactivation, such that the currents were not fully inactivated at the end of the 500-ms sweep. F : a summary of 12 such experiments showing that the mean peak inward current increased in amplitude and that the voltage at which current peaked shifted negatively by 10 mV. Peak inward current increased by 308% from a control value (■) of 93 ± 17 pA to 380 ± 58 pA in the presence of FPL (▲; n = 12; P
    Figure Legend Snippet: A and B : family of currents (evoked by the same protocol as that described in Fig. 4 ) before ( A ) and in the presence of nifedipine ( B ). The transient inward current was blocked, indicating that it was an L-type calcium current. C : summary of 6 such experiments. Mean inward current (■) peaked at 0 mV and reversed at +23 mV. In the presence of nifedipine, inward current was abolished, leaving only the outward current carried by Cs + . D and E : effects of the calcium channel agonist FPL-64176. The control inward currents ( D ) were greatly enhanced by 300 nM FPL 64176 (FPL; E ). This was accompanied by somewhat slower activation kinetics and by very much slower inactivation, such that the currents were not fully inactivated at the end of the 500-ms sweep. F : a summary of 12 such experiments showing that the mean peak inward current increased in amplitude and that the voltage at which current peaked shifted negatively by 10 mV. Peak inward current increased by 308% from a control value (■) of 93 ± 17 pA to 380 ± 58 pA in the presence of FPL (▲; n = 12; P

    Techniques Used: Activation Assay, Mass Spectrometry

    Top : pseudo linescan of a synoviocyte loaded with the calcium indicator fluo-4 (see materials and methods ); shown are the effects of increasing external K + concentration for 5 s (indicated by the black bar) before and in the presence of 1 μM nifedipine. Bottom : F/F 0 plot of the same experiment. Depolarization of the membrane with high potassium caused a large increase in intracellular calcium, and this effect was greatly attenuated in the presence of nifedipine.
    Figure Legend Snippet: Top : pseudo linescan of a synoviocyte loaded with the calcium indicator fluo-4 (see materials and methods ); shown are the effects of increasing external K + concentration for 5 s (indicated by the black bar) before and in the presence of 1 μM nifedipine. Bottom : F/F 0 plot of the same experiment. Depolarization of the membrane with high potassium caused a large increase in intracellular calcium, and this effect was greatly attenuated in the presence of nifedipine.

    Techniques Used: Concentration Assay

    9) Product Images from "Morphological, immunocytochemical, and functional characterization of esophageal enteric neurons in primary culture"

    Article Title: Morphological, immunocytochemical, and functional characterization of esophageal enteric neurons in primary culture

    Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

    doi: 10.1152/ajpgi.00040.2013

    Effect of high potassium and nifedipine on [Ca 2+ ] cyt in esophageal enteric neurons in 2 mM Ca 2+ normal PSS. A : after basal lines were stable, addition of high K + (100 mM) to 2 mM Ca 2+ normal PSS is indicated by a line above the tracings. B : after esophageal enteric neurons were pretreated with nifedipine (10 μM) in 2 mM Ca 2+ normal PSS for 10 min, addition of high K + (100 mM) is indicated by a line above the tracings. Values are means ± SE. C : histograms of the summary data of neuronal response to high K + in the absence or the presence of nifedipine in 2 mM Ca 2+ PSS. ** P
    Figure Legend Snippet: Effect of high potassium and nifedipine on [Ca 2+ ] cyt in esophageal enteric neurons in 2 mM Ca 2+ normal PSS. A : after basal lines were stable, addition of high K + (100 mM) to 2 mM Ca 2+ normal PSS is indicated by a line above the tracings. B : after esophageal enteric neurons were pretreated with nifedipine (10 μM) in 2 mM Ca 2+ normal PSS for 10 min, addition of high K + (100 mM) is indicated by a line above the tracings. Values are means ± SE. C : histograms of the summary data of neuronal response to high K + in the absence or the presence of nifedipine in 2 mM Ca 2+ PSS. ** P

    Techniques Used:

    10) Product Images from "Protease‐activated receptor 2 activates CRAC‐mediated Ca2+ influx to cause prostate smooth muscle contraction"

    Article Title: Protease‐activated receptor 2 activates CRAC‐mediated Ca2+ influx to cause prostate smooth muscle contraction

    Journal: FASEB bioAdvances

    doi: 10.1096/fba.2018-00024

    CRAC channels are involved in contraction of prostate smooth muscle cells. (A) qRT‐PCR analysis to determine expression of various CRAC and L‐type voltage channels in PSMC. (B and C) collagen hydrogels showing significantly reduced contractility upon BTP2 (12 µM) pretreatment but not after nifedipine (10 µM) pretreatment. (D and E) BTP2 (12 µM) pretreatment reduced the amplitude of the secondary Ca 2+ oscillations in PSMC (grey line), resulting in significantly reduced area of secondary oscillations. Data represent mean ± SEM of three independent experiments. qRT‐PCR samples of respective Ca 2+ channel mRNA relative to the expression of GAPDH as a housekeeping gene. Diameter of collagen hydrogels were measured in ImageJ (version 1.50i) and significance analyzed in Prism (version 7.04) with one‐way ANOVA followed by Tukey's multiple comparison test. [Ca2+] i was monitored using Fura‐2AM fluorescence and represented as the 340/380 nm ratio. Area of the secondary oscillations was determined by area under the curve analysis performed in Prism (version 7.04) with unpaired two tailed Student's t test. * P
    Figure Legend Snippet: CRAC channels are involved in contraction of prostate smooth muscle cells. (A) qRT‐PCR analysis to determine expression of various CRAC and L‐type voltage channels in PSMC. (B and C) collagen hydrogels showing significantly reduced contractility upon BTP2 (12 µM) pretreatment but not after nifedipine (10 µM) pretreatment. (D and E) BTP2 (12 µM) pretreatment reduced the amplitude of the secondary Ca 2+ oscillations in PSMC (grey line), resulting in significantly reduced area of secondary oscillations. Data represent mean ± SEM of three independent experiments. qRT‐PCR samples of respective Ca 2+ channel mRNA relative to the expression of GAPDH as a housekeeping gene. Diameter of collagen hydrogels were measured in ImageJ (version 1.50i) and significance analyzed in Prism (version 7.04) with one‐way ANOVA followed by Tukey's multiple comparison test. [Ca2+] i was monitored using Fura‐2AM fluorescence and represented as the 340/380 nm ratio. Area of the secondary oscillations was determined by area under the curve analysis performed in Prism (version 7.04) with unpaired two tailed Student's t test. * P

    Techniques Used: Quantitative RT-PCR, Expressing, Fluorescence, Two Tailed Test

    11) Product Images from "Differential Calcium Signaling Mediated by Voltage-Gated Calcium Channels in Rat Retinal Ganglion Cells and Their Unmyelinated Axons"

    Article Title: Differential Calcium Signaling Mediated by Voltage-Gated Calcium Channels in Rat Retinal Ganglion Cells and Their Unmyelinated Axons

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0084507

    L-type VGCC subtypes contribute to calcium signalling in ganglion cell axons. A. Fluo-4 labelling of RGC axons in the wholemount retina. Scale bar is 20 µm. B. Application of nifedipine (NIF; 10 µM), an L-type Ca channel antagonist, reduced the second high K + -evoked calcium signal. C. Summary of Ca 2+ imaging results from RGC axons showing the following changes in paired pulse Ca 2+ signal in response to drugs (applied during the second K + pulse) compared to their control paired K + pulses (K): 10 µM nifedipine (20%±6%; p = 0.0053; n = 12), 100 µM verapamil (VPM; 52%±9%; p
    Figure Legend Snippet: L-type VGCC subtypes contribute to calcium signalling in ganglion cell axons. A. Fluo-4 labelling of RGC axons in the wholemount retina. Scale bar is 20 µm. B. Application of nifedipine (NIF; 10 µM), an L-type Ca channel antagonist, reduced the second high K + -evoked calcium signal. C. Summary of Ca 2+ imaging results from RGC axons showing the following changes in paired pulse Ca 2+ signal in response to drugs (applied during the second K + pulse) compared to their control paired K + pulses (K): 10 µM nifedipine (20%±6%; p = 0.0053; n = 12), 100 µM verapamil (VPM; 52%±9%; p

    Techniques Used: Imaging

    Many VGCC subtypes contribute to calcium signalling in ganglion cell bodies. A. Fluo-4 labelling of RGC somata in the wholemount retina. Scale bar is 20 µm. B. Application of nifedipine (NIF; 10 µM), an L-type Ca channel antagonist, reduced the second high K + -evoked calcium signal. C. Summary of Ca 2+ imaging results in RGC somata showing the following changes in paired pulse Ca 2+ signal in response to drugs (applied during the second K + pulse) compared to their control paired K + pulses (K): 10 µM nifedipine (29%±7%; p = 0.0003; n = 20), 100 µM verapamil (VPM; 39%±5%; p
    Figure Legend Snippet: Many VGCC subtypes contribute to calcium signalling in ganglion cell bodies. A. Fluo-4 labelling of RGC somata in the wholemount retina. Scale bar is 20 µm. B. Application of nifedipine (NIF; 10 µM), an L-type Ca channel antagonist, reduced the second high K + -evoked calcium signal. C. Summary of Ca 2+ imaging results in RGC somata showing the following changes in paired pulse Ca 2+ signal in response to drugs (applied during the second K + pulse) compared to their control paired K + pulses (K): 10 µM nifedipine (29%±7%; p = 0.0003; n = 20), 100 µM verapamil (VPM; 39%±5%; p

    Techniques Used: Imaging

    12) Product Images from "Dynamic disorganization of synaptic NMDA receptors triggered by autoantibodies from psychotic patients"

    Article Title: Dynamic disorganization of synaptic NMDA receptors triggered by autoantibodies from psychotic patients

    Journal: Nature Communications

    doi: 10.1038/s41467-017-01700-3

    NMDAR-Ab from Healthy + subjects and PSY + patients do not affect NMDAR-mediated Ca 2+ transients in spines of hippocampal neurons. a Representative time-lapse images of a spontaneous NMDAR-mediated Ca 2+ transient in basal condition (in the presence of nifedipine 5 µM and bicuculline 5 µM). Scale bar, 2 µm. Lower panel, representative examples of NMDAR-mediated Ca 2+ transients recorded in spines (expressed as Δ F / F ratio) exposed to purified IgG from Healthy −, Healthy +, or PSY + individuals. Note that all events were abolished by the NMDAR-competitive antagonist D-AP5 (50 µM). b Normalized frequency (ratio of Ca 2+ transients frequency post-application of NMDAR-Ab relative to the baseline acquisition) of spontaneous NMDAR-mediated Ca 2+ transients in control condition with no IgG ( n = 38 spines, N = 4 neurons) or in the presence of Healthy − purified IgG ( n = 38, N = 5), Healthy + NMDAR-Ab ( n = 68, N = 10), or PSY + NMDAR-Ab ( n = 131, N = 15). Data are expressed as mean ± SEM. One out of one Healthy − , three out of three Healthy + , and four out of nine PSY + were used and pooled for comparisons. P > 0.05, Krukal–Wallis test
    Figure Legend Snippet: NMDAR-Ab from Healthy + subjects and PSY + patients do not affect NMDAR-mediated Ca 2+ transients in spines of hippocampal neurons. a Representative time-lapse images of a spontaneous NMDAR-mediated Ca 2+ transient in basal condition (in the presence of nifedipine 5 µM and bicuculline 5 µM). Scale bar, 2 µm. Lower panel, representative examples of NMDAR-mediated Ca 2+ transients recorded in spines (expressed as Δ F / F ratio) exposed to purified IgG from Healthy −, Healthy +, or PSY + individuals. Note that all events were abolished by the NMDAR-competitive antagonist D-AP5 (50 µM). b Normalized frequency (ratio of Ca 2+ transients frequency post-application of NMDAR-Ab relative to the baseline acquisition) of spontaneous NMDAR-mediated Ca 2+ transients in control condition with no IgG ( n = 38 spines, N = 4 neurons) or in the presence of Healthy − purified IgG ( n = 38, N = 5), Healthy + NMDAR-Ab ( n = 68, N = 10), or PSY + NMDAR-Ab ( n = 131, N = 15). Data are expressed as mean ± SEM. One out of one Healthy − , three out of three Healthy + , and four out of nine PSY + were used and pooled for comparisons. P > 0.05, Krukal–Wallis test

    Techniques Used: Purification

    13) Product Images from "Disruption of Cav1.2-mediated signaling is a pathway for ketamine-induced pathology"

    Article Title: Disruption of Cav1.2-mediated signaling is a pathway for ketamine-induced pathology

    Journal: Nature Communications

    doi: 10.1038/s41467-020-18167-4

    Ketamine and nifedipine regulated mouse urodynamics resembling ketamine cystitis in humans. a , b Representative CMG traces of ketamine cystitis-like voiding phenotypes induced by intravesical ketamine ( a 100, 500 µg ml −1 ) and nifedipine ( b 10, 100 µM) are reversed by Bay k8644 infusion (200 nM). Summarized CMG data ( c – l n = 5 mice for ketamine group and n = 7 mice for nifedipine group) show that decreased voiding interval ( c , h ), peak pressure ( f , k ), and compliance ( g , l ), were each rescued by Bay k8644 infusion. Data are shown as box and whiskers, center line is the median of the data set, box represents 75% of the data, and bars indicates whiskers from minimum to maximum. Data were analysed by paired two tail Student’s t -tests. P
    Figure Legend Snippet: Ketamine and nifedipine regulated mouse urodynamics resembling ketamine cystitis in humans. a , b Representative CMG traces of ketamine cystitis-like voiding phenotypes induced by intravesical ketamine ( a 100, 500 µg ml −1 ) and nifedipine ( b 10, 100 µM) are reversed by Bay k8644 infusion (200 nM). Summarized CMG data ( c – l n = 5 mice for ketamine group and n = 7 mice for nifedipine group) show that decreased voiding interval ( c , h ), peak pressure ( f , k ), and compliance ( g , l ), were each rescued by Bay k8644 infusion. Data are shown as box and whiskers, center line is the median of the data set, box represents 75% of the data, and bars indicates whiskers from minimum to maximum. Data were analysed by paired two tail Student’s t -tests. P

