Structured Review

Alomone Labs nifedipine
Effect of ion channel blockers on L55P TTR-induced calcium influx and analysis of sensitivity to icilin and capsaicin , (A) L55P was applied to DRG growth cones in the presence of VGCC inhibitors <t>(nifedipine,</t> ω-agatoxin IVA, ω-conotoxin GIVA), Na V inhibitors (tetrodotoxin, ambroxol and carbamazepine) and TRP inhibitors (SKF-96365, BCTC). The resulting maximal calcium influx (max ΔF/F 0 ) calculated over the imaging period (7 min) was calculated. (B) Effect of capsaicin (1 μM) and icilin (100 μM) on cytosolic calcium in DRG growth cones in culture. When DRG cultures were pre-treated with ambroxol (5 μM), icilin-induced calcium fluorescence was significantly decreased. All graphs show maximal ΔF/F 0 ± SEM for n = 12-24 growth cones. Significant differences from control values are depicted as: * p
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Images

1) Product Images from "TRPM8 and Nav1.8 sodium channels are required for transthyretin-induced calcium influx in growth cones of small-diameter TrkA-positive sensory neurons"

Article Title: TRPM8 and Nav1.8 sodium channels are required for transthyretin-induced calcium influx in growth cones of small-diameter TrkA-positive sensory neurons

Journal: Molecular Neurodegeneration

doi: 10.1186/1750-1326-6-19

Effect of ion channel blockers on L55P TTR-induced calcium influx and analysis of sensitivity to icilin and capsaicin , (A) L55P was applied to DRG growth cones in the presence of VGCC inhibitors (nifedipine, ω-agatoxin IVA, ω-conotoxin GIVA), Na V inhibitors (tetrodotoxin, ambroxol and carbamazepine) and TRP inhibitors (SKF-96365, BCTC). The resulting maximal calcium influx (max ΔF/F 0 ) calculated over the imaging period (7 min) was calculated. (B) Effect of capsaicin (1 μM) and icilin (100 μM) on cytosolic calcium in DRG growth cones in culture. When DRG cultures were pre-treated with ambroxol (5 μM), icilin-induced calcium fluorescence was significantly decreased. All graphs show maximal ΔF/F 0 ± SEM for n = 12-24 growth cones. Significant differences from control values are depicted as: * p
Figure Legend Snippet: Effect of ion channel blockers on L55P TTR-induced calcium influx and analysis of sensitivity to icilin and capsaicin , (A) L55P was applied to DRG growth cones in the presence of VGCC inhibitors (nifedipine, ω-agatoxin IVA, ω-conotoxin GIVA), Na V inhibitors (tetrodotoxin, ambroxol and carbamazepine) and TRP inhibitors (SKF-96365, BCTC). The resulting maximal calcium influx (max ΔF/F 0 ) calculated over the imaging period (7 min) was calculated. (B) Effect of capsaicin (1 μM) and icilin (100 μM) on cytosolic calcium in DRG growth cones in culture. When DRG cultures were pre-treated with ambroxol (5 μM), icilin-induced calcium fluorescence was significantly decreased. All graphs show maximal ΔF/F 0 ± SEM for n = 12-24 growth cones. Significant differences from control values are depicted as: * p

Techniques Used: Imaging, Fluorescence

2) Product Images from "Homer regulates calcium signalling in growth cone turning"

Article Title: Homer regulates calcium signalling in growth cone turning

Journal: Neural Development

doi: 10.1186/1749-8104-4-29

Spontaneous calcium transients and growth cone turning are sensitive to blockage of store-operated channels . (A) Individual control morphant growth cones exhibited sparse spontaneous calcium transients, occurring at a rate of approximately one transient per three minutes. (B) Homer1 morphant growth cones exhibited significantly greater frequency, at a rate of at least one spontaneous transient per minute. (C) A trace from a single Homer1 morphant growth cone showed a decrease in spontaneous calcium transient frequency in the presence of bath applied SKF-96365. (D) Quantification of spontaneous calcium transient frequencies in Homer1 morphant growth cones. Removing calcium from the media (Ca free) or bath application of La 3+ (La) or SKF-96365 (SKF) reduced spontaneous transient frequencies in Homer1 morphant growth cones to control (ctrl) levels. Bath application of a voltage-gated calcium channel (VGCC) inhibitor cocktail or nifedipine alone had little effect on the frequency of spontaneous calcium transients in Homer1 morphant growth cones. (E) Calcium-dependent brain derived neurotrophic factor (BDNF)-induced turning is mediated through store-operated channels. BDNF attraction was abolished when TRPC channels were inactivated with bath application of SKF-96365 or La 3+ . Inhibition of VGCCs with nifedipine or ω-conotoxin-MVIIC had no effect on control and Homer1 morphant growth cone turning. (F) Inhibition of store-operated channels did not alter axon extension rates. Error bars indicate standard error of the mean. Cocktail = nifedipine, ω-conotoxin-MVIIC plus Ni ++ . The scale bar in (C) applies also to (A, B).
Figure Legend Snippet: Spontaneous calcium transients and growth cone turning are sensitive to blockage of store-operated channels . (A) Individual control morphant growth cones exhibited sparse spontaneous calcium transients, occurring at a rate of approximately one transient per three minutes. (B) Homer1 morphant growth cones exhibited significantly greater frequency, at a rate of at least one spontaneous transient per minute. (C) A trace from a single Homer1 morphant growth cone showed a decrease in spontaneous calcium transient frequency in the presence of bath applied SKF-96365. (D) Quantification of spontaneous calcium transient frequencies in Homer1 morphant growth cones. Removing calcium from the media (Ca free) or bath application of La 3+ (La) or SKF-96365 (SKF) reduced spontaneous transient frequencies in Homer1 morphant growth cones to control (ctrl) levels. Bath application of a voltage-gated calcium channel (VGCC) inhibitor cocktail or nifedipine alone had little effect on the frequency of spontaneous calcium transients in Homer1 morphant growth cones. (E) Calcium-dependent brain derived neurotrophic factor (BDNF)-induced turning is mediated through store-operated channels. BDNF attraction was abolished when TRPC channels were inactivated with bath application of SKF-96365 or La 3+ . Inhibition of VGCCs with nifedipine or ω-conotoxin-MVIIC had no effect on control and Homer1 morphant growth cone turning. (F) Inhibition of store-operated channels did not alter axon extension rates. Error bars indicate standard error of the mean. Cocktail = nifedipine, ω-conotoxin-MVIIC plus Ni ++ . The scale bar in (C) applies also to (A, B).