    Techniques Used: Mouse Assay

    Ketamine inhibits Cav1.2-mediated calcium influx in mouse BSM cells. a – c Representative Fluo-4 Ca 2+ images of primary cultured mouse BSM cells treated without ( a ) or with Bay k8644 (10 nM) ( b ), or treated first with ketamine (100 µg ml −1 ) and then with added Bay k8644 (10 nM) ( c ). Scale bar: 40 µm. d Nonlinear curve fit of Bay k8644 concentration-dependent increase in mouse BSM cell [Ca 2+ ] i with EC 50 of 9.6 nM ( n = 10, 23, 18, 19, 10, and 29 BSM cells for respective [Bay k8644] = 0, 0.1, 1, 10, 200, and 1000 nM). Bars indicate the SD of the means. e 10 nM Bay k8644-induced increase in BSM intracellular [Ca 2+ ] ( n = 39 BSM cells) was inhibited by 100 µg ml −1 ketamine ( n = 25 BSM cells)) and by 10 µM nifedipine ( n = 39 BSM cells). f Hundred millimolar of KCl-stimulated increase in BSM intracellular [Ca 2+ ] ( n = 39) was inhibited by 100 µg ml −1 ketamine ( n = 25 BSM cells) and by 10 µM nifedipine ( n = 39 BSM cells). g Hundred micromolar of carbachol-stimulated increase in BSM intracellular [Ca 2+ ] ( n = 27 BSM cells) was inhibited by 100 µg ml −1 ketamine ( n = 27 BSM cells), and by 10 µM nifedipine ( n = 30 BSM cells). h Hundred micromolar of ATP-stimulated increase in BSM intracellular [Ca 2+ ] ( n = 43 BSM cells) was inhibited by 100 µg ml −1 ketamine ( n = 22 BSM cells) and by 10 µM nifedipine ( n = 21 BSM cells). Data are shown as box and whiskers, center line is the median of the data set, box represents 75% of the data, and bars indicates whiskers from minimum to maximum. Data were analysed by two tailed Student’s t -test. P
    Figure Legend Snippet: Ketamine inhibits Cav1.2-mediated calcium influx in mouse BSM cells. a – c Representative Fluo-4 Ca 2+ images of primary cultured mouse BSM cells treated without ( a ) or with Bay k8644 (10 nM) ( b ), or treated first with ketamine (100 µg ml −1 ) and then with added Bay k8644 (10 nM) ( c ). Scale bar: 40 µm. d Nonlinear curve fit of Bay k8644 concentration-dependent increase in mouse BSM cell [Ca 2+ ] i with EC 50 of 9.6 nM ( n = 10, 23, 18, 19, 10, and 29 BSM cells for respective [Bay k8644] = 0, 0.1, 1, 10, 200, and 1000 nM). Bars indicate the SD of the means. e 10 nM Bay k8644-induced increase in BSM intracellular [Ca 2+ ] ( n = 39 BSM cells) was inhibited by 100 µg ml −1 ketamine ( n = 25 BSM cells)) and by 10 µM nifedipine ( n = 39 BSM cells). f Hundred millimolar of KCl-stimulated increase in BSM intracellular [Ca 2+ ] ( n = 39) was inhibited by 100 µg ml −1 ketamine ( n = 25 BSM cells) and by 10 µM nifedipine ( n = 39 BSM cells). g Hundred micromolar of carbachol-stimulated increase in BSM intracellular [Ca 2+ ] ( n = 27 BSM cells) was inhibited by 100 µg ml −1 ketamine ( n = 27 BSM cells), and by 10 µM nifedipine ( n = 30 BSM cells). h Hundred micromolar of ATP-stimulated increase in BSM intracellular [Ca 2+ ] ( n = 43 BSM cells) was inhibited by 100 µg ml −1 ketamine ( n = 22 BSM cells) and by 10 µM nifedipine ( n = 21 BSM cells). Data are shown as box and whiskers, center line is the median of the data set, box represents 75% of the data, and bars indicates whiskers from minimum to maximum. Data were analysed by two tailed Student’s t -test. P

    Techniques Used: Cell Culture, Concentration Assay, Two Tailed Test

    Ketamine reduces Cav1.2-stimulated mRNA and protein levels in BSM cells. Mouse BSM strips were subjected to 50 mM KCl activation of Cav1.2 for 0–120 min and then lysed for mRNA preparation. Changes in c-fos ( a n = 9 BSM strips) and c-jun ( b n = 9 BSM strips) mRNA were measured by quantitative RT-PCR. Upregulation of both c-fos and c-jun were inhibited by 100 µg ml −1 ketamine and by 10 µM nifedipine. c Representative immunoblot from two independent experiments showing that upregulation of c-fos and c-jun by 30 min treatment with 50 mM KCl to activate Cav1.2 was inhibited by ketamine (100 µg ml −1 ) and by nifedipine (10 µg ml −1 ). d summarized data ( n = 5 BSM strips) of experiments similar to that shown in c . e 50 mM KCl upregulated expression and nuclear translocation of c-fos and c-jun in human BSM cells in a manner inhibited by ketamine (100 µg ml −1 ) and rescued by Bay k8644 (200 nM). Scale bar: 20 µm. These images, representative of two separate triplicate experiments, are summarized in f ( n = 38–46 BSM cells). Data are shown as box and whiskers, center line is the median of the data set, box represents 75% of the data, and bars indicates whiskers from minimum to maximum. Data are analysed by two tailed Student’s t -test. P
    Figure Legend Snippet: Ketamine reduces Cav1.2-stimulated mRNA and protein levels in BSM cells. Mouse BSM strips were subjected to 50 mM KCl activation of Cav1.2 for 0–120 min and then lysed for mRNA preparation. Changes in c-fos ( a n = 9 BSM strips) and c-jun ( b n = 9 BSM strips) mRNA were measured by quantitative RT-PCR. Upregulation of both c-fos and c-jun were inhibited by 100 µg ml −1 ketamine and by 10 µM nifedipine. c Representative immunoblot from two independent experiments showing that upregulation of c-fos and c-jun by 30 min treatment with 50 mM KCl to activate Cav1.2 was inhibited by ketamine (100 µg ml −1 ) and by nifedipine (10 µg ml −1 ). d summarized data ( n = 5 BSM strips) of experiments similar to that shown in c . e 50 mM KCl upregulated expression and nuclear translocation of c-fos and c-jun in human BSM cells in a manner inhibited by ketamine (100 µg ml −1 ) and rescued by Bay k8644 (200 nM). Scale bar: 20 µm. These images, representative of two separate triplicate experiments, are summarized in f ( n = 38–46 BSM cells). Data are shown as box and whiskers, center line is the median of the data set, box represents 75% of the data, and bars indicates whiskers from minimum to maximum. Data are analysed by two tailed Student’s t -test. P

    Techniques Used: Activation Assay, Quantitative RT-PCR, Expressing, Translocation Assay, Two Tailed Test

    Ketamine and nifedipine dose-dependently inhibit human BSM cell proliferation. Primary cultured human BSM cells were incubated with ketamine or nifedipine for 1–7 days at the indicated concentrations, cell proliferation was assessed by alamar blue assay in the presence of ketamine ( a n = 4) or nifedipine ( b n = 4). Ketamine and nifedipine inhibited hBSM cell proliferation. c Immunofluorescent staining of ki67 (green) in hBSM cells was inhibited by pretreatment with ketamine (100 µg ml −1 ) or nifedipine (10 µM), but inhibition was rescued by 200 nM Bay k8644, representative images are from two independent experiments with at least three samples each group at each experiment. Scale bar: 40 µm. Data are presented as mean values ± SD. Source data are provided as a Source Data file.
    Figure Legend Snippet: Ketamine and nifedipine dose-dependently inhibit human BSM cell proliferation. Primary cultured human BSM cells were incubated with ketamine or nifedipine for 1–7 days at the indicated concentrations, cell proliferation was assessed by alamar blue assay in the presence of ketamine ( a n = 4) or nifedipine ( b n = 4). Ketamine and nifedipine inhibited hBSM cell proliferation. c Immunofluorescent staining of ki67 (green) in hBSM cells was inhibited by pretreatment with ketamine (100 µg ml −1 ) or nifedipine (10 µM), but inhibition was rescued by 200 nM Bay k8644, representative images are from two independent experiments with at least three samples each group at each experiment. Scale bar: 40 µm. Data are presented as mean values ± SD. Source data are provided as a Source Data file.

    Techniques Used: Cell Culture, Incubation, Alamar Blue Assay, Staining, Inhibition

    Ketamine inhibits Cav1.2-mediated calcium channel activity. a – c are representative Ba 2+ current traces of two microelectrode voltage-clamped Xenopus oocytes, previously injected with water ( a , n = 5 oocytes) or with cRNA encoding Cav1.2 subunits, recorded in the absence ( b , n = 10 oocytes), or presence of ketamine ( c n = 10 oocytes). d , e summarize data from a – c showing dose-dependent inhibition of Cav1.2-mediated Ba 2+ current by ketamine ( d n = 10 oocytes) or nifedipine ( e n = 5 oocytes). f , g are representative whole cell current traces of fresh isolated BSM cells in the absence ( f n = 8 BSM cells) or presence ( g n = 8 BSM cells) of 100 µg ml −1 ketamine. h Summarizes data showing ketamine inhibition on Cav1.2-mediated Ba 2+ current in freshly isolated mouse BSM cells as shown in f , g . Data are presented as mean values ± SD. Source data are provided as a Source Data file.
    Figure Legend Snippet: Ketamine inhibits Cav1.2-mediated calcium channel activity. a – c are representative Ba 2+ current traces of two microelectrode voltage-clamped Xenopus oocytes, previously injected with water ( a , n = 5 oocytes) or with cRNA encoding Cav1.2 subunits, recorded in the absence ( b , n = 10 oocytes), or presence of ketamine ( c n = 10 oocytes). d , e summarize data from a – c showing dose-dependent inhibition of Cav1.2-mediated Ba 2+ current by ketamine ( d n = 10 oocytes) or nifedipine ( e n = 5 oocytes). f , g are representative whole cell current traces of fresh isolated BSM cells in the absence ( f n = 8 BSM cells) or presence ( g n = 8 BSM cells) of 100 µg ml −1 ketamine. h Summarizes data showing ketamine inhibition on Cav1.2-mediated Ba 2+ current in freshly isolated mouse BSM cells as shown in f , g . Data are presented as mean values ± SD. Source data are provided as a Source Data file.

    Techniques Used: Activity Assay, Injection, Inhibition, Isolation

    Ketamine and Cav1.2 agonist Bay k8644 are mutual antagonists. a Representative traces of Bay k8644-mediated potentiation of EFS-stimulated BSM contraction, summarized in d ( n = 7 BSM strips). b Representative traces of Bay k8644-mediated potentiation of EFS-stimulated BSM contraction fully inhibited by ketamine and by nifedipine in dose-dependent manners, summarized in e ( n = 8 BSM strips) and f ( n = 12 BSM strips). c representative traces of ketamine-induced and nifedipine-induced inhibition of EFS-stimulated BSM contraction rescued by 50 or 200 nM Bay k8644, summarized in g ( n = 17 BSM strips) and h ( n = 13 BSM strips). Data are presented as mean values ± SD. These data support ketamine as an inhibitor of Cav1.2-mediated BSM contraction. Source data are provided as a Source Data file.
    Figure Legend Snippet: Ketamine and Cav1.2 agonist Bay k8644 are mutual antagonists. a Representative traces of Bay k8644-mediated potentiation of EFS-stimulated BSM contraction, summarized in d ( n = 7 BSM strips). b Representative traces of Bay k8644-mediated potentiation of EFS-stimulated BSM contraction fully inhibited by ketamine and by nifedipine in dose-dependent manners, summarized in e ( n = 8 BSM strips) and f ( n = 12 BSM strips). c representative traces of ketamine-induced and nifedipine-induced inhibition of EFS-stimulated BSM contraction rescued by 50 or 200 nM Bay k8644, summarized in g ( n = 17 BSM strips) and h ( n = 13 BSM strips). Data are presented as mean values ± SD. These data support ketamine as an inhibitor of Cav1.2-mediated BSM contraction. Source data are provided as a Source Data file.

    Techniques Used: Inhibition

    14) Product Images from "Saikosaponin d causes apoptotic death of cultured neocortical neurons by increasing membrane permeability and elevating intracellular Ca2+ concentration"

    Article Title: Saikosaponin d causes apoptotic death of cultured neocortical neurons by increasing membrane permeability and elevating intracellular Ca2+ concentration

    Journal: Neurotoxicology

    doi: 10.1016/j.neuro.2018.11.006

    Major Ca 2+ influx routes are not involved in SSd-elevated [Ca 2+ ] i . Representative traces of nifedipine (A), KB-R7943 (B), MK-801 (C), CNQX (D), SB366791 (E), and RR (F) effect on SSd-stimulated [Ca 2+ ] i elevation as a function of time. This experiment was performed in three independent cultures, each in triplicates with similar results. The first arrow indicates the addition of Veh or inhibitor and the second arrow indicates the addition of Veh or SSd (3 µM). Veh indicates 0.1% DMSO.
    Figure Legend Snippet: Major Ca 2+ influx routes are not involved in SSd-elevated [Ca 2+ ] i . Representative traces of nifedipine (A), KB-R7943 (B), MK-801 (C), CNQX (D), SB366791 (E), and RR (F) effect on SSd-stimulated [Ca 2+ ] i elevation as a function of time. This experiment was performed in three independent cultures, each in triplicates with similar results. The first arrow indicates the addition of Veh or inhibitor and the second arrow indicates the addition of Veh or SSd (3 µM). Veh indicates 0.1% DMSO.

    Techniques Used:

    15) Product Images from "How Modeling Can Reconcile Apparently Discrepant Experimental Results: The Case of Pacemaking in Dopaminergic Neurons"

    Article Title: How Modeling Can Reconcile Apparently Discrepant Experimental Results: The Case of Pacemaking in Dopaminergic Neurons

    Journal: PLoS Computational Biology

    doi: 10.1371/journal.pcbi.1002050

    Effect of sodium and L-type calcium channel blockade on the firing of SNc dopaminergic neurons in vitro . ( A1 ) Extracellular recording of a DA cell in control conditions (left) and after application of 20 M nifedipine (right). ( A2 ) Same as ( A1 ) after a 80 reduction of the sodium conductance by the superfusion of 30 nM TTX. ( B ) Evolution of the mean firing rate (samples of 2 minutes) of a DA cell over time. ( C ) Mean firing frequency (N = 6) for each condition (mean sem). A simultaneous application of TTX and nifedipine affects the firing of the cells more strongly, as compared to the application of either of the two compounds alone. All experiments were performed in the presence of blockers of synaptic transmission. Note that the superfusion of the blockers produces an excitation of the neurons, which can be attributed to the block of inhibitory D2 autoreceptors. *P 0.05, **P 0.01, ***P 0.001.
    Figure Legend Snippet: Effect of sodium and L-type calcium channel blockade on the firing of SNc dopaminergic neurons in vitro . ( A1 ) Extracellular recording of a DA cell in control conditions (left) and after application of 20 M nifedipine (right). ( A2 ) Same as ( A1 ) after a 80 reduction of the sodium conductance by the superfusion of 30 nM TTX. ( B ) Evolution of the mean firing rate (samples of 2 minutes) of a DA cell over time. ( C ) Mean firing frequency (N = 6) for each condition (mean sem). A simultaneous application of TTX and nifedipine affects the firing of the cells more strongly, as compared to the application of either of the two compounds alone. All experiments were performed in the presence of blockers of synaptic transmission. Note that the superfusion of the blockers produces an excitation of the neurons, which can be attributed to the block of inhibitory D2 autoreceptors. *P 0.05, **P 0.01, ***P 0.001.