Techniques Used: Derivative Assay, Inhibition

3) Product Images from "Calcium Channels in Postnatal Development of Rat Pancreatic Beta Cells and Their Role in Insulin Secretion"

Article Title: Calcium Channels in Postnatal Development of Rat Pancreatic Beta Cells and Their Role in Insulin Secretion

Journal: Frontiers in Endocrinology

doi: 10.3389/fendo.2018.00040

Effect of calcium channel inhibitors on basal and glucose-induced insulin secretion in adult beta cells. (A) Overall insulin secretory activity (insulin secretion index) of adult beta cells incubated with nifedipine (5 µM), mibefradil (1 µM), NiCl 2 (50 µM) and TTA-A 2 (50 µM), exposed at basal (5.6 mM glucose), and stimulating (15.6 mM glucose) conditions. Bars represent the mean ± SEM of three different experiments by duplicate. * p ≤ 0.05 denotes significant differences with respect to control cells at 5.6 and 15.5 mM glucose. Dunnet test (analysis of variance). (B,C) Frequency distribution of functional subpopulations of beta cells incubated with inhibitors of (A) observed in basal (B) and stimulating (C) glucose conditions.
Figure Legend Snippet: Effect of calcium channel inhibitors on basal and glucose-induced insulin secretion in adult beta cells. (A) Overall insulin secretory activity (insulin secretion index) of adult beta cells incubated with nifedipine (5 µM), mibefradil (1 µM), NiCl 2 (50 µM) and TTA-A 2 (50 µM), exposed at basal (5.6 mM glucose), and stimulating (15.6 mM glucose) conditions. Bars represent the mean ± SEM of three different experiments by duplicate. * p ≤ 0.05 denotes significant differences with respect to control cells at 5.6 and 15.5 mM glucose. Dunnet test (analysis of variance). (B,C) Frequency distribution of functional subpopulations of beta cells incubated with inhibitors of (A) observed in basal (B) and stimulating (C) glucose conditions.

Techniques Used: Activity Assay, Incubation, Functional Assay

4) Product Images from "Calcium Channels in Postnatal Development of Rat Pancreatic Beta Cells and Their Role in Insulin Secretion"

Article Title: Calcium Channels in Postnatal Development of Rat Pancreatic Beta Cells and Their Role in Insulin Secretion

Journal: Frontiers in Endocrinology

doi: 10.3389/fendo.2018.00040

Effect of calcium channel inhibitors on low-voltage-activated (LVA) and high-voltage-activated (HVA) calcium currents in adult beta cells. (A–F) Representative recordings of global calcium currents observed in adult beta cells before and after of calcium channel inhibitors: mibefradil (1 and 10 µM), NiCl 2 (50 µM), TTA-A 2 (5 and 50 µM), and nifedipine (5 µM), respectively. Protocol: voltage ramp from −80 to +60 mV, 500 ms duration, and 0.5 mV/ms slope. (G) Normalized calcium current after of calcium channel inhibitors: 1 µM mibefradil ( n = 5), 10 µM mibefradil ( n = 6), NiCl 2 ( n = 6), 5 µM TTA-A 2 ( n = 5), 50 µM TTA-A 2 ( n = 3), and nifedipine ( n = 6). * p ≤ 0.05 denotes significant differences compared with cells without inhibitors, paired t -test.
Figure Legend Snippet: Effect of calcium channel inhibitors on low-voltage-activated (LVA) and high-voltage-activated (HVA) calcium currents in adult beta cells. (A–F) Representative recordings of global calcium currents observed in adult beta cells before and after of calcium channel inhibitors: mibefradil (1 and 10 µM), NiCl 2 (50 µM), TTA-A 2 (5 and 50 µM), and nifedipine (5 µM), respectively. Protocol: voltage ramp from −80 to +60 mV, 500 ms duration, and 0.5 mV/ms slope. (G) Normalized calcium current after of calcium channel inhibitors: 1 µM mibefradil ( n = 5), 10 µM mibefradil ( n = 6), NiCl 2 ( n = 6), 5 µM TTA-A 2 ( n = 5), 50 µM TTA-A 2 ( n = 3), and nifedipine ( n = 6). * p ≤ 0.05 denotes significant differences compared with cells without inhibitors, paired t -test.

Techniques Used: Mass Spectrometry

Effect of calcium channel inhibitors on basal and glucose-induced insulin secretion in adult beta cells. (A) Overall insulin secretory activity (insulin secretion index) of adult beta cells incubated with nifedipine (5 µM), mibefradil (1 µM), NiCl 2 (50 µM) and TTA-A 2 (50 µM), exposed at basal (5.6 mM glucose), and stimulating (15.6 mM glucose) conditions. Bars represent the mean ± SEM of three different experiments by duplicate. * p ≤ 0.05 denotes significant differences with respect to control cells at 5.6 and 15.5 mM glucose. Dunnet test (analysis of variance). (B,C) Frequency distribution of functional subpopulations of beta cells incubated with inhibitors of (A) observed in basal (B) and stimulating (C) glucose conditions.
Figure Legend Snippet: Effect of calcium channel inhibitors on basal and glucose-induced insulin secretion in adult beta cells. (A) Overall insulin secretory activity (insulin secretion index) of adult beta cells incubated with nifedipine (5 µM), mibefradil (1 µM), NiCl 2 (50 µM) and TTA-A 2 (50 µM), exposed at basal (5.6 mM glucose), and stimulating (15.6 mM glucose) conditions. Bars represent the mean ± SEM of three different experiments by duplicate. * p ≤ 0.05 denotes significant differences with respect to control cells at 5.6 and 15.5 mM glucose. Dunnet test (analysis of variance). (B,C) Frequency distribution of functional subpopulations of beta cells incubated with inhibitors of (A) observed in basal (B) and stimulating (C) glucose conditions.

Techniques Used: Activity Assay, Incubation, Functional Assay

5) Product Images from "Mechanistic insights into the detection of free fatty and bile acids by ileal glucagon-like peptide-1 secreting cells"

Article Title: Mechanistic insights into the detection of free fatty and bile acids by ileal glucagon-like peptide-1 secreting cells

Journal: Molecular Metabolism

doi: 10.1016/j.molmet.2017.11.005

Electrophysiological responses of organoid-derived ileal L-cells to GPBAR1 agonists. (A) Perforated-patch current clamp recording of an L-cell firing action potentials evoked by depolarizing current injections before (i), during (ii) and after (iii) application of GPBAR-A (3 μM). Current was injected to maintain the cell at −70 mV, and a series of 500 ms current pulses was applied, increasing in magnitude by 2 pA. (Aiv) Mean number (n = 9) of action potentials (threshold −10 mV) elicited during current injections as in Ai-iii, with error bars representing SEM. (Bi) Current–voltage relationship as assessed by voltage ramps over 500 ms from −100 to −50 mV, from a holding potential of −80 mV. Twenty ramps per condition in each cell (n = 11 cells) were averaged to represent baseline (black trace) and GPBAR-A treatment (3 μM, red trace). Recording of an L-cell studied by the same protocol as (A), before (Bii), during application of GPBAR-A (3 μM, Biii), and additional application of the HCN channel blocker, ZD7288 (10 μM, Biv). Perforated-patch voltage clamp recordings of I Ca before (Ci), during (Cii) and after (Ciii) application of GPBAR-A (3 μM). (Civ) I Ca –voltage relationship of ileal L-cells as assessed with 160 ms voltage ramps from a holding potential of −80 mV to +80 mV, during application of GPBAR-A (3 μM) and nifedipine (50 μM). Ten voltage ramps were averaged per treatment for each cell (n = 6) and normalized to the baseline peak I Ca amplitude. Recording of an ileal L-cell, elicited by the same protocol as (A) before (Di), during (Dii) and after (Diii) application of BayK8644 (10 μM). (Div) Mean number of action potentials (threshold −10 mV) elicited during current injections as in Di-iii, with error bars representing SEM (n = 4). Statistical significance was assessed using multiple t-tests with Holm-Sidak multiple comparisons correction (Aiv and Div), p
Figure Legend Snippet: Electrophysiological responses of organoid-derived ileal L-cells to GPBAR1 agonists. (A) Perforated-patch current clamp recording of an L-cell firing action potentials evoked by depolarizing current injections before (i), during (ii) and after (iii) application of GPBAR-A (3 μM). Current was injected to maintain the cell at −70 mV, and a series of 500 ms current pulses was applied, increasing in magnitude by 2 pA. (Aiv) Mean number (n = 9) of action potentials (threshold −10 mV) elicited during current injections as in Ai-iii, with error bars representing SEM. (Bi) Current–voltage relationship as assessed by voltage ramps over 500 ms from −100 to −50 mV, from a holding potential of −80 mV. Twenty ramps per condition in each cell (n = 11 cells) were averaged to represent baseline (black trace) and GPBAR-A treatment (3 μM, red trace). Recording of an L-cell studied by the same protocol as (A), before (Bii), during application of GPBAR-A (3 μM, Biii), and additional application of the HCN channel blocker, ZD7288 (10 μM, Biv). Perforated-patch voltage clamp recordings of I Ca before (Ci), during (Cii) and after (Ciii) application of GPBAR-A (3 μM). (Civ) I Ca –voltage relationship of ileal L-cells as assessed with 160 ms voltage ramps from a holding potential of −80 mV to +80 mV, during application of GPBAR-A (3 μM) and nifedipine (50 μM). Ten voltage ramps were averaged per treatment for each cell (n = 6) and normalized to the baseline peak I Ca amplitude. Recording of an ileal L-cell, elicited by the same protocol as (A) before (Di), during (Dii) and after (Diii) application of BayK8644 (10 μM). (Div) Mean number of action potentials (threshold −10 mV) elicited during current injections as in Di-iii, with error bars representing SEM (n = 4). Statistical significance was assessed using multiple t-tests with Holm-Sidak multiple comparisons correction (Aiv and Div), p