    Techniques Used: In Vitro, Transmission Assay, Blocking Assay

    16) Product Images from "Anaphylatoxins Activate Ca2+, Akt/PI3-Kinase, and FOXO1/FoxP3 in the Retinal Pigment Epithelium"

    Article Title: Anaphylatoxins Activate Ca2+, Akt/PI3-Kinase, and FOXO1/FoxP3 in the Retinal Pigment Epithelium

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2017.00703

    Role of PI3-kinase and Akt in anaphylatoxin-evoked Ca 2+ transients. (A,D) Effect of the PI3-kinase blocker LY294002 (50 µM) on C3a-evoked (A) or C5a-evoked (D) Ca 2+ transients in ARPE-19 cells. (B,E) Effect of the Akt blocker API-2 (10 µM) on C3a-evoked (B) or C5a-evoked (C) Ca 2+ transients in ARPE-19 cells. (C,F) Effect of the L-type channel blocker nifedipine (10 µM) on C3a-evoked (C) or C5a-evoked (F) Ca 2+ transients in ARPE-19 cells. (G,H) Statistical comparison of blocker application effects on C3a-evoked (G) and C5a-evoked (H) Ca 2+ -transients at the peak and late phases. Anaphylatoxins were applied at concentrations of 260 nM (C3a) and 52 nM (C5a). (A–F) Black rim indicates SEM. (G,H) data are mean + SEM, number of cells as indicated in the bars from six to nine independent experiments, * p
    Figure Legend Snippet: Role of PI3-kinase and Akt in anaphylatoxin-evoked Ca 2+ transients. (A,D) Effect of the PI3-kinase blocker LY294002 (50 µM) on C3a-evoked (A) or C5a-evoked (D) Ca 2+ transients in ARPE-19 cells. (B,E) Effect of the Akt blocker API-2 (10 µM) on C3a-evoked (B) or C5a-evoked (C) Ca 2+ transients in ARPE-19 cells. (C,F) Effect of the L-type channel blocker nifedipine (10 µM) on C3a-evoked (C) or C5a-evoked (F) Ca 2+ transients in ARPE-19 cells. (G,H) Statistical comparison of blocker application effects on C3a-evoked (G) and C5a-evoked (H) Ca 2+ -transients at the peak and late phases. Anaphylatoxins were applied at concentrations of 260 nM (C3a) and 52 nM (C5a). (A–F) Black rim indicates SEM. (G,H) data are mean + SEM, number of cells as indicated in the bars from six to nine independent experiments, * p

    Techniques Used:

    17) Product Images from "Molecular basis of ancestral vertebrate electroreception"

    Article Title: Molecular basis of ancestral vertebrate electroreception

    Journal: Nature

    doi: 10.1038/nature21401

    I Cav and I K tune voltage oscillations and electroreceptive behaviors a. Representative traces showing membrane voltage-dependent oscillations at indicated membrane potentials (V m ). Scale: 5 mV, 500 ms. b. Normalized amplitude of membrane voltage oscillations (from rest, averaged over 500 ms) at indicated V m (n = 4). Overlaid normalized I Cav window current (blue trace). c. Current injection (10 pA, 5 ms at arrow) at −65 mV elicited oscillations or a sustained depolarization in the presence of TEA + (representative of n = 3). Scale bar: 5 mV, 100 ms. d. Representative V m oscillations were inhibited by TEA + or nifedipine. Scale bar: 5 mV, 100 ms. e. Average oscillation amplitude and frequency. Each circle depicts one experiment; p
    Figure Legend Snippet: I Cav and I K tune voltage oscillations and electroreceptive behaviors a. Representative traces showing membrane voltage-dependent oscillations at indicated membrane potentials (V m ). Scale: 5 mV, 500 ms. b. Normalized amplitude of membrane voltage oscillations (from rest, averaged over 500 ms) at indicated V m (n = 4). Overlaid normalized I Cav window current (blue trace). c. Current injection (10 pA, 5 ms at arrow) at −65 mV elicited oscillations or a sustained depolarization in the presence of TEA + (representative of n = 3). Scale bar: 5 mV, 100 ms. d. Representative V m oscillations were inhibited by TEA + or nifedipine. Scale bar: 5 mV, 100 ms. e. Average oscillation amplitude and frequency. Each circle depicts one experiment; p

    Techniques Used: Mass Spectrometry, Injection

    18) Product Images from "Membrane depolarization causes a direct activation of G protein-coupled receptors leading to local Ca2+ release in smooth muscle"

    Article Title: Membrane depolarization causes a direct activation of G protein-coupled receptors leading to local Ca2+ release in smooth muscle

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi: 10.1073/pnas.0813307106

    Membrane depolarization-induced local Ca 2+ release is independent of VDCCs and associated extracellular Ca 2+ influx in airway SMCs. ( A ) Application of nifedipine (Nif, 10 μM) for 5 min to inhibit VDCCs or incubation with nominally Ca 2+ -free plus
    Figure Legend Snippet: Membrane depolarization-induced local Ca 2+ release is independent of VDCCs and associated extracellular Ca 2+ influx in airway SMCs. ( A ) Application of nifedipine (Nif, 10 μM) for 5 min to inhibit VDCCs or incubation with nominally Ca 2+ -free plus

    Techniques Used: Incubation

    19) Product Images from "A Critical Role for Protein Tyrosine Phosphatase Nonreceptor Type 5 in Determining Individual Susceptibility to Develop Stress-Related Cognitive and Morphological Changes"

    Article Title: A Critical Role for Protein Tyrosine Phosphatase Nonreceptor Type 5 in Determining Individual Susceptibility to Develop Stress-Related Cognitive and Morphological Changes

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.5902-11.2012

    PTPN5 loss of function increases excitatory overload. A , Representative immunoblots and corresponding densitometric analysis showing Ca V 1.2 protein expression in hippocampal CA1 region of NS, US, or SUS rats at 1 week after stress procedure ( n = 4 in each group). B , Correlation analysis of the discrimination index in the OLM and Ca V 1.2 protein expression in the DH at 1 week after stress procedure. C , Correlation analysis of the number of dendritic spines in hippocampal CA1 pyramidal cells and Ca V 1.2 protein expression in the DH at 1 week after stress procedure. D , E , Summary of experiments showing the relative rate of cell death using the DNA fragmentation assay ( D ) or the LDH release assay ( E ) in slices from sh-DsRed-treated or sh-PTPN5-treated rats after treatment with different glutamate concentrations ( n = 5 in each group). LD 50 represents the median lethal dose. F , G , Summary of experiments showing the relative rate of cell death using the DNA fragmentation assay ( F ) or the LDH release assay ( G ) in slices from sh-DsRed-treated or sh-PTPN5-treated rats after treatment with different Bay K8644 concentrations ( n = 5 in each group). H , Schematic representation of the experimental designs for examining the stress-induced impairment of the OLM in rats receiving bilateral intra-DH injections of sh-PTPN5 before stress and nifedipine (2 mg · kg −1 · d −1 ) treatment at different time points after stress. I , Pie chart and bar graph showing the relative distribution of the OLM in rats by subtracting poststress values from prestress values at 1 week after stress procedure with nifedipine or saline treatment. The susceptibility was defined as index
    Figure Legend Snippet: PTPN5 loss of function increases excitatory overload. A , Representative immunoblots and corresponding densitometric analysis showing Ca V 1.2 protein expression in hippocampal CA1 region of NS, US, or SUS rats at 1 week after stress procedure ( n = 4 in each group). B , Correlation analysis of the discrimination index in the OLM and Ca V 1.2 protein expression in the DH at 1 week after stress procedure. C , Correlation analysis of the number of dendritic spines in hippocampal CA1 pyramidal cells and Ca V 1.2 protein expression in the DH at 1 week after stress procedure. D , E , Summary of experiments showing the relative rate of cell death using the DNA fragmentation assay ( D ) or the LDH release assay ( E ) in slices from sh-DsRed-treated or sh-PTPN5-treated rats after treatment with different glutamate concentrations ( n = 5 in each group). LD 50 represents the median lethal dose. F , G , Summary of experiments showing the relative rate of cell death using the DNA fragmentation assay ( F ) or the LDH release assay ( G ) in slices from sh-DsRed-treated or sh-PTPN5-treated rats after treatment with different Bay K8644 concentrations ( n = 5 in each group). H , Schematic representation of the experimental designs for examining the stress-induced impairment of the OLM in rats receiving bilateral intra-DH injections of sh-PTPN5 before stress and nifedipine (2 mg · kg −1 · d −1 ) treatment at different time points after stress. I , Pie chart and bar graph showing the relative distribution of the OLM in rats by subtracting poststress values from prestress values at 1 week after stress procedure with nifedipine or saline treatment. The susceptibility was defined as index

    Techniques Used: Western Blot, Expressing, Relative Rate, DNA Fragmentation Assay, Lactate Dehydrogenase Assay

    20) Product Images from "The Relationship Between Basal and Regulated Gnrhr Expression in Rodent Pituitary Gonadotrophs"

    Article Title: The Relationship Between Basal and Regulated Gnrhr Expression in Rodent Pituitary Gonadotrophs

    Journal: Molecular and cellular endocrinology

    doi: 10.1016/j.mce.2016.08.040

    The ineffectiveness of calcium, PKC, and cAMP on the regulation of Gnrhr mRNA levels in mouse LβT2 gonadotrophs. A and B, Effects of BayK 8644 and nifedipine on calcium signaling (A) and Gnrhr expression (B). C, The lack of effects of PMA on Gnrhr expressions during 1, 3, and 5 h of incubation. D, Forskolin-induced cAMP production, and the lack of effect on basal Gnrhr expression for 6 h incubation.
    Figure Legend Snippet: The ineffectiveness of calcium, PKC, and cAMP on the regulation of Gnrhr mRNA levels in mouse LβT2 gonadotrophs. A and B, Effects of BayK 8644 and nifedipine on calcium signaling (A) and Gnrhr expression (B). C, The lack of effects of PMA on Gnrhr expressions during 1, 3, and 5 h of incubation. D, Forskolin-induced cAMP production, and the lack of effect on basal Gnrhr expression for 6 h incubation.

    Techniques Used: Expressing, Incubation

    GnRH also stimulates mouse pituitary Gnrhr expression through calcium and PKC-ERK1/2 signaling pathways. A, Basal and GnRH-stimulated G nrhr expression in cultured pituitary cells from different mice strains. Asterisks indicate significant differences between pairs. B-F, Cultured pituitary cells from C57BL/6J mice. B, A time course study of GnRH-stimulated Gnrhr expression. C, The lack of effect of 10 nM GnRH on Gnrhr expression in the presence of 1 μM cetrorelix acetate, a GnRHR antagonist, and inhibition of GnRH-stimulated Gnrhr expression by U0126. D and E, Effect of BayK 8644, an L-type voltage-gated calcium channel agonist, on calcium influx (D) and Gnrhr expression (E). Notice the lack of effects of nifedipine—an L-type calcium channel antagonist—on Gnrhr expression. In calcium measurements, the identification of gonadotrophs was done by application of GnRH at the end of recording (not shown). The effects of PMA (100 nM) on Gnrhr expression (F). In all experiments Gnrhr expression was evaluated after 6 h. Experiments were performed in mouse pituitary cells 24 h after dispersion. In A, C, E, and F, asterisks indicate significant differences (P
    Figure Legend Snippet: GnRH also stimulates mouse pituitary Gnrhr expression through calcium and PKC-ERK1/2 signaling pathways. A, Basal and GnRH-stimulated G nrhr expression in cultured pituitary cells from different mice strains. Asterisks indicate significant differences between pairs. B-F, Cultured pituitary cells from C57BL/6J mice. B, A time course study of GnRH-stimulated Gnrhr expression. C, The lack of effect of 10 nM GnRH on Gnrhr expression in the presence of 1 μM cetrorelix acetate, a GnRHR antagonist, and inhibition of GnRH-stimulated Gnrhr expression by U0126. D and E, Effect of BayK 8644, an L-type voltage-gated calcium channel agonist, on calcium influx (D) and Gnrhr expression (E). Notice the lack of effects of nifedipine—an L-type calcium channel antagonist—on Gnrhr expression. In calcium measurements, the identification of gonadotrophs was done by application of GnRH at the end of recording (not shown). The effects of PMA (100 nM) on Gnrhr expression (F). In all experiments Gnrhr expression was evaluated after 6 h. Experiments were performed in mouse pituitary cells 24 h after dispersion. In A, C, E, and F, asterisks indicate significant differences (P

    Techniques Used: Expressing, Cell Culture, Mouse Assay, Inhibition

    21) Product Images from "GABA Maintains the Proliferation of Progenitors in the Developing Chick Ciliary Marginal Zone and Non-Pigmented Ciliary Epithelium"

    Article Title: GABA Maintains the Proliferation of Progenitors in the Developing Chick Ciliary Marginal Zone and Non-Pigmented Ciliary Epithelium

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0036874

    Expression of cyclin-dependent protein kinase inhibitors p27 KIP1 and p21 CIP in cultured NPE cells. mRNA levels in cultured NPE cells were analysed by qRT-PCR and normalised to β-actin and TATA box binding protein. Relative expression of (A) p27 KIP1 in control (1 µM GABA), FGF-2- (1.5 µg/ml), bicuculline- (20 µM bicuculline, 1 µM GABA), or nifedipine-treated (10 µM nifedipine, 1 µM GABA) cells. (B) Relative mRNA levels of p21 CIP in control (1 µM GABA) or bicuculline-treated cells (20 µM bicuculline, 1 µM GABA). Fixed dissociated cells were stained with the nuclear stain DAPI and an antibody against p27 KIP1 . (C) Percentage of p27 KIP1 cells in the control, FGF-2-, bicuculline- and nifedipine-treated cells. Error bars ±SD, n = 4 independent cultures. Statistical test was one-way ANOVA, Tukey's multi-comparison post hoc test; p
    Figure Legend Snippet: Expression of cyclin-dependent protein kinase inhibitors p27 KIP1 and p21 CIP in cultured NPE cells. mRNA levels in cultured NPE cells were analysed by qRT-PCR and normalised to β-actin and TATA box binding protein. Relative expression of (A) p27 KIP1 in control (1 µM GABA), FGF-2- (1.5 µg/ml), bicuculline- (20 µM bicuculline, 1 µM GABA), or nifedipine-treated (10 µM nifedipine, 1 µM GABA) cells. (B) Relative mRNA levels of p21 CIP in control (1 µM GABA) or bicuculline-treated cells (20 µM bicuculline, 1 µM GABA). Fixed dissociated cells were stained with the nuclear stain DAPI and an antibody against p27 KIP1 . (C) Percentage of p27 KIP1 cells in the control, FGF-2-, bicuculline- and nifedipine-treated cells. Error bars ±SD, n = 4 independent cultures. Statistical test was one-way ANOVA, Tukey's multi-comparison post hoc test; p