Techniques Used: Derivative Assay, Injection, Mass Spectrometry

6) Product Images from "The Neural Cell Adhesion Molecule Promotes FGFR-Dependent Phosphorylation and Membrane Targeting of the Exocyst Complex to Induce Exocytosis in Growth Cones"

Article Title: The Neural Cell Adhesion Molecule Promotes FGFR-Dependent Phosphorylation and Membrane Targeting of the Exocyst Complex to Induce Exocytosis in Growth Cones

Journal: The Journal of Neuroscience

doi: 10.1523/JNEUROSCI.3109-10.2011

Specific triggering of NCAM functions by application of NCAM antibodies to isolated growth cones enhances the association of NCAM with the exocyst complex and induces depletion of the internal membrane pool. A , NCAM immunoprecipitates from NCAM+/+ growth cones analyzed by Western blot with NCAM, exo70, and sec8 antibodies. Mock immunoprecipitation with nonspecific IgG served as control. Growth cones were pretreated with nonspecific rabbit IgG or NCAM antibodies to cluster NCAM at the surface of growth cones. Note that coimmunoprecipitation of exo70 and sec8 with NCAM is increased in NCAM antibody-treated growth cones. B–E , Graphs show internal membrane pools in NCAM antibody-treated growth cones (mean + SEM from 3 experiments) normalized to the size of the internal membrane pool in preimmune serum-treated growth cones set to 100% (dashed line). Note that the internal membrane pool is reduced in NCAM+/+ growth cones treated with NCAM antibodies, an effect that is blocked in NCAM+/+ growth cones pretreated with BAPTA ( B ), tetanus toxin ( C ), or the FGFR inhibitor and the L-type VDCC inhibitor nifedipine ( D ) or when growth cones were treated with NCAM antibody at 25°C or 4°C ( C ). NCAM−/− growth cones served as control ( B ). Inhibitor of T-type VDCC pimozide ( D ) does not influence, while inhibitor of dynamin-dependent endocytosis dynasore ( E ) increases, the effect of NCAM antibodies. * p
Figure Legend Snippet: Specific triggering of NCAM functions by application of NCAM antibodies to isolated growth cones enhances the association of NCAM with the exocyst complex and induces depletion of the internal membrane pool. A , NCAM immunoprecipitates from NCAM+/+ growth cones analyzed by Western blot with NCAM, exo70, and sec8 antibodies. Mock immunoprecipitation with nonspecific IgG served as control. Growth cones were pretreated with nonspecific rabbit IgG or NCAM antibodies to cluster NCAM at the surface of growth cones. Note that coimmunoprecipitation of exo70 and sec8 with NCAM is increased in NCAM antibody-treated growth cones. B–E , Graphs show internal membrane pools in NCAM antibody-treated growth cones (mean + SEM from 3 experiments) normalized to the size of the internal membrane pool in preimmune serum-treated growth cones set to 100% (dashed line). Note that the internal membrane pool is reduced in NCAM+/+ growth cones treated with NCAM antibodies, an effect that is blocked in NCAM+/+ growth cones pretreated with BAPTA ( B ), tetanus toxin ( C ), or the FGFR inhibitor and the L-type VDCC inhibitor nifedipine ( D ) or when growth cones were treated with NCAM antibody at 25°C or 4°C ( C ). NCAM−/− growth cones served as control ( B ). Inhibitor of T-type VDCC pimozide ( D ) does not influence, while inhibitor of dynamin-dependent endocytosis dynasore ( E ) increases, the effect of NCAM antibodies. * p

Techniques Used: Isolation, Western Blot, Immunoprecipitation

7) Product Images from "The Neural Cell Adhesion Molecule Promotes FGFR-Dependent Phosphorylation and Membrane Targeting of the Exocyst Complex to Induce Exocytosis in Growth Cones"

Article Title: The Neural Cell Adhesion Molecule Promotes FGFR-Dependent Phosphorylation and Membrane Targeting of the Exocyst Complex to Induce Exocytosis in Growth Cones