    Techniques Used: Expressing, Cell Culture, Quantitative RT-PCR, Binding Assay, Staining

    Effects of GABA A receptor and voltage-gated Ca 2+ channel inhibitors on NPE cell proliferation. Bar graphs show the relative proliferation levels of dissociated NPE cells determined by incorporation of [ 3 H]-thymidine. (A) Proliferation levels of cells treated with FGF-2 (1.5 µg/ml), bicuculline (20 µM bicuculline, 1 µM GABA), SR-95331 (50 µM SR-95531, 1 µM GABA), picrotoxin (50 µM picrotoxin, 1 µM GABA) and muscimol (50 µM muscimol, 1 µM GABA) in relation to control cells (1 µM GABA), (B) Proliferation levels of cells treated with the VGCC antagonist nifedipine (10 µM nifedipine, 1 µM GABA), KCl (20 mM, 1 µM GABA), bicuculline (20 µM, 1 µM GABA) or KCl + bicuculline (20 µM bicuculline, 20 mM KCl, 1 µM GABA) in relation to control cells (1 µM GABA). Vehicle and control for nifedipine treatment was DMSO (0.01%). Error bars ±SD, n = 4 independent cultures. Statistical test was one-way ANOVA, Tukey's multi-comparison post-hoc test; p
    Figure Legend Snippet: Effects of GABA A receptor and voltage-gated Ca 2+ channel inhibitors on NPE cell proliferation. Bar graphs show the relative proliferation levels of dissociated NPE cells determined by incorporation of [ 3 H]-thymidine. (A) Proliferation levels of cells treated with FGF-2 (1.5 µg/ml), bicuculline (20 µM bicuculline, 1 µM GABA), SR-95331 (50 µM SR-95531, 1 µM GABA), picrotoxin (50 µM picrotoxin, 1 µM GABA) and muscimol (50 µM muscimol, 1 µM GABA) in relation to control cells (1 µM GABA), (B) Proliferation levels of cells treated with the VGCC antagonist nifedipine (10 µM nifedipine, 1 µM GABA), KCl (20 mM, 1 µM GABA), bicuculline (20 µM, 1 µM GABA) or KCl + bicuculline (20 µM bicuculline, 20 mM KCl, 1 µM GABA) in relation to control cells (1 µM GABA). Vehicle and control for nifedipine treatment was DMSO (0.01%). Error bars ±SD, n = 4 independent cultures. Statistical test was one-way ANOVA, Tukey's multi-comparison post-hoc test; p

    Techniques Used:

    22) Product Images from "Hyperoxic Vasoconstriction of Human Pulmonary Arteries: A Novel Insight into Acute Ventricular Septal Defects"

    Article Title: Hyperoxic Vasoconstriction of Human Pulmonary Arteries: A Novel Insight into Acute Ventricular Septal Defects

    Journal: ISRN Cardiology

    doi: 10.1155/2013/685735

    Effect of Nifedipine on the vasoconstrictive response to hyperoxia.
    Figure Legend Snippet: Effect of Nifedipine on the vasoconstrictive response to hyperoxia.

    Techniques Used:

    23) Product Images from "Bidirectional NMDA receptor plasticity controls CA3 output and heterosynaptic metaplasticity"

    Article Title: Bidirectional NMDA receptor plasticity controls CA3 output and heterosynaptic metaplasticity

    Journal: Nature neuroscience

    doi: 10.1038/nn.3461

    Mechanistic properties of tLTP N and tLTD N a ) tLTD N requires NMDAR activation. Transient application of d–APV (25 μM) prior to induction blocked tLTD N . In all panels, representative averaged traces under each experimental condition are shown right. b ) tLTD N requires Ca 2+ influx through L–type calcium channels. Delivering the POST–PRE induction in the presence of 10 μM nifedipine abolished tLTD N c ) Pre–treatment (30 min prior to induction) and bath application of 30 μM cyclopiazonic acid (CPA) had no effect on tLTD N relative to interleaved controls. d ) Depletion of intracellular Ca 2+ stores by CPA abolished tLTP N , demonstrating the unique additional requirement of store Ca 2+ for tLTP N . Interleaved control experiments are shown in black. e ) tLTD N is blocked in the presence of 1 μM okadaic acid implicating phosphatase activity in the expression of tLTD N . f) Intracellular loading of 600 μM GDPβS abolishes tLTD N indicating that a GTP dependent process is required for tLTD N . g ) tLTD N is blocked by intracellular loading of dynamin inhibitory peptide (DIP, 50 μM) implicating dynamin dependent endocytosis in the expression of tLTD N . h ) Summary data for all experimental groups representing the mean ± s.e.m. *p
    Figure Legend Snippet: Mechanistic properties of tLTP N and tLTD N a ) tLTD N requires NMDAR activation. Transient application of d–APV (25 μM) prior to induction blocked tLTD N . In all panels, representative averaged traces under each experimental condition are shown right. b ) tLTD N requires Ca 2+ influx through L–type calcium channels. Delivering the POST–PRE induction in the presence of 10 μM nifedipine abolished tLTD N c ) Pre–treatment (30 min prior to induction) and bath application of 30 μM cyclopiazonic acid (CPA) had no effect on tLTD N relative to interleaved controls. d ) Depletion of intracellular Ca 2+ stores by CPA abolished tLTP N , demonstrating the unique additional requirement of store Ca 2+ for tLTP N . Interleaved control experiments are shown in black. e ) tLTD N is blocked in the presence of 1 μM okadaic acid implicating phosphatase activity in the expression of tLTD N . f) Intracellular loading of 600 μM GDPβS abolishes tLTD N indicating that a GTP dependent process is required for tLTD N . g ) tLTD N is blocked by intracellular loading of dynamin inhibitory peptide (DIP, 50 μM) implicating dynamin dependent endocytosis in the expression of tLTD N . h ) Summary data for all experimental groups representing the mean ± s.e.m. *p

    Techniques Used: Activation Assay, Activity Assay, Expressing

    24) Product Images from "Decreased cardiac excitability secondary to reduction of sodium current may be a significant contributor to reduced contractility in a rat model of sepsis"

    Article Title: Decreased cardiac excitability secondary to reduction of sodium current may be a significant contributor to reduced contractility in a rat model of sepsis

    Journal: Critical Care

    doi: 10.1186/cc13800

    Block of sodium channels triggers significant reduction in contractility. (a) Shown are force traces from a papillary muscle paced at 1 Hz before and after application of tetrodotoxin (TTX) and nifedipine. After each drug is washed out, contractility returns to baseline. (b) Shown is a bar graph showing the mean force at baseline, following TTX, washout of TTX (post TTX), following nifedipine, and washout of nifedipine (post Nifed) (n = 3 rats). ** P
    Figure Legend Snippet: Block of sodium channels triggers significant reduction in contractility. (a) Shown are force traces from a papillary muscle paced at 1 Hz before and after application of tetrodotoxin (TTX) and nifedipine. After each drug is washed out, contractility returns to baseline. (b) Shown is a bar graph showing the mean force at baseline, following TTX, washout of TTX (post TTX), following nifedipine, and washout of nifedipine (post Nifed) (n = 3 rats). ** P

    Techniques Used: Blocking Assay

    25) Product Images from "Plasticity of GABAA receptor diffusion dynamics at the axon initial segment"

    Article Title: Plasticity of GABAA receptor diffusion dynamics at the axon initial segment

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2014.00151

    Distal shift in AIS position and increased GABA A R lateral mobility depend on L-type VGCCs. (A) Example ankG staining from control (top), KCl (middle) and KCl + 5 μM nifedipine conditions (bottom). (B) Analysis of AIS start position. One-way ANOVA omnibus test p = 0.01. Pairwise test p -values are Bonferroni-corrected. KCl treatment caused a distal shift in AIS start position ( p
    Figure Legend Snippet: Distal shift in AIS position and increased GABA A R lateral mobility depend on L-type VGCCs. (A) Example ankG staining from control (top), KCl (middle) and KCl + 5 μM nifedipine conditions (bottom). (B) Analysis of AIS start position. One-way ANOVA omnibus test p = 0.01. Pairwise test p -values are Bonferroni-corrected. KCl treatment caused a distal shift in AIS start position ( p

    Techniques Used: Staining

    26) Product Images from "Molecular tuning of electroreception in sharks and skates"

    Article Title: Molecular tuning of electroreception in sharks and skates

    Journal: Nature

    doi: 10.1038/s41586-018-0160-9

    Shark I CaV properties a. Isolated shark ampullary organs with attached canals and nerve fibers ( Top, scale 100μm) and a representative electrosensory cell patch clamp experiment ( Bottom, scale 10μm). b. I Cav currents elicited by increasing voltage pulses from −100mV ( Left ) and average current–voltage ( I – V ) relationship ( Right , n = 7). c. I Cav exhibited an L-type Ca V pharmacological profile: Peak currents were regulated by Bay K (agonist), Cd 2+ (blocker), nifedipine (antagonist), but not mibefradil (T-type antagonist). n = 4. p
    Figure Legend Snippet: Shark I CaV properties a. Isolated shark ampullary organs with attached canals and nerve fibers ( Top, scale 100μm) and a representative electrosensory cell patch clamp experiment ( Bottom, scale 10μm). b. I Cav currents elicited by increasing voltage pulses from −100mV ( Left ) and average current–voltage ( I – V ) relationship ( Right , n = 7). c. I Cav exhibited an L-type Ca V pharmacological profile: Peak currents were regulated by Bay K (agonist), Cd 2+ (blocker), nifedipine (antagonist), but not mibefradil (T-type antagonist). n = 4. p

    Techniques Used: Isolation, Patch Clamp

    27) Product Images from "Saikosaponin d causes apoptotic death of cultured neocortical neurons by increasing membrane permeability and elevating intracellular Ca2+ concentration"

    Article Title: Saikosaponin d causes apoptotic death of cultured neocortical neurons by increasing membrane permeability and elevating intracellular Ca2+ concentration

    Journal: Neurotoxicology

    doi: 10.1016/j.neuro.2018.11.006

    Major Ca 2+ influx routes are not involved in SSd-elevated [Ca 2+ ] i . Representative traces of nifedipine (A), KB-R7943 (B), MK-801 (C), CNQX (D), SB366791 (E), and RR (F) effect on SSd-stimulated [Ca 2+ ] i elevation as a function of time. This experiment was performed in three independent cultures, each in triplicates with similar results. The first arrow indicates the addition of Veh or inhibitor and the second arrow indicates the addition of Veh or SSd (3 µM). Veh indicates 0.1% DMSO.
    Figure Legend Snippet: Major Ca 2+ influx routes are not involved in SSd-elevated [Ca 2+ ] i . Representative traces of nifedipine (A), KB-R7943 (B), MK-801 (C), CNQX (D), SB366791 (E), and RR (F) effect on SSd-stimulated [Ca 2+ ] i elevation as a function of time. This experiment was performed in three independent cultures, each in triplicates with similar results. The first arrow indicates the addition of Veh or inhibitor and the second arrow indicates the addition of Veh or SSd (3 µM). Veh indicates 0.1% DMSO.

    Techniques Used:

    28) Product Images from "Molecular tuning of electroreception in sharks and skates"

    Article Title: Molecular tuning of electroreception in sharks and skates

    Journal: Nature

    doi: 10.1038/s41586-018-0160-9

    Shark I CaV properties a. Isolated shark ampullary organs with attached canals and nerve fibers ( Top, scale 100μm) and a representative electrosensory cell patch clamp experiment ( Bottom, scale 10μm). b. I Cav currents elicited by increasing voltage pulses from −100mV ( Left ) and average current–voltage ( I – V ) relationship ( Right , n = 7). c. I Cav exhibited an L-type Ca V pharmacological profile: Peak currents were regulated by Bay K (agonist), Cd 2+ (blocker), nifedipine (antagonist), but not mibefradil (T-type antagonist). n = 4. p
    Figure Legend Snippet: Shark I CaV properties a. Isolated shark ampullary organs with attached canals and nerve fibers ( Top, scale 100μm) and a representative electrosensory cell patch clamp experiment ( Bottom, scale 10μm). b. I Cav currents elicited by increasing voltage pulses from −100mV ( Left ) and average current–voltage ( I – V ) relationship ( Right , n = 7). c. I Cav exhibited an L-type Ca V pharmacological profile: Peak currents were regulated by Bay K (agonist), Cd 2+ (blocker), nifedipine (antagonist), but not mibefradil (T-type antagonist). n = 4. p

    Techniques Used: Isolation, Patch Clamp

    29) Product Images from "Matrix Metalloprotease-1 and Elastase Are Novel Uterotonic Agents Acting Through Protease-Activated Receptor 1"

    Article Title: Matrix Metalloprotease-1 and Elastase Are Novel Uterotonic Agents Acting Through Protease-Activated Receptor 1

    Journal: Reproductive Sciences

    doi: 10.1177/1933719117732162

    Summary of matrix metalloproteinase-1 (MMP-1) and elastase results. Myometrial uterine contractility induced by MMP-1 (n = 13) was prevented by protease-activated receptor 1 (PAR-1) inhibition (n = 4) or inositol trisphosphate receptor (IP 3 R) blockade (n = 5; A). Elastase produced a dose-dependent increase in uterine contractility (B, n = 4). Elastase-induced increases in uterine contractility (n = 15) were prevented by inhibition of PAR-1 (n = 10 low dose, n = 3 high dose), IP 3 R blockade (n = 7) and nifedipine (n = 6) but not by indomethacin (n = 7; C). *** P
    Figure Legend Snippet: Summary of matrix metalloproteinase-1 (MMP-1) and elastase results. Myometrial uterine contractility induced by MMP-1 (n = 13) was prevented by protease-activated receptor 1 (PAR-1) inhibition (n = 4) or inositol trisphosphate receptor (IP 3 R) blockade (n = 5; A). Elastase produced a dose-dependent increase in uterine contractility (B, n = 4). Elastase-induced increases in uterine contractility (n = 15) were prevented by inhibition of PAR-1 (n = 10 low dose, n = 3 high dose), IP 3 R blockade (n = 7) and nifedipine (n = 6) but not by indomethacin (n = 7; C). *** P

    Techniques Used: Inhibition, Produced

    30) Product Images from "Store-Operated Calcium Entry via STIM1 Contributes to MRGPRX2 Induced Mast Cell Functions"

    Article Title: Store-Operated Calcium Entry via STIM1 Contributes to MRGPRX2 Induced Mast Cell Functions