Journal: The Journal of Neuroscience

doi: 10.1523/JNEUROSCI.3109-10.2011

Specific triggering of NCAM functions by application of NCAM antibodies to isolated growth cones enhances the association of NCAM with the exocyst complex and induces depletion of the internal membrane pool. A , NCAM immunoprecipitates from NCAM+/+ growth cones analyzed by Western blot with NCAM, exo70, and sec8 antibodies. Mock immunoprecipitation with nonspecific IgG served as control. Growth cones were pretreated with nonspecific rabbit IgG or NCAM antibodies to cluster NCAM at the surface of growth cones. Note that coimmunoprecipitation of exo70 and sec8 with NCAM is increased in NCAM antibody-treated growth cones. B–E , Graphs show internal membrane pools in NCAM antibody-treated growth cones (mean + SEM from 3 experiments) normalized to the size of the internal membrane pool in preimmune serum-treated growth cones set to 100% (dashed line). Note that the internal membrane pool is reduced in NCAM+/+ growth cones treated with NCAM antibodies, an effect that is blocked in NCAM+/+ growth cones pretreated with BAPTA ( B ), tetanus toxin ( C ), or the FGFR inhibitor and the L-type VDCC inhibitor nifedipine ( D ) or when growth cones were treated with NCAM antibody at 25°C or 4°C ( C ). NCAM−/− growth cones served as control ( B ). Inhibitor of T-type VDCC pimozide ( D ) does not influence, while inhibitor of dynamin-dependent endocytosis dynasore ( E ) increases, the effect of NCAM antibodies. * p
Figure Legend Snippet: Specific triggering of NCAM functions by application of NCAM antibodies to isolated growth cones enhances the association of NCAM with the exocyst complex and induces depletion of the internal membrane pool. A , NCAM immunoprecipitates from NCAM+/+ growth cones analyzed by Western blot with NCAM, exo70, and sec8 antibodies. Mock immunoprecipitation with nonspecific IgG served as control. Growth cones were pretreated with nonspecific rabbit IgG or NCAM antibodies to cluster NCAM at the surface of growth cones. Note that coimmunoprecipitation of exo70 and sec8 with NCAM is increased in NCAM antibody-treated growth cones. B–E , Graphs show internal membrane pools in NCAM antibody-treated growth cones (mean + SEM from 3 experiments) normalized to the size of the internal membrane pool in preimmune serum-treated growth cones set to 100% (dashed line). Note that the internal membrane pool is reduced in NCAM+/+ growth cones treated with NCAM antibodies, an effect that is blocked in NCAM+/+ growth cones pretreated with BAPTA ( B ), tetanus toxin ( C ), or the FGFR inhibitor and the L-type VDCC inhibitor nifedipine ( D ) or when growth cones were treated with NCAM antibody at 25°C or 4°C ( C ). NCAM−/− growth cones served as control ( B ). Inhibitor of T-type VDCC pimozide ( D ) does not influence, while inhibitor of dynamin-dependent endocytosis dynasore ( E ) increases, the effect of NCAM antibodies. * p

Techniques Used: Isolation, Western Blot, Immunoprecipitation

8) Product Images from "GABAB receptors modulate Ca2+ but not G protein‐gated inwardly rectifying K+ channels in cerebrospinal‐fluid contacting neurones of mouse brainstem"

Article Title: GABAB receptors modulate Ca2+ but not G protein‐gated inwardly rectifying K+ channels in cerebrospinal‐fluid contacting neurones of mouse brainstem

Journal: The Journal of Physiology

doi: 10.1113/JP277172

CSF‐cNs express N‐type voltage‐gated Ca 2+ channels A , representative whole‐cell current traces recorded in response to voltage steps from −60 mV to +30 mV ( V Step , +10 mV increments, protocol illustrated under the current traces) from a holding potential of −70 mV ( V h ) to elicit Ca 2+ current in a CSF‐cN. The inset represents the recorded CSF‐cN after cell dialysis with Alexa 594 (10 μM) to confirm the morphology. CC: central canal. B , average current‐voltage relationship for the Ca 2+ currents recorded in CSF‐cNs ( n = 13). Data are fitted using a Boltzmann function (red trace, see Methods for more details). The inset in red gives the values defining the properties of the Ca 2+ current in CSF‐cNs obtained from the Boltzmann fit of the average data (see text for details). C , summary box‐and‐whiskers plots of the averaged percentage of Ca 2+ current blockade in the presence of cadmium (Cd 2+ ; 105 ± 3%; black box, n = 12), ω‐conotoxin GVIA (ω‐CnTx GVIA; 64 ± 6%; grey box, n = 7), ω‐agatoxin IVA (ω‐AgaTx IVA; 11 ± 2%, light grey box, n = 11), and nifedipine (14 ± 3%; white box, n = 9). Ca 2+ current sensitivity to cadmium and ω‐CnTx GVIA is significantly higher compared to that observed in the presence of ω‐agatoxin IVA ( **** P
Figure Legend Snippet: CSF‐cNs express N‐type voltage‐gated Ca 2+ channels A , representative whole‐cell current traces recorded in response to voltage steps from −60 mV to +30 mV ( V Step , +10 mV increments, protocol illustrated under the current traces) from a holding potential of −70 mV ( V h ) to elicit Ca 2+ current in a CSF‐cN. The inset represents the recorded CSF‐cN after cell dialysis with Alexa 594 (10 μM) to confirm the morphology. CC: central canal. B , average current‐voltage relationship for the Ca 2+ currents recorded in CSF‐cNs ( n = 13). Data are fitted using a Boltzmann function (red trace, see Methods for more details). The inset in red gives the values defining the properties of the Ca 2+ current in CSF‐cNs obtained from the Boltzmann fit of the average data (see text for details). C , summary box‐and‐whiskers plots of the averaged percentage of Ca 2+ current blockade in the presence of cadmium (Cd 2+ ; 105 ± 3%; black box, n = 12), ω‐conotoxin GVIA (ω‐CnTx GVIA; 64 ± 6%; grey box, n = 7), ω‐agatoxin IVA (ω‐AgaTx IVA; 11 ± 2%, light grey box, n = 11), and nifedipine (14 ± 3%; white box, n = 9). Ca 2+ current sensitivity to cadmium and ω‐CnTx GVIA is significantly higher compared to that observed in the presence of ω‐agatoxin IVA ( **** P

Techniques Used:

9) Product Images from "Ca2+ entry-independent effects of L-type Ca2+ channel modulators on Ca2+ sparks in ventricular myocytes"

Article Title: Ca2+ entry-independent effects of L-type Ca2+ channel modulators on Ca2+ sparks in ventricular myocytes

Journal: American journal of physiology. Cell physiology

doi: 10.1152/ajpcell.00437.2006

DHPR channel blocker nifedipine did not affect SR Ca 2+ load of permeabilized myocytes Confocal linescan images and correspondingΔF/F0 profiles of Ca 2+ release induced by application of 20 mM caffeine under control conditions, and after addition of 5 μM nifedipine.
Figure Legend Snippet: DHPR channel blocker nifedipine did not affect SR Ca 2+ load of permeabilized myocytes Confocal linescan images and correspondingΔF/F0 profiles of Ca 2+ release induced by application of 20 mM caffeine under control conditions, and after addition of 5 μM nifedipine.

Techniques Used:

Verapamil did not affect Ca 2+ sparks in permeabilized myocytes A. Top , confocal linescan images of Ca2+ sparks. Bottom, local ΔF/F 0 profiles of Ca 2+ release events.ΔF/F 0 plots were obtained by averaging fluo-3 fluorescence from 1 μm-wide region marked by boxes. Measurements were done under control conditions, and after subsequent addition of verapamil (10 μM), and then of nifepidine (5 μM). B. Average data of spark frequency under the named conditions, control, verapamil and verapamil plus nifedipine. *Statistically different at P
Figure Legend Snippet: Verapamil did not affect Ca 2+ sparks in permeabilized myocytes A. Top , confocal linescan images of Ca2+ sparks. Bottom, local ΔF/F 0 profiles of Ca 2+ release events.ΔF/F 0 plots were obtained by averaging fluo-3 fluorescence from 1 μm-wide region marked by boxes. Measurements were done under control conditions, and after subsequent addition of verapamil (10 μM), and then of nifepidine (5 μM). B. Average data of spark frequency under the named conditions, control, verapamil and verapamil plus nifedipine. *Statistically different at P

Techniques Used: Fluorescence

DHPR channel agonists and blockers did not affect SR Ca 2+ uptake by cardiac SR vesicles A. SR Ca 2+ uptake measured in control conditions, in the presence of nifedipine (10 μM) and in the presence of BayK (5 μM). Ca 2+ uptake was initiated by addition of CaCl 2 (20 μM). Experimental data were fitted by a single exponential function from which the time constant of Ca 2+ uptake was derived. Average time constant under control conditions was 130 ± 35 s (n = 6). B. Relative time constants of SR Ca 2+ uptake (expressed as % of control values, n=6 each) for Nifedipine (10 μM), Nimodipine (5 μM), Calciseptine (1 μM), FS-2 (1 μM), Verapamil (10 μM), BayK (5 μM), and FPL (5 μM). Values between groups were not statistically different.
Figure Legend Snippet: DHPR channel agonists and blockers did not affect SR Ca 2+ uptake by cardiac SR vesicles A. SR Ca 2+ uptake measured in control conditions, in the presence of nifedipine (10 μM) and in the presence of BayK (5 μM). Ca 2+ uptake was initiated by addition of CaCl 2 (20 μM). Experimental data were fitted by a single exponential function from which the time constant of Ca 2+ uptake was derived. Average time constant under control conditions was 130 ± 35 s (n = 6). B. Relative time constants of SR Ca 2+ uptake (expressed as % of control values, n=6 each) for Nifedipine (10 μM), Nimodipine (5 μM), Calciseptine (1 μM), FS-2 (1 μM), Verapamil (10 μM), BayK (5 μM), and FPL (5 μM). Values between groups were not statistically different.