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2019.03143

    Mast cell degranulation and cytokine production are inhibited by SOCE antagonists. (A–D) CST-14-induced degranulation in LAD2 mast cells as quantified by β-hexosaminidase release in the presence of (A) YM, (B) SKF, (C) Nifedipine, and (D) A425619 is shown. Values are plotted as percentages of total cell lysate β-hexosaminidase content. (E,F) Bar graphs show IL-2 and TNF-α production by LAD2 mast cells stimulated with the indicated concentrations of CST-14. Data shown are mean ± S.E. of 3–5 independent experiments. Statistical significance was determined by two-way ANOVA. * p
    Figure Legend Snippet: Mast cell degranulation and cytokine production are inhibited by SOCE antagonists. (A–D) CST-14-induced degranulation in LAD2 mast cells as quantified by β-hexosaminidase release in the presence of (A) YM, (B) SKF, (C) Nifedipine, and (D) A425619 is shown. Values are plotted as percentages of total cell lysate β-hexosaminidase content. (E,F) Bar graphs show IL-2 and TNF-α production by LAD2 mast cells stimulated with the indicated concentrations of CST-14. Data shown are mean ± S.E. of 3–5 independent experiments. Statistical significance was determined by two-way ANOVA. * p

    Techniques Used:

    MRGPRX2-induced Ca 2+ mobilization is reduced by SOCE inhibition. (A–D) Intracellular Ca 2+ mobilization in LAD2 human mast cells was determined following incubation with varying concentrations of (A) YM, (B) SKF, (C) Nifedipine, and (D) A425619 for 30 min. Cells were treated with half log doses of the MRGPRX2 agonist cortistatin-14 (CST-14), and changes in fluorescence intensities were recorded for 120 s. Data are plotted as the change in fluorescence [minimum (Min) subtracted from maximum (Max) value] normalized to the maximal change in fluorescence. (E) Traces show SOCE assay following SKF pretreatment. LAD2 cells were suspended in Ca 2+ -free buffer and stimulated with 300 nM CST-14. CaCl 2 (Ca 2+ ) at a final concentration of 2 mM was added to the cells at the indicated timepoint. Plotted curves are the average (mean ± S.E.) of 3–6 independent experiments. Data are analyzed with two-way ANOVA. * p
    Figure Legend Snippet: MRGPRX2-induced Ca 2+ mobilization is reduced by SOCE inhibition. (A–D) Intracellular Ca 2+ mobilization in LAD2 human mast cells was determined following incubation with varying concentrations of (A) YM, (B) SKF, (C) Nifedipine, and (D) A425619 for 30 min. Cells were treated with half log doses of the MRGPRX2 agonist cortistatin-14 (CST-14), and changes in fluorescence intensities were recorded for 120 s. Data are plotted as the change in fluorescence [minimum (Min) subtracted from maximum (Max) value] normalized to the maximal change in fluorescence. (E) Traces show SOCE assay following SKF pretreatment. LAD2 cells were suspended in Ca 2+ -free buffer and stimulated with 300 nM CST-14. CaCl 2 (Ca 2+ ) at a final concentration of 2 mM was added to the cells at the indicated timepoint. Plotted curves are the average (mean ± S.E.) of 3–6 independent experiments. Data are analyzed with two-way ANOVA. * p

    Techniques Used: Inhibition, Incubation, Fluorescence, Concentration Assay

    31) Product Images from "Activation of transient receptor potential ankyrin 1 induces CGRP release from spinal cord synaptosomes. Activation of transient receptor potential ankyrin 1 induces CGRP release from spinal cord synaptosomes"

    Article Title: Activation of transient receptor potential ankyrin 1 induces CGRP release from spinal cord synaptosomes. Activation of transient receptor potential ankyrin 1 induces CGRP release from spinal cord synaptosomes

    Journal: Pharmacology Research & Perspectives

    doi: 10.1002/prp2.191

    Blocking voltage‐gated calcium channels ( VGCC s) inhibits depolarization‐evoked calcitonin gene‐related peptide ( CGRP ) release but has no effect on cinnamaldehyde‐induced CGRP release. The effect of VGCC ‐blockade on 100 μ mol/L cinnamaldehyde‐induced CGRP release from rat dorsal spinal cord homogenate was examined. (A) 100 μ mol/L cinnamaldehyde‐induced CGRP release (control) was not significantly affected in the presence of 5 μ mol/L nifedipine, 200 nmol/L ω ‐conotoxin MVIIC ( CTX ) or 10 μ mol/L mibefradil dihydrochloride. Columns represent mean ± SEM ( ANOVA ; n = 4 experiments). (B) Moreover, 100 μ mol/L cinnamaldehyde‐induced CGRP release (control) was not significantly altered in the presence of 1 μ mol/L ω ‐conotoxin MVIIC ( CTX ) or a cocktail of VGCC blockers (containing 5 μ mol/L nifidepine, 1 μ mol/L ω ‐conotoxin MVIIC and 10 μ mol/L mibefradil dihydrochloride). Data are normalized to 40 mmol/L KC l‐induced release. Columns represent mean ± SEM ( ANOVA ; n = 3 experiments). (C) The effect of VGCC ‐blockade on depolarization‐induced (40 mmol/L KC l) CGRP release from rat dorsal spinal cord homogenate was also examined. 40 mmol/L KC l evoked CGRP release which was significantly decreased in the presence of the t‐type VGCC blocker, mibefradil dihydrochloride (10 μ mol/L) and a cocktail of VGCC inhibitors (containing 5 μ mol/L nifidepine, 1 μ mol/L ω ‐conotoxin MVIIC and 10 μ mol/L mibefradil dihydrochloride). There was a trend for homogenate treated with 1 μ mol/L ω ‐conotoxin MVIIC ( CTX ) to exhibit a reduced release to 40 mmol/L KC l although this was not significant. Treatment with 5 μ mol/L nifedipine and 200 nmol/L ω ‐conotoxin MVIIC had no effect on KC l‐induced release. Data is normalized to 40 mmol/L KC l‐induced release (control). Columns represent mean ± SEM (*** P
    Figure Legend Snippet: Blocking voltage‐gated calcium channels ( VGCC s) inhibits depolarization‐evoked calcitonin gene‐related peptide ( CGRP ) release but has no effect on cinnamaldehyde‐induced CGRP release. The effect of VGCC ‐blockade on 100 μ mol/L cinnamaldehyde‐induced CGRP release from rat dorsal spinal cord homogenate was examined. (A) 100 μ mol/L cinnamaldehyde‐induced CGRP release (control) was not significantly affected in the presence of 5 μ mol/L nifedipine, 200 nmol/L ω ‐conotoxin MVIIC ( CTX ) or 10 μ mol/L mibefradil dihydrochloride. Columns represent mean ± SEM ( ANOVA ; n = 4 experiments). (B) Moreover, 100 μ mol/L cinnamaldehyde‐induced CGRP release (control) was not significantly altered in the presence of 1 μ mol/L ω ‐conotoxin MVIIC ( CTX ) or a cocktail of VGCC blockers (containing 5 μ mol/L nifidepine, 1 μ mol/L ω ‐conotoxin MVIIC and 10 μ mol/L mibefradil dihydrochloride). Data are normalized to 40 mmol/L KC l‐induced release. Columns represent mean ± SEM ( ANOVA ; n = 3 experiments). (C) The effect of VGCC ‐blockade on depolarization‐induced (40 mmol/L KC l) CGRP release from rat dorsal spinal cord homogenate was also examined. 40 mmol/L KC l evoked CGRP release which was significantly decreased in the presence of the t‐type VGCC blocker, mibefradil dihydrochloride (10 μ mol/L) and a cocktail of VGCC inhibitors (containing 5 μ mol/L nifidepine, 1 μ mol/L ω ‐conotoxin MVIIC and 10 μ mol/L mibefradil dihydrochloride). There was a trend for homogenate treated with 1 μ mol/L ω ‐conotoxin MVIIC ( CTX ) to exhibit a reduced release to 40 mmol/L KC l although this was not significant. Treatment with 5 μ mol/L nifedipine and 200 nmol/L ω ‐conotoxin MVIIC had no effect on KC l‐induced release. Data is normalized to 40 mmol/L KC l‐induced release (control). Columns represent mean ± SEM (*** P

    Techniques Used: Blocking Assay

    32) Product Images from "The effect of sphingosine-1-phosphate on colonic smooth muscle contractility: Modulation by TNBS-induced colitis"

    Article Title: The effect of sphingosine-1-phosphate on colonic smooth muscle contractility: Modulation by TNBS-induced colitis

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0170792

    The Role of calcium and calcium sensitization pathways in S1P induced contraction in control and colitic colon. Colonic segments from control (n = 3–6) and colitic (n = 3–7) rats were equilibrated in Krebs solution for 30 min and contracted twice with KCL with consecutive washes after the maximal contraction was reached. Tissues were then preincubated with L-type calcium channel blocker (nifedipine, 1μM) or SERCA antagonist (thapsigargin, 10μM) (A) or with PKC antagonist (GF 102903x, 1μM), ROCK inhibitor (Y-27632, 10μM) or inhibitor cocktails (B) for 30 min before the addition of S1P (40μM). Data is mean ± SEM of S1P induced contraction expressed relative to the second KCl-induced contraction, * P
    Figure Legend Snippet: The Role of calcium and calcium sensitization pathways in S1P induced contraction in control and colitic colon. Colonic segments from control (n = 3–6) and colitic (n = 3–7) rats were equilibrated in Krebs solution for 30 min and contracted twice with KCL with consecutive washes after the maximal contraction was reached. Tissues were then preincubated with L-type calcium channel blocker (nifedipine, 1μM) or SERCA antagonist (thapsigargin, 10μM) (A) or with PKC antagonist (GF 102903x, 1μM), ROCK inhibitor (Y-27632, 10μM) or inhibitor cocktails (B) for 30 min before the addition of S1P (40μM). Data is mean ± SEM of S1P induced contraction expressed relative to the second KCl-induced contraction, * P

    Techniques Used:

    33) Product Images from "Exercise induces hippocampal BDNF through a PGC-1α/FNDC5 pathway"

    Article Title: Exercise induces hippocampal BDNF through a PGC-1α/FNDC5 pathway

    Journal: Cell metabolism

    doi: 10.1016/j.cmet.2013.09.008

    Neuronal Fndc5 gene expression is regulated by a PGC-1α (A) Primary cortical neurons at DIV 7 were treated with either forskolin (10 μM), a stimulator intracellular cAMP levels, or vehicle for overnight. (B) Primary cortical neurons at DIV 7 were treated with nifedipine (5 μM), a L-type calcium channel blocker, or vehicle for overnight. (C) Primary cortical neurons at DIV 7 were transduced with either PGC-1α or GFP adenovirus and harvested 48 hrs later. (D) Primary cortical neurons at DIV 5 were transduced with lentivirus carrying the specified shRNA hairpins against Pgc1a or luciferase (Luc) as control and were harvested four days later. (E) Cortices were harvested from either male five months old Pgc1a KO ( Pgc1a −/− ) or wild type mice ( Pgc1a +/+ .
    Figure Legend Snippet: Neuronal Fndc5 gene expression is regulated by a PGC-1α (A) Primary cortical neurons at DIV 7 were treated with either forskolin (10 μM), a stimulator intracellular cAMP levels, or vehicle for overnight. (B) Primary cortical neurons at DIV 7 were treated with nifedipine (5 μM), a L-type calcium channel blocker, or vehicle for overnight. (C) Primary cortical neurons at DIV 7 were transduced with either PGC-1α or GFP adenovirus and harvested 48 hrs later. (D) Primary cortical neurons at DIV 5 were transduced with lentivirus carrying the specified shRNA hairpins against Pgc1a or luciferase (Luc) as control and were harvested four days later. (E) Cortices were harvested from either male five months old Pgc1a KO ( Pgc1a −/− ) or wild type mice ( Pgc1a +/+ .

    Techniques Used: Expressing, Pyrolysis Gas Chromatography, Transduction, shRNA, Luciferase, Mouse Assay

    34) Product Images from "Non-Hebbian Synaptic Plasticity Induced by Repetitive Postsynaptic Action Potentials"

    Article Title: Non-Hebbian Synaptic Plasticity Induced by Repetitive Postsynaptic Action Potentials

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.5881-08.2009

    Pharmacological characterization of depolarizing pulse-induced LTP. A , Depolarizing pulse (arrow)-induced LTP in the presence of nifedipine, an L-VDCC blocker (filled circles; n = 9), and DMSO alone (open circles; n = 8). B , Depolarizing pulse (arrow)-induced LTP in the presence of KN-93, a CaMKII inhibitor (filled circles; n = 14), and KN-92, an inactive analog of KN-93 (open circles; n = 11). C , Depolarizing pulse (arrow)-induced LTP in the presence (filled circles; n = 10) and absence (open circles; n = 7) of MPEP, an mGluR5 antagonist.
    Figure Legend Snippet: Pharmacological characterization of depolarizing pulse-induced LTP. A , Depolarizing pulse (arrow)-induced LTP in the presence of nifedipine, an L-VDCC blocker (filled circles; n = 9), and DMSO alone (open circles; n = 8). B , Depolarizing pulse (arrow)-induced LTP in the presence of KN-93, a CaMKII inhibitor (filled circles; n = 14), and KN-92, an inactive analog of KN-93 (open circles; n = 11). C , Depolarizing pulse (arrow)-induced LTP in the presence (filled circles; n = 10) and absence (open circles; n = 7) of MPEP, an mGluR5 antagonist.

    Techniques Used:

    35) Product Images from "Acetylcholine synergizes with netrin-1 to drive persistent firing in the entorhinal cortex"

    Article Title: Acetylcholine synergizes with netrin-1 to drive persistent firing in the entorhinal cortex

    Journal: bioRxiv

    doi: 10.1101/2020.07.08.194274

    Netrin-1 induces DCC-dependent increases in [Ca2+]i in cortical neurons. A-F. Group data show that netrin-1 (2.7 nM) alone induces a long-lasting increase in fura-2 ratio (A) that requires extracellular Ca 2+ (B), expression of netrin-1 receptor DCC (C), and is blocked by 2-APB (D; 100 μM), flufenamic acid (E; 100 μM), and nifedipine (F; 10 μM).
    Figure Legend Snippet: Netrin-1 induces DCC-dependent increases in [Ca2+]i in cortical neurons. A-F. Group data show that netrin-1 (2.7 nM) alone induces a long-lasting increase in fura-2 ratio (A) that requires extracellular Ca 2+ (B), expression of netrin-1 receptor DCC (C), and is blocked by 2-APB (D; 100 μM), flufenamic acid (E; 100 μM), and nifedipine (F; 10 μM).

    Techniques Used: Droplet Countercurrent Chromatography, Expressing

    Netrin-1 induces an inward current that is dependent on netrin-1 receptor DCC but not L-type Ca 2+ channels. Current responses in a layer V entorhinal neuron to a series of hyperpolarizing and depolarizing voltage steps prior to (black) and following bath application of netrin-1 (2.7 nM, blue) in the presence of nifedipine (A; 10 μM), and conditional deletion of DCC (D; DCC cKO). B, E. Group data show current subtraction of responses in the presence of netrin-1 from baseline values and holding current at −70 mV in the presence of nifedipine (B-C) or DCC cKO (E-F).
    Figure Legend Snippet: Netrin-1 induces an inward current that is dependent on netrin-1 receptor DCC but not L-type Ca 2+ channels. Current responses in a layer V entorhinal neuron to a series of hyperpolarizing and depolarizing voltage steps prior to (black) and following bath application of netrin-1 (2.7 nM, blue) in the presence of nifedipine (A; 10 μM), and conditional deletion of DCC (D; DCC cKO). B, E. Group data show current subtraction of responses in the presence of netrin-1 from baseline values and holding current at −70 mV in the presence of nifedipine (B-C) or DCC cKO (E-F).

    Techniques Used: Droplet Countercurrent Chromatography

    36) Product Images from "Neuronal Expression of the Human Neuropeptide S Receptor NPSR1 Identifies NPS-Induced Calcium Signaling Pathways"

    Article Title: Neuronal Expression of the Human Neuropeptide S Receptor NPSR1 Identifies NPS-Induced Calcium Signaling Pathways

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0117319

    SOCE blockers inhibit the generation of the slow, extracellular component of NPSR1-mediated calcium signals. (A) Mean fluorescence values calculated from 103 NPSR1-expressing neurons recorded in the presence of ML-9 [50 μM]. (B) Mean fluorescence values of 127 cells treated with SKF96365 [15 μM]. (C) Overlay of mean fluorescence values from 229 cells recorded under control conditions, i.e. extracellular solution supplemented with 3 mM CaCl 2 (black, see also Fig. 2B ), 103 neurons recorded in presence of ML-9 (grey, see also Fig. 7A ), 127 cells treated with SKF96365 (empty circles, see also Fig. 7B ), and 65 neurons recorded under calcium-depleted conditions (empty squares, see Fig. 6B ). (D) Statistical analysis of the data shown in (C). The response amplitude has been integrated over time and averaged for different experimental conditions as indicated. (E) Overlay of mean fluorescence of 15 cells treated with NPS and ML-9 [100μM] as indicated (grey) and 207 cells measured under control conditions (black). (F) Normalized mean fluorescence values from 148 neurons expressing NPSR1 from a first application of NPS and a consecutive second application of NPS in presence of Mibefradil [4 μM], Nifedipine [5 μM] and Conotoxin MVIIC [250 nM]. Standard deviations have been omitted for clarification in (C) and (E). Calcium signals were evoked with 500 nM NPS as indicated.
    Figure Legend Snippet: SOCE blockers inhibit the generation of the slow, extracellular component of NPSR1-mediated calcium signals. (A) Mean fluorescence values calculated from 103 NPSR1-expressing neurons recorded in the presence of ML-9 [50 μM]. (B) Mean fluorescence values of 127 cells treated with SKF96365 [15 μM]. (C) Overlay of mean fluorescence values from 229 cells recorded under control conditions, i.e. extracellular solution supplemented with 3 mM CaCl 2 (black, see also Fig. 2B ), 103 neurons recorded in presence of ML-9 (grey, see also Fig. 7A ), 127 cells treated with SKF96365 (empty circles, see also Fig. 7B ), and 65 neurons recorded under calcium-depleted conditions (empty squares, see Fig. 6B ). (D) Statistical analysis of the data shown in (C). The response amplitude has been integrated over time and averaged for different experimental conditions as indicated. (E) Overlay of mean fluorescence of 15 cells treated with NPS and ML-9 [100μM] as indicated (grey) and 207 cells measured under control conditions (black). (F) Normalized mean fluorescence values from 148 neurons expressing NPSR1 from a first application of NPS and a consecutive second application of NPS in presence of Mibefradil [4 μM], Nifedipine [5 μM] and Conotoxin MVIIC [250 nM]. Standard deviations have been omitted for clarification in (C) and (E). Calcium signals were evoked with 500 nM NPS as indicated.

    Techniques Used: Fluorescence, Expressing, Clarification Assay

    37) Product Images from "Stimulation of GABA-Induced Ca2+ Influx Enhances Maturation of Human Induced Pluripotent Stem Cell-Derived Neurons"

    Article Title: Stimulation of GABA-Induced Ca2+ Influx Enhances Maturation of Human Induced Pluripotent Stem Cell-Derived Neurons

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0081031

    Effect of ACM on functional expression of voltage-activated Ca 2+ channels. A. Mean traces of the ratio of intensity (I 340 /I 380 ) from fura-2 Ca 2+ imaging for control medium (solid line) and ACM-treated (dashed line) cells at week 1. Ca 2+ influx was evoked using 50mM K + solution (High K + ) to depolarise the neurons. To measure the influence of different sub-types of voltage activated Ca 2+ channel on the depolarisation-evoked peak as a whole (the sum of the voltage activated Ca 2+ influx) antagonists of specific channels were added to the High K + solution: 10µM nifedipine (L-type Ca 2+ channels), 100nM conotoxin (N-type Ca 2+ channels), 100nM agatoxin (P/Q- type Ca 2+ channels) and 100nM SNX482 (R-type Ca 2+ channels). B. Bar graph comparing the proportion (%) of neurons which showed significant ( > 5%) inhibition by each antagonist for control medium- and ACM-treated cells at week 1, compared by chi 2 tests. ***P
    Figure Legend Snippet: Effect of ACM on functional expression of voltage-activated Ca 2+ channels. A. Mean traces of the ratio of intensity (I 340 /I 380 ) from fura-2 Ca 2+ imaging for control medium (solid line) and ACM-treated (dashed line) cells at week 1. Ca 2+ influx was evoked using 50mM K + solution (High K + ) to depolarise the neurons. To measure the influence of different sub-types of voltage activated Ca 2+ channel on the depolarisation-evoked peak as a whole (the sum of the voltage activated Ca 2+ influx) antagonists of specific channels were added to the High K + solution: 10µM nifedipine (L-type Ca 2+ channels), 100nM conotoxin (N-type Ca 2+ channels), 100nM agatoxin (P/Q- type Ca 2+ channels) and 100nM SNX482 (R-type Ca 2+ channels). B. Bar graph comparing the proportion (%) of neurons which showed significant ( > 5%) inhibition by each antagonist for control medium- and ACM-treated cells at week 1, compared by chi 2 tests. ***P

    Techniques Used: Functional Assay, Expressing, Imaging, Inhibition

    The effects of manipulating Ca 2+ and GABA signaling in the culture medium. Bar graphs comparing the proportion of cells firing sAPs (A) and mean V m (B) following 3 weeks of differentiation in ACM alone, or ACM with 10µM bicuculline (a GABA A antagonist), with 2 µM nifedipine (an L-type Ca 2+ channel antagonist), with 100 nM conotoxin (a N-type Ca 2+ channel toxin) or with 100 nM SNX482 (an R- type Ca 2+ channel toxin). Chi 2 tests were performed comparing the ACM with each toxin against ACM alone. ± P
    Figure Legend Snippet: The effects of manipulating Ca 2+ and GABA signaling in the culture medium. Bar graphs comparing the proportion of cells firing sAPs (A) and mean V m (B) following 3 weeks of differentiation in ACM alone, or ACM with 10µM bicuculline (a GABA A antagonist), with 2 µM nifedipine (an L-type Ca 2+ channel antagonist), with 100 nM conotoxin (a N-type Ca 2+ channel toxin) or with 100 nM SNX482 (an R- type Ca 2+ channel toxin). Chi 2 tests were performed comparing the ACM with each toxin against ACM alone. ± P

    Techniques Used:

    Manipulation of GABA A and Ca 2+ currents in high Ca 2+ medium: effects and functional rescue. Bar graph comparing the proportion of cells firing sAPs (A) and mean V m (B) at week 2 when treated with control medium (0.6mM Ca 2+ ), high Ca 2+ medium (1.8mM Ca 2+ ) and high Ca 2+ medium with 10µM bicuculline, with 2µM nifedipine and with 100nM conotoxin and, with 100nM agatoxin (a potent P/Q- type Ca 2+ channel toxin). Chi 2 tests were performed to compare the high Ca 2+ medium with each toxin against high Ca 2+ medium alone. ±P
    Figure Legend Snippet: Manipulation of GABA A and Ca 2+ currents in high Ca 2+ medium: effects and functional rescue. Bar graph comparing the proportion of cells firing sAPs (A) and mean V m (B) at week 2 when treated with control medium (0.6mM Ca 2+ ), high Ca 2+ medium (1.8mM Ca 2+ ) and high Ca 2+ medium with 10µM bicuculline, with 2µM nifedipine and with 100nM conotoxin and, with 100nM agatoxin (a potent P/Q- type Ca 2+ channel toxin). Chi 2 tests were performed to compare the high Ca 2+ medium with each toxin against high Ca 2+ medium alone. ±P

    Techniques Used: Functional Assay

    38) Product Images from "The tobacco-specific carcinogen-operated calcium channel promotes lung tumorigenesis via IGF2 exocytosis in lung epithelial cells"

    Article Title: The tobacco-specific carcinogen-operated calcium channel promotes lung tumorigenesis via IGF2 exocytosis in lung epithelial cells

    Journal: Nature Communications

    doi: 10.1038/ncomms12961

    NNK-mediated increase in intracellular Ca 2+ is important for IGF2 secretion and IGF-1R activation. ( a ) BEAS-2B/GFP-IGF2 cells were stimulated with NNK for 15 min after pretreatment with the mecamylamine (MCA) for 3 h. IGF-1R phosphorylation in WCL or IGF2 secretion in the CM were determined by western blot (WB) analysis. ( b , f ) BEAS-2B/GFP-IGF2 cells were transfected with indicated siRNA, and then stimulated with NNK for 15 min. IGF-1R phosphorylation in WCL or IGF2 secretion in the CM were subjected to WB analysis. ( c , d ) HBEL/p53i cells were treated with ionomycin (Iono) or thapsigargin (Thapsi) for 15 min ( c ) or incubated with indicated concentration of Ca 2+ and NNK for 15 min ( d ). Activation of IGF-1R or Akt was determined by WB analysis. ( e , g ) HBEL/p53i or BEAS-2B/GFP-IGF2 cells were stimulated with NNK for 15 min after pretreatment with the indicated inhibitors for 3 h. IGF-1R phosphorylation in WCL or IGF2 secretion in CM were subjected to WB analysis. BAP: BAPTA-AM; Amlo: amlodipine; Nife: nifedipine. ( h ) Time-lapse imaging analysis for GFP-IGF2 secretion from BEAS-2B/GFP-IGF2 cells. Cells were pretreated with amlodipine (Amlo) or nifedipine (Nife) for 3 h and further stimulated with NNK. White arrows indicate secreted GFP-IGF2. Right: secreted GFP-IGF2 out of 25 BEAS-2B cells stimulated with NNK in the presence or absence of indicated inhibitors at 30 min after NNK treatment was quantified using Harmony high content imaging and analysis software. Data are presented as the mean±s.d. *** P
    Figure Legend Snippet: NNK-mediated increase in intracellular Ca 2+ is important for IGF2 secretion and IGF-1R activation. ( a ) BEAS-2B/GFP-IGF2 cells were stimulated with NNK for 15 min after pretreatment with the mecamylamine (MCA) for 3 h. IGF-1R phosphorylation in WCL or IGF2 secretion in the CM were determined by western blot (WB) analysis. ( b , f ) BEAS-2B/GFP-IGF2 cells were transfected with indicated siRNA, and then stimulated with NNK for 15 min. IGF-1R phosphorylation in WCL or IGF2 secretion in the CM were subjected to WB analysis. ( c , d ) HBEL/p53i cells were treated with ionomycin (Iono) or thapsigargin (Thapsi) for 15 min ( c ) or incubated with indicated concentration of Ca 2+ and NNK for 15 min ( d ). Activation of IGF-1R or Akt was determined by WB analysis. ( e , g ) HBEL/p53i or BEAS-2B/GFP-IGF2 cells were stimulated with NNK for 15 min after pretreatment with the indicated inhibitors for 3 h. IGF-1R phosphorylation in WCL or IGF2 secretion in CM were subjected to WB analysis. BAP: BAPTA-AM; Amlo: amlodipine; Nife: nifedipine. ( h ) Time-lapse imaging analysis for GFP-IGF2 secretion from BEAS-2B/GFP-IGF2 cells. Cells were pretreated with amlodipine (Amlo) or nifedipine (Nife) for 3 h and further stimulated with NNK. White arrows indicate secreted GFP-IGF2. Right: secreted GFP-IGF2 out of 25 BEAS-2B cells stimulated with NNK in the presence or absence of indicated inhibitors at 30 min after NNK treatment was quantified using Harmony high content imaging and analysis software. Data are presented as the mean±s.d. *** P

    Techniques Used: Activation Assay, Western Blot, Transfection, Incubation, Concentration Assay, Imaging, Software

    Suppression of NNK-induced acquisition of transformed phenotypes in vitro and lung tumour formation in vivo by blockade of Ca 2+ influx. ( a – c ) Anchorage-dependent colony formation ( n =3, mean±s.d.) ( a ), cell viability ( n =3, mean±s.d.) ( b ), and anchorage-independent colony formation ( n =4, mean±s.d.) ( c ) of BEAS-2B cells treated with NNK in combination with BAPTA-AM (BAP), mecamylamine (MCA), nifedipine (Nife), or amlodipine (Amlo). * P
    Figure Legend Snippet: Suppression of NNK-induced acquisition of transformed phenotypes in vitro and lung tumour formation in vivo by blockade of Ca 2+ influx. ( a – c ) Anchorage-dependent colony formation ( n =3, mean±s.d.) ( a ), cell viability ( n =3, mean±s.d.) ( b ), and anchorage-independent colony formation ( n =4, mean±s.d.) ( c ) of BEAS-2B cells treated with NNK in combination with BAPTA-AM (BAP), mecamylamine (MCA), nifedipine (Nife), or amlodipine (Amlo). * P

    Techniques Used: Transformation Assay, In Vitro, In Vivo

    39) Product Images from "Multiple excitatory actions of orexins upon thalamo-cortical neurons in dorsal lateral geniculate nucleus - implications for vision modulation by arousal"

    Article Title: Multiple excitatory actions of orexins upon thalamo-cortical neurons in dorsal lateral geniculate nucleus - implications for vision modulation by arousal