Techniques Used: Derivative Assay

Nifedipine and nimodipine decreased Ca 2+ spark frequency in saponin-permeabilized rat ventricular myocytes A (a) Confocal linescan images of Ca 2+ sparks in control conditions, and 5 minutes after addition of nifedipine (5 μM). Bottom traces are local ΔF/F0 profiles of Ca 2+ release events. These ΔF/F 0 plots were obtained by averaging fluo-3 fluorescence from 1 μm wide region marked by boxes on the left of the linescan images. (b) Average linescan images of sparks (n=18 events each) observed under control conditions and with nifedipine (5 μM). (c, d, e, f) Numerical data of spark characteristics (frequency, amplitude, duration and width) under control conditions (Ctrl, black) and in the presence of nifedipine (Nif, red). B (a) Confocal linescan images of Ca 2+ sparks in control conditions and in the presence of nimodipine (1 μM). Bottom traces are localΔF/F 0 profiles of Ca 2+ release events in the region marked by boxes. (b, c, d, e) Average data of Ca 2+ release events (frequency, amplitude, duration and width) under control conditions (Ctrl, black) and in the presence of nimodipine (Nimod, red). *Significant nifedipine or nimodipine effects on Ca 2+ spark frequency compared to control, P
Figure Legend Snippet: Nifedipine and nimodipine decreased Ca 2+ spark frequency in saponin-permeabilized rat ventricular myocytes A (a) Confocal linescan images of Ca 2+ sparks in control conditions, and 5 minutes after addition of nifedipine (5 μM). Bottom traces are local ΔF/F0 profiles of Ca 2+ release events. These ΔF/F 0 plots were obtained by averaging fluo-3 fluorescence from 1 μm wide region marked by boxes on the left of the linescan images. (b) Average linescan images of sparks (n=18 events each) observed under control conditions and with nifedipine (5 μM). (c, d, e, f) Numerical data of spark characteristics (frequency, amplitude, duration and width) under control conditions (Ctrl, black) and in the presence of nifedipine (Nif, red). B (a) Confocal linescan images of Ca 2+ sparks in control conditions and in the presence of nimodipine (1 μM). Bottom traces are localΔF/F 0 profiles of Ca 2+ release events in the region marked by boxes. (b, c, d, e) Average data of Ca 2+ release events (frequency, amplitude, duration and width) under control conditions (Ctrl, black) and in the presence of nimodipine (Nimod, red). *Significant nifedipine or nimodipine effects on Ca 2+ spark frequency compared to control, P

Techniques Used: Fluorescence

Nifedipine decreased Ca 2+ spark frequency in patch-clamped cat ventricular myocytes bathed with Ca 2+ -free solutions Intact myocytes were loaded with Fluo-4 by internal perfusion via a patch pipette. Pipette (intracellular) and bathing solutions were the same as the intracellular solution utilized for bathing saponin permeabilized myocytes (see Methods). The figure shows confocal linescan images of Ca 2+ sparks in control conditions and after addition of nifedipine (5 μM). In all cases, local ΔF/F 0 profiles of Ca 2+ release events are shown, which were obtained by averaging fluo-3 fluorescence from 1 μm wide region marked by boxes.
Figure Legend Snippet: Nifedipine decreased Ca 2+ spark frequency in patch-clamped cat ventricular myocytes bathed with Ca 2+ -free solutions Intact myocytes were loaded with Fluo-4 by internal perfusion via a patch pipette. Pipette (intracellular) and bathing solutions were the same as the intracellular solution utilized for bathing saponin permeabilized myocytes (see Methods). The figure shows confocal linescan images of Ca 2+ sparks in control conditions and after addition of nifedipine (5 μM). In all cases, local ΔF/F 0 profiles of Ca 2+ release events are shown, which were obtained by averaging fluo-3 fluorescence from 1 μm wide region marked by boxes.

Techniques Used: Transferring, Fluorescence

10) Product Images from "α-Synuclein oligomers mediate the aberrant form of spike-induced calcium release from IP3 receptor"

Article Title: α-Synuclein oligomers mediate the aberrant form of spike-induced calcium release from IP3 receptor

Journal: Scientific Reports

doi: 10.1038/s41598-019-52135-3

α-Synuclein oligomers prolonged AHP by spike-induced Ca 2+ release from IP 3 receptor coupled with L-VDCC and SK channel. (a ) Specimen recordings of action potentials during positive current pulses (300 ms, 0.3 nA) in neurons with αSN or αSNo under the application of the L-VDCC blocker nifedipine (10 μM), the SK channel blocker apamin (100 nM) and the IP 3 R blocker heparin. These blockers canceled αSNo-mediated reduction of spike frequency. Scale bars, 100 ms and 10 mV. ( b ) Mean spike frequencies during 0.3 nA positive current steps under the application of various blockers of channels or receptors controlling intracellular Ca 2+ dynamics. * p
Figure Legend Snippet: α-Synuclein oligomers prolonged AHP by spike-induced Ca 2+ release from IP 3 receptor coupled with L-VDCC and SK channel. (a ) Specimen recordings of action potentials during positive current pulses (300 ms, 0.3 nA) in neurons with αSN or αSNo under the application of the L-VDCC blocker nifedipine (10 μM), the SK channel blocker apamin (100 nM) and the IP 3 R blocker heparin. These blockers canceled αSNo-mediated reduction of spike frequency. Scale bars, 100 ms and 10 mV. ( b ) Mean spike frequencies during 0.3 nA positive current steps under the application of various blockers of channels or receptors controlling intracellular Ca 2+ dynamics. * p

Techniques Used: Mass Spectrometry

11) Product Images from "NCAM induces CaMKII?-mediated RPTP? phosphorylation to enhance its catalytic activity and neurite outgrowth"

Article Title: NCAM induces CaMKII?-mediated RPTP? phosphorylation to enhance its catalytic activity and neurite outgrowth