    Journal: Scientific Reports

    doi: 10.1038/s41598-017-08202-8

    In DLG TC neurons, OXA evokes calcium influx through voltage-gated calcium channels. ( A , B ) Application of OXA (200 nM, red bars) produced a depolarisation that was heavily reduced by NiCl 2 (10 mM, light grey bar) and CdCl 2 (1 mM, grey bar). ( C ) Mibefradil (Mib, 30 μM, dark grey bar), reduced OXA-evoked depolarisation but in a less effective manner. ( D ) Nifedipine (Nif, 1 mM, black bar) also caused a reduction in the OXA effect. Responses to OXA (in%) in the presence of the blockers mentioned above are summarised as a bar graph ( O ). ( E , H , K ) Electrophysiological tests to elucidate calcium conductances were applied under control conditions (in TTX) and during the maximal response to OXA (200 nM). ( E ) Low voltage steps were used to evoke T-type calcium currents (I T ). ( F , G ) Application of OXA enhanced the amplitude of I T (in red). ( H ) In order to evoke HVA calcium currents, high voltage steps were used. ( I ) OXA caused the potentiation of HVA calcium spikes and a shift in their voltage dependency (in red). ( J ) Application of OXA resulted in an increase in calcium spike amplitude (amp.) and quantity (qtty). ( K ) Slow voltage ramps were also performed. Current responses under control conditions were further collated with those during responses to OXA (in red). ( L ) The first group of neurons examined (n = 7/25) was characterised by calcium spikes evoked by OXA application. ( M ) The second group tested (n = 9/25) lacked calcium spikes but elicited an inward current as a result of OXA treatment with a reversal potential of −80 mV and a significant augmentation in the voltage range between −45 mV and 0 mV ( P ). ( N ) The last group of neurons tested with slow voltage ramps (n = 9/25) showed calcium spikes under both control conditions and during the OXA effect. ( R ) The potential at which the first calcium spike was generated was shifted during OXA-evoked depolarisations. * p
    Figure Legend Snippet: In DLG TC neurons, OXA evokes calcium influx through voltage-gated calcium channels. ( A , B ) Application of OXA (200 nM, red bars) produced a depolarisation that was heavily reduced by NiCl 2 (10 mM, light grey bar) and CdCl 2 (1 mM, grey bar). ( C ) Mibefradil (Mib, 30 μM, dark grey bar), reduced OXA-evoked depolarisation but in a less effective manner. ( D ) Nifedipine (Nif, 1 mM, black bar) also caused a reduction in the OXA effect. Responses to OXA (in%) in the presence of the blockers mentioned above are summarised as a bar graph ( O ). ( E , H , K ) Electrophysiological tests to elucidate calcium conductances were applied under control conditions (in TTX) and during the maximal response to OXA (200 nM). ( E ) Low voltage steps were used to evoke T-type calcium currents (I T ). ( F , G ) Application of OXA enhanced the amplitude of I T (in red). ( H ) In order to evoke HVA calcium currents, high voltage steps were used. ( I ) OXA caused the potentiation of HVA calcium spikes and a shift in their voltage dependency (in red). ( J ) Application of OXA resulted in an increase in calcium spike amplitude (amp.) and quantity (qtty). ( K ) Slow voltage ramps were also performed. Current responses under control conditions were further collated with those during responses to OXA (in red). ( L ) The first group of neurons examined (n = 7/25) was characterised by calcium spikes evoked by OXA application. ( M ) The second group tested (n = 9/25) lacked calcium spikes but elicited an inward current as a result of OXA treatment with a reversal potential of −80 mV and a significant augmentation in the voltage range between −45 mV and 0 mV ( P ). ( N ) The last group of neurons tested with slow voltage ramps (n = 9/25) showed calcium spikes under both control conditions and during the OXA effect. ( R ) The potential at which the first calcium spike was generated was shifted during OXA-evoked depolarisations. * p

    Techniques Used: Produced, Generated

    40) Product Images from "Regulation of cpg15 by signaling pathways that mediate synaptic plasticity"

    Article Title: Regulation of cpg15 by signaling pathways that mediate synaptic plasticity

    Journal: Molecular and cellular neurosciences

    doi:

    cpg15 is an IEG induced by synaptic activity through activation of NMDA receptors and L-type VSCCs. (A) Northern blots of total RNA prepared from cortical cultures treated for 9 h at 14 div. Cultures were untreated (−) or treated with TTX (1 µM), PTX (50 µM), or KCl (50 mM) in the absence or presence of EGTA (2 mM), CPP (10 µM), or nifedipine (Nif, 5 µM) as indicated above. (B) Quantification of cpg15 mRNA levels shown in A normalized to a GAPDH loading control. cpg15 expression in TTX-treated cultures was designated 1. Cultures treated with PTX or KCl and CPP showed significantly higher cpg15 expression compared to TTX-treated cultures (* P
    Figure Legend Snippet: cpg15 is an IEG induced by synaptic activity through activation of NMDA receptors and L-type VSCCs. (A) Northern blots of total RNA prepared from cortical cultures treated for 9 h at 14 div. Cultures were untreated (−) or treated with TTX (1 µM), PTX (50 µM), or KCl (50 mM) in the absence or presence of EGTA (2 mM), CPP (10 µM), or nifedipine (Nif, 5 µM) as indicated above. (B) Quantification of cpg15 mRNA levels shown in A normalized to a GAPDH loading control. cpg15 expression in TTX-treated cultures was designated 1. Cultures treated with PTX or KCl and CPP showed significantly higher cpg15 expression compared to TTX-treated cultures (* P

    Techniques Used: Activity Assay, Activation Assay, Northern Blot, Conditioned Place Preference, Expressing

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    Article Snippet: Nifedipine, CPA, Pyr6 and kinase inhibitors (PD-98059, LY-294002, GF-109203X, and SB-203580) were obtained from Tocris Cookson (Bristol, United Kingdom).

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    Article Snippet: D-(−)-2-amino-5-phosphonopentanoic acid (APV), bicuculline, (S)-(−)-blebbistatin, (R)-(+)-blebbistatin, thapsigargin and nifedipine were purchased from Tocris (Ellisville, MO, USA).

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    Spontaneous neuronal calcium activity in GC-P and PGN-P in the RMS, RMS-OB and deep GCL. A. Schematic representation of an olfactory bulb sagittal slice. B. Ai14/GCaMP6s P0 animals received lateral or medial electroporation of a Cre mRNAs. C. Calcium activity was recorded on acute brain slices between 6 and 10 dpe. Red and green cells represent medial and lateral cells migrating in the RMS, RMS-OB or in the deep GCL. D.F.H. Raster plot of calcium activity of GC-P (left) and PGN-P (right) recorded in the RMS (D), RMS OB (F) and deep GCL (H). E.G.I. Percentage of active cells, frequency and mean amplitude for GC-P and PGN-P in the RMS (E), RMS-OB (G) and in the deep GCL (I). Cells were defined as active if they showed at least one detectable calcium transient. The calcium activity of GC-P greatly increased upon arrival in the RMS-OB and the deep GCL, in contrast with PGN-P activity. N = 6 slices per condition. Error bars are SEM. J. Left: Raster plot of calcium activity of GC-P in the deep GCL in control and calcium-free medium (No Calcium + 2mM EGTA). Right: The percentage of active cells is highly decreased in calcium free medium. K. Left: Raster plot of calcium activity of GC-P in the deep GCL in control condition and <t>nifedipine</t> (10 μM) supplemented medium. Right: The percentage of active after incubation with the L-Type Voltage Gated Calcium Channels antagonist Nifedipine at 10 μM is highly decreased.
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    Spontaneous neuronal calcium activity in GC-P and PGN-P in the RMS, RMS-OB and deep GCL. A. Schematic representation of an olfactory bulb sagittal slice. B. Ai14/GCaMP6s P0 animals received lateral or medial electroporation of a Cre mRNAs. C. Calcium activity was recorded on acute brain slices between 6 and 10 dpe. Red and green cells represent medial and lateral cells migrating in the RMS, RMS-OB or in the deep GCL. D.F.H. Raster plot of calcium activity of GC-P (left) and PGN-P (right) recorded in the RMS (D), RMS OB (F) and deep GCL (H). E.G.I. Percentage of active cells, frequency and mean amplitude for GC-P and PGN-P in the RMS (E), RMS-OB (G) and in the deep GCL (I). Cells were defined as active if they showed at least one detectable calcium transient. The calcium activity of GC-P greatly increased upon arrival in the RMS-OB and the deep GCL, in contrast with PGN-P activity. N = 6 slices per condition. Error bars are SEM. J. Left: Raster plot of calcium activity of GC-P in the deep GCL in control and calcium-free medium (No Calcium + 2mM EGTA). Right: The percentage of active cells is highly decreased in calcium free medium. K. Left: Raster plot of calcium activity of GC-P in the deep GCL in control condition and nifedipine (10 μM) supplemented medium. Right: The percentage of active after incubation with the L-Type Voltage Gated Calcium Channels antagonist Nifedipine at 10 μM is highly decreased.

    Journal: bioRxiv

    Article Title: Intrinsic neuronal activity during migration controls the recruitment of specific interneuron subtypes in the postnatal mouse olfactory bulb

    doi: 10.1101/2020.07.28.224568

    Figure Lengend Snippet: Spontaneous neuronal calcium activity in GC-P and PGN-P in the RMS, RMS-OB and deep GCL. A. Schematic representation of an olfactory bulb sagittal slice. B. Ai14/GCaMP6s P0 animals received lateral or medial electroporation of a Cre mRNAs. C. Calcium activity was recorded on acute brain slices between 6 and 10 dpe. Red and green cells represent medial and lateral cells migrating in the RMS, RMS-OB or in the deep GCL. D.F.H. Raster plot of calcium activity of GC-P (left) and PGN-P (right) recorded in the RMS (D), RMS OB (F) and deep GCL (H). E.G.I. Percentage of active cells, frequency and mean amplitude for GC-P and PGN-P in the RMS (E), RMS-OB (G) and in the deep GCL (I). Cells were defined as active if they showed at least one detectable calcium transient. The calcium activity of GC-P greatly increased upon arrival in the RMS-OB and the deep GCL, in contrast with PGN-P activity. N = 6 slices per condition. Error bars are SEM. J. Left: Raster plot of calcium activity of GC-P in the deep GCL in control and calcium-free medium (No Calcium + 2mM EGTA). Right: The percentage of active cells is highly decreased in calcium free medium. K. Left: Raster plot of calcium activity of GC-P in the deep GCL in control condition and nifedipine (10 μM) supplemented medium. Right: The percentage of active after incubation with the L-Type Voltage Gated Calcium Channels antagonist Nifedipine at 10 μM is highly decreased.

    Article Snippet: PharmacologyAntagonists were bath applied at the following concentrations: D-APV (Tocris Bioscience, 50μM), NBQX (Tocris Bioscience, 10μM), MPEP (Tocris Bioscience, 30μM), Bicuculline (Tocris Bioscience, 10μM), Strychnine (Tocris Bioscience, 20μM), Nifedipine (Tocris Bioscience, 10μM).

    Techniques: Activity Assay, Electroporation, Incubation

    Spontaneous neuronal calcium activity in GC-P in the deep GCL is not affected by classical antagonists. Incubation with a calcium free medium decrease the frequency of calcium transients. (A) The L-type voltage-dependent calcium channel blocker nifedipine decrease the frequency of calcium transients. (B) The NMDA receptors antagonist D-APV (C), AMPA/Kainate receptors antagonist NBQX (D), metabotropic glutamate receptor 5 antagonist MPEP (E), GABAA receptors antagonist Bicuculline (F) and glycine receptor antagonist strychnine (G) do no modify the percentage of active cells or the amplitude of calcium transient.

    Journal: bioRxiv

    Article Title: Intrinsic neuronal activity during migration controls the recruitment of specific interneuron subtypes in the postnatal mouse olfactory bulb

    doi: 10.1101/2020.07.28.224568

    Figure Lengend Snippet: Spontaneous neuronal calcium activity in GC-P in the deep GCL is not affected by classical antagonists. Incubation with a calcium free medium decrease the frequency of calcium transients. (A) The L-type voltage-dependent calcium channel blocker nifedipine decrease the frequency of calcium transients. (B) The NMDA receptors antagonist D-APV (C), AMPA/Kainate receptors antagonist NBQX (D), metabotropic glutamate receptor 5 antagonist MPEP (E), GABAA receptors antagonist Bicuculline (F) and glycine receptor antagonist strychnine (G) do no modify the percentage of active cells or the amplitude of calcium transient.

    Article Snippet: PharmacologyAntagonists were bath applied at the following concentrations: D-APV (Tocris Bioscience, 50μM), NBQX (Tocris Bioscience, 10μM), MPEP (Tocris Bioscience, 30μM), Bicuculline (Tocris Bioscience, 10μM), Strychnine (Tocris Bioscience, 20μM), Nifedipine (Tocris Bioscience, 10μM).

    Techniques: Activity Assay, Incubation

    Effects of various inhibitors of Ca 2+ entry on DA-actin distribution. Neurons (21 DIV) were incubated in normal medium containing 50 µM APV (A), 20 mM EGTA (B), 20 µM nifedipine (C), or 1 µM thapsigargin (D) for 30 min. The neurons were then stimulated with 100 µM glutamate for an additional 10 min. F-actin images indicate that spines kept their structure during the experiment although their shapes were changed. Scale bars, 5 µm. ( A ) APV pretreatment significantly increased both the drebrin and actin SDRs (n = 30 cells; p

    Journal: PLoS ONE

    Article Title: Myosin II ATPase Activity Mediates the Long-Term Potentiation-Induced Exodus of Stable F-Actin Bound by Drebrin A from Dendritic Spines

    doi: 10.1371/journal.pone.0085367

    Figure Lengend Snippet: Effects of various inhibitors of Ca 2+ entry on DA-actin distribution. Neurons (21 DIV) were incubated in normal medium containing 50 µM APV (A), 20 mM EGTA (B), 20 µM nifedipine (C), or 1 µM thapsigargin (D) for 30 min. The neurons were then stimulated with 100 µM glutamate for an additional 10 min. F-actin images indicate that spines kept their structure during the experiment although their shapes were changed. Scale bars, 5 µm. ( A ) APV pretreatment significantly increased both the drebrin and actin SDRs (n = 30 cells; p

    Article Snippet: D-(−)-2-amino-5-phosphonopentanoic acid (APV), bicuculline, (S)-(−)-blebbistatin, (R)-(+)-blebbistatin, thapsigargin and nifedipine were purchased from Tocris (Ellisville, MO, USA).

    Techniques: Incubation

    α 1 -Adrenoceptor-elicited vasoconstriction in resistance arteries is mostly due to Ca 2+ entry through voltage-dependent L-type channels. (A,B) Average inhibitory effects of the selective L-type Ca 2+ channel blocker nifedipine (0.3 μM) (A) or the inhibitor of the Orai1–mediated Ca 2+ entry Pyr6 (3 μM) alone or in combination with the SERCA inhibitor CPA (10 μM) (B ) on the CaCl 2 concentration-response curves (CRCs) in endothelium-denuded mesenteric resistance arteries kept in nominally Ca 2+ -free medium and stimulated with 10 μM PE. (C,D ) Summarized data showing the effects of SR Ca 2+ store depletion by SERCA inhibition with CPA (10 μM) alone or CPA plus nifedipine (0.3 μM) on the changes in [Ca 2+ ] i (C) and contraction (D) in response to 10 μM PE in resistance arteries kept in a nominally Ca 2+ -free medium (0 mM Ca 2+ , open bar) after Ca 2+ readmission (1 mM CaCl 2 , closed bar). Results are expressed as a percentage of control maximal responses (A,B) or the KPSS responses (C,D) . Values are means ± SEM of n = 6 arteries (one from each animal). ∗ P

    Journal: Frontiers in Physiology

    Article Title: Role of Phosphatidylinositol 3-Kinase (PI3K), Mitogen-Activated Protein Kinase (MAPK), and Protein Kinase C (PKC) in Calcium Signaling Pathways Linked to the α1-Adrenoceptor in Resistance Arteries

    doi: 10.3389/fphys.2019.00055

    Figure Lengend Snippet: α 1 -Adrenoceptor-elicited vasoconstriction in resistance arteries is mostly due to Ca 2+ entry through voltage-dependent L-type channels. (A,B) Average inhibitory effects of the selective L-type Ca 2+ channel blocker nifedipine (0.3 μM) (A) or the inhibitor of the Orai1–mediated Ca 2+ entry Pyr6 (3 μM) alone or in combination with the SERCA inhibitor CPA (10 μM) (B ) on the CaCl 2 concentration-response curves (CRCs) in endothelium-denuded mesenteric resistance arteries kept in nominally Ca 2+ -free medium and stimulated with 10 μM PE. (C,D ) Summarized data showing the effects of SR Ca 2+ store depletion by SERCA inhibition with CPA (10 μM) alone or CPA plus nifedipine (0.3 μM) on the changes in [Ca 2+ ] i (C) and contraction (D) in response to 10 μM PE in resistance arteries kept in a nominally Ca 2+ -free medium (0 mM Ca 2+ , open bar) after Ca 2+ readmission (1 mM CaCl 2 , closed bar). Results are expressed as a percentage of control maximal responses (A,B) or the KPSS responses (C,D) . Values are means ± SEM of n = 6 arteries (one from each animal). ∗ P

    Article Snippet: Nifedipine, CPA, Pyr6 and kinase inhibitors (PD-98059, LY-294002, GF-109203X, and SB-203580) were obtained from Tocris Cookson (Bristol, United Kingdom).

    Techniques: Concentration Assay, Inhibition

    L-type channel inactivation processes upon β-adrenergic stimulus. Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cell in a newborn rat cardiomyocyte overexpressing RFP (A), Ca V β 2a (B), CaM wt (D) , or CaM 34 (E). Bar graphs are mean ± SEM ( n = 8) of maximal current normalized by cell capacitance (pA/pF), total time of current normalized by action potential duration (TTC norm ), and the total current integral normalized by cell capacitance (Q total ) from a cardiomyocyte overexpressing RFP (empty bars) and Ca V β 2a (plum bars). CaM wt (empty bars; B) or CaM 34 (blue bars; D). Data are presented as percentages of their respective control situation [RFP for C and CaM wt for F]. *, P

    Journal: The Journal of General Physiology

    Article Title: Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

    doi: 10.1085/jgp.201812236

    Figure Lengend Snippet: L-type channel inactivation processes upon β-adrenergic stimulus. Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cell in a newborn rat cardiomyocyte overexpressing RFP (A), Ca V β 2a (B), CaM wt (D) , or CaM 34 (E). Bar graphs are mean ± SEM ( n = 8) of maximal current normalized by cell capacitance (pA/pF), total time of current normalized by action potential duration (TTC norm ), and the total current integral normalized by cell capacitance (Q total ) from a cardiomyocyte overexpressing RFP (empty bars) and Ca V β 2a (plum bars). CaM wt (empty bars; B) or CaM 34 (blue bars; D). Data are presented as percentages of their respective control situation [RFP for C and CaM wt for F]. *, P

    Article Snippet: To accomplish this, APs and nifedipine-sensitive currents were recorded from cardiomyocytes treated with the NCX inhibitor SEA0400 (Tocris, 1 µM).

    Techniques: Chick Chorioallantoic Membrane Assay

    L-type calcium current during an AP upon β-adrenergic stimulus. (A and B) Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cell in control (A) and isoproterenol-treated (B) newborn rat cardiomyocytes. (C) Bar graph of maximal current normalized by cell capacitance (pA/pF); total time of nifedipine-sensitive current normalized by its APD (TTC norm ); and the total current integral normalized by cell capacitance (Q total ). Data are presented as percentages with respect to the controls. The bar graph shows mean ± SEM; empty bars represent control cardiomyocytes and green bars correspond to isoproterenol-treated cardiomyocytes ( n = 6; *P

    Journal: The Journal of General Physiology

    Article Title: Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

    doi: 10.1085/jgp.201812236

    Figure Lengend Snippet: L-type calcium current during an AP upon β-adrenergic stimulus. (A and B) Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cell in control (A) and isoproterenol-treated (B) newborn rat cardiomyocytes. (C) Bar graph of maximal current normalized by cell capacitance (pA/pF); total time of nifedipine-sensitive current normalized by its APD (TTC norm ); and the total current integral normalized by cell capacitance (Q total ). Data are presented as percentages with respect to the controls. The bar graph shows mean ± SEM; empty bars represent control cardiomyocytes and green bars correspond to isoproterenol-treated cardiomyocytes ( n = 6; *P

    Article Snippet: To accomplish this, APs and nifedipine-sensitive currents were recorded from cardiomyocytes treated with the NCX inhibitor SEA0400 (Tocris, 1 µM).

    Techniques:

    APs and L-type calcium currents in CDI-impaired cardiomyocytes. (A) Representative AP waveforms from a newborn rat cardiomyocyte overexpressing CaM wt (solid black line) or CaM 34 (dashed blue line). APs were elicited by 2–5 ms depolarizing current injections (100–200 pA) at 1 Hz. The horizontal line indicates zero level. (B) Bar graph of APD estimated at 20% (APD 20 ), 50% (APD 50 ), and 90% (APD 90 ) of the repolarization phase. (C) Phase plot of the normalized first derivative of membrane potential (dV/dt) against membrane potential (V m ) for the APs shown in A. Empty symbols correspond to data from cardiomyocytes overexpressing CaM wt and blue symbols for cardiomyocytes overexpressing CaM 34 . (D) Bar graph of overshoot, threshold potentials, and mean DMPs. (E) Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cardiomyocyte overexpressing CaM 34 . (F) Bar graph of maximal current normalized by cell capacitance (pA/pF), total time of nifedipine-sensitive current normalized by its APD (TTC norm ), and the total current integral normalized by cell capacitance (Q total ). Data are shown as percentages with respect to CaM wt -overexpressing cardiomyocytes. Bar graphs are mean ± SEM; empty bars represent cardiomyocytes overexpressing CaM wt , and blue bars correspond to those overexpressing CaM 34 ( n = 7; *, P

    Journal: The Journal of General Physiology

    Article Title: Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

    doi: 10.1085/jgp.201812236

    Figure Lengend Snippet: APs and L-type calcium currents in CDI-impaired cardiomyocytes. (A) Representative AP waveforms from a newborn rat cardiomyocyte overexpressing CaM wt (solid black line) or CaM 34 (dashed blue line). APs were elicited by 2–5 ms depolarizing current injections (100–200 pA) at 1 Hz. The horizontal line indicates zero level. (B) Bar graph of APD estimated at 20% (APD 20 ), 50% (APD 50 ), and 90% (APD 90 ) of the repolarization phase. (C) Phase plot of the normalized first derivative of membrane potential (dV/dt) against membrane potential (V m ) for the APs shown in A. Empty symbols correspond to data from cardiomyocytes overexpressing CaM wt and blue symbols for cardiomyocytes overexpressing CaM 34 . (D) Bar graph of overshoot, threshold potentials, and mean DMPs. (E) Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cardiomyocyte overexpressing CaM 34 . (F) Bar graph of maximal current normalized by cell capacitance (pA/pF), total time of nifedipine-sensitive current normalized by its APD (TTC norm ), and the total current integral normalized by cell capacitance (Q total ). Data are shown as percentages with respect to CaM wt -overexpressing cardiomyocytes. Bar graphs are mean ± SEM; empty bars represent cardiomyocytes overexpressing CaM wt , and blue bars correspond to those overexpressing CaM 34 ( n = 7; *, P

    Article Snippet: To accomplish this, APs and nifedipine-sensitive currents were recorded from cardiomyocytes treated with the NCX inhibitor SEA0400 (Tocris, 1 µM).

    Techniques: Chick Chorioallantoic Membrane Assay, Mass Spectrometry

    Physiological temperature modifies APs and L-type calcium currents in cardiomyocytes. (A) Representative AP waveforms from newborn rat cardiomyocytes at 23°–25°C (black dashed line) or 35°–37°C (brown line). (B) Representative AP waveforms at 35–37°C before (brown line) and after treatment with 1 µM SEA0400 (light blue line). APs were elicited by 2–5 ms depolarizing current injections (100–200 pA) at 1 Hz. (C) Bar graph of the APD percentage change upon isoproterenol treatment, estimated at 20% (APD 20 ), 50% (APD 50 ), and 90% (APD 90 ) of the repolarization phase. (D and E) Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cell at 35–37°C in control cardiomyocytes (D) or treated with 1 µM SEA0400 (E). (F) Bar graph of maximal current normalized by cell capacitance (pA/pF), total time of nifedipine-sensitive current normalized by its APD (TTC norm ), and the total current integral normalized by cell capacitance (Q total ). Data are presented as percentages with respect to control cardiomyocytes at 23–25°C. Bar graphs are mean ± SEM; empty bars represent control cardiomyocytes, brown bars correspond to cardiomyocytes at 35–37°C, and light blue bars correspond to cardiomyocytes at 35–37°C treated with 1 µM SEA0400. *, P

    Journal: The Journal of General Physiology

    Article Title: Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

    doi: 10.1085/jgp.201812236

    Figure Lengend Snippet: Physiological temperature modifies APs and L-type calcium currents in cardiomyocytes. (A) Representative AP waveforms from newborn rat cardiomyocytes at 23°–25°C (black dashed line) or 35°–37°C (brown line). (B) Representative AP waveforms at 35–37°C before (brown line) and after treatment with 1 µM SEA0400 (light blue line). APs were elicited by 2–5 ms depolarizing current injections (100–200 pA) at 1 Hz. (C) Bar graph of the APD percentage change upon isoproterenol treatment, estimated at 20% (APD 20 ), 50% (APD 50 ), and 90% (APD 90 ) of the repolarization phase. (D and E) Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cell at 35–37°C in control cardiomyocytes (D) or treated with 1 µM SEA0400 (E). (F) Bar graph of maximal current normalized by cell capacitance (pA/pF), total time of nifedipine-sensitive current normalized by its APD (TTC norm ), and the total current integral normalized by cell capacitance (Q total ). Data are presented as percentages with respect to control cardiomyocytes at 23–25°C. Bar graphs are mean ± SEM; empty bars represent control cardiomyocytes, brown bars correspond to cardiomyocytes at 35–37°C, and light blue bars correspond to cardiomyocytes at 35–37°C treated with 1 µM SEA0400. *, P

    Article Snippet: To accomplish this, APs and nifedipine-sensitive currents were recorded from cardiomyocytes treated with the NCX inhibitor SEA0400 (Tocris, 1 µM).

    Techniques: Mass Spectrometry

    APs and L-type calcium currents in VDI-impaired newborn rat cardiomyocytes. (A) Representative AP waveforms from a newborn rat cardiomyocyte overexpressing RFP (solid black line) or Ca V β 2a (dashed plum line). APs were elicited by 2–5 ms depolarizing current injections (100–200 pA) at 1 Hz. (B) Bar graph of APD estimated at 20% (APD 20 ), 50% (APD 50 ), and 90% (APD 90 ) of the repolarization phase. (C) Phase plot of the normalized first derivative of membrane potential (dV/dt) against membrane potential (V m ) for the APs shown in A. Cardiomyocytes overexpressing RFP are shown with empty symbols and cardiomyocytes overexpressing Ca V β 2a with plum symbols. (D) Bar graph of overshoot, threshold potentials, and mean DMPs. (E) Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cardiomyocyte overexpressing Ca V β 2a . (F) Bar graph of maximal current normalized by cell capacitance (pA/pF), total time of nifedipine-sensitive current normalized by its APD (TTC norm ), and the total current integral normalized by cell capacitance (Q total ). Data are presented as percentages with respect to RFP-transduced cardiomyocytes. Bar graphs are mean ± SEM; empty bars represent cardiomyocytes overexpressing RFP, and plum bars correspond to those overexpressing Ca V β 2a ( n = 6; *, P

    Journal: The Journal of General Physiology

    Article Title: Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

    doi: 10.1085/jgp.201812236

    Figure Lengend Snippet: APs and L-type calcium currents in VDI-impaired newborn rat cardiomyocytes. (A) Representative AP waveforms from a newborn rat cardiomyocyte overexpressing RFP (solid black line) or Ca V β 2a (dashed plum line). APs were elicited by 2–5 ms depolarizing current injections (100–200 pA) at 1 Hz. (B) Bar graph of APD estimated at 20% (APD 20 ), 50% (APD 50 ), and 90% (APD 90 ) of the repolarization phase. (C) Phase plot of the normalized first derivative of membrane potential (dV/dt) against membrane potential (V m ) for the APs shown in A. Cardiomyocytes overexpressing RFP are shown with empty symbols and cardiomyocytes overexpressing Ca V β 2a with plum symbols. (D) Bar graph of overshoot, threshold potentials, and mean DMPs. (E) Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cardiomyocyte overexpressing Ca V β 2a . (F) Bar graph of maximal current normalized by cell capacitance (pA/pF), total time of nifedipine-sensitive current normalized by its APD (TTC norm ), and the total current integral normalized by cell capacitance (Q total ). Data are presented as percentages with respect to RFP-transduced cardiomyocytes. Bar graphs are mean ± SEM; empty bars represent cardiomyocytes overexpressing RFP, and plum bars correspond to those overexpressing Ca V β 2a ( n = 6; *, P

    Article Snippet: To accomplish this, APs and nifedipine-sensitive currents were recorded from cardiomyocytes treated with the NCX inhibitor SEA0400 (Tocris, 1 µM).

    Techniques: Mass Spectrometry

    Role of L-type channel inactivation processes during a simulated AP. (A) Simulated L-type calcium current for the control condition (black line) or for cardiomyocytes with increased L-type channel conductance alone (light gray line) or simultaneously with an increased CDI (violet line) or VDI (pink line). (B) Experimental data showing the maximal nifedipine-sensitive current from control, Ca V β 2a , and CaM 34 before (empty bars) or after (green bars) isoproterenol stimulation. #, P

    Journal: The Journal of General Physiology

    Article Title: Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

    doi: 10.1085/jgp.201812236

    Figure Lengend Snippet: Role of L-type channel inactivation processes during a simulated AP. (A) Simulated L-type calcium current for the control condition (black line) or for cardiomyocytes with increased L-type channel conductance alone (light gray line) or simultaneously with an increased CDI (violet line) or VDI (pink line). (B) Experimental data showing the maximal nifedipine-sensitive current from control, Ca V β 2a , and CaM 34 before (empty bars) or after (green bars) isoproterenol stimulation. #, P

    Article Snippet: To accomplish this, APs and nifedipine-sensitive currents were recorded from cardiomyocytes treated with the NCX inhibitor SEA0400 (Tocris, 1 µM).

    Techniques: Chick Chorioallantoic Membrane Assay