Journal: The Journal of Cell Biology

doi: 10.1083/jcb.200803045

NCAM-induced CaMKIIα activation depends on Ca 2+ influx via T- and L-type VDCC. (A) Cultured hippocampal neurons were incubated with pimozide and nifedipine, inhibitors of T-and L-type VDCC, respectively. Neurons were then stimulated with rat NCAM monoclonal antibodies (H28live) or nonspecific rat IgG, then fixed and colabeled with antibodies against activated Thr286-phosphorylated CaMKIIα. Representative images are shown. Note that clustering of NCAM without inhibitors induces an increase in active CaMKIIα levels along neurites and that active CaMKIIα accumulates in NCAM clusters. Pimozide and nifedipine inhibit CaMKIIα activation. Graph shows mean levels ± SEM in arbitrary units (AU) of active CaMKIIα along neurites. n > 45 neurites from 30 neurons from 3 coverslips analyzed in each group. Bar, 20 μm. (B) Cultured cortical neurons were treated with nonspecific rabbit IgG or NCAM polyclonal antibodies in the absence or presence of pimozide and nifedipine. Lysates of these cells and fyn immunoprecipitates from the lysates were then probed with the indicated antibodies by Western blotting. Note that pimozide and nifedipine inhibited fyn and CaMKIIα activation in response to NCAM antibodies. Graphs show quantitation of the blots (mean ± SEM), with the levels in cells treated with nonspecific IgG without inhibitors set to 100%. *, P
Figure Legend Snippet: NCAM-induced CaMKIIα activation depends on Ca 2+ influx via T- and L-type VDCC. (A) Cultured hippocampal neurons were incubated with pimozide and nifedipine, inhibitors of T-and L-type VDCC, respectively. Neurons were then stimulated with rat NCAM monoclonal antibodies (H28live) or nonspecific rat IgG, then fixed and colabeled with antibodies against activated Thr286-phosphorylated CaMKIIα. Representative images are shown. Note that clustering of NCAM without inhibitors induces an increase in active CaMKIIα levels along neurites and that active CaMKIIα accumulates in NCAM clusters. Pimozide and nifedipine inhibit CaMKIIα activation. Graph shows mean levels ± SEM in arbitrary units (AU) of active CaMKIIα along neurites. n > 45 neurites from 30 neurons from 3 coverslips analyzed in each group. Bar, 20 μm. (B) Cultured cortical neurons were treated with nonspecific rabbit IgG or NCAM polyclonal antibodies in the absence or presence of pimozide and nifedipine. Lysates of these cells and fyn immunoprecipitates from the lysates were then probed with the indicated antibodies by Western blotting. Note that pimozide and nifedipine inhibited fyn and CaMKIIα activation in response to NCAM antibodies. Graphs show quantitation of the blots (mean ± SEM), with the levels in cells treated with nonspecific IgG without inhibitors set to 100%. *, P

Techniques Used: Activation Assay, Cell Culture, Incubation, Western Blot, Quantitation Assay

Related Articles

other:

Article Title: Calcium Channels in Postnatal Development of Rat Pancreatic Beta Cells and Their Role in Insulin Secretion
Article Snippet: Reagents were obtained from the following sources: collagenase P, bovine serum albumin (BSA), Ficoll 400, trypan blue, 4-(2-hydroxyethyl)-1 piperazineethanesulfonic acid (HEPES), poly-L-lysine, Staphylococcus aureus protein A, trypsin, insulin, guinea-pig complement, nickel chloride (II), and all salts of electrophysiological recordings from Sigma-Aldrich (St. Louis, MO, USA); mibefradil, nifedipine, anti-VGCC rabbit polyclonal IgG from Alomone Labs (Jerusalem, Israel); FITC-conjugated anti-guinea pig, and Alexa Fluor 647-conjugated anti-rabbit IgG from Jackson ImmunoResearch (West Grove, USA).

Article Title: Calcium Channels in Postnatal Development of Rat Pancreatic Beta Cells and Their Role in Insulin Secretion
Article Snippet: Chemical and Reagents Reagents were obtained from the following sources: collagenase P, bovine serum albumin (BSA), Ficoll 400, trypan blue, 4-(2-hydroxyethyl)-1 piperazineethanesulfonic acid (HEPES), poly-L-lysine, Staphylococcus aureus protein A, trypsin, insulin, guinea-pig complement, nickel chloride (II), and all salts of electrophysiological recordings from Sigma-Aldrich (St. Louis, MO, USA); mibefradil, nifedipine, anti-VGCC rabbit polyclonal IgG from Alomone Labs (Jerusalem, Israel); FITC-conjugated anti-guinea pig, and Alexa Fluor 647-conjugated anti-rabbit IgG from Jackson ImmunoResearch (West Grove, USA).

Article Title: Homer regulates calcium signalling in growth cone turning
Article Snippet: Reagents Control (TGgTGAAcATAcGTTGTTgCCCgAT) and specific Homer1 (TGCTGAAGATAGTTGTTCCCCCAT) morpholine oligonucleotides labelled with either fluoro-isothiocyanate or biotin (designed by GeneTools, LLC, Philomath, OR, USA); KN-93 and KN-92 (Calbiochem, San Diego, CA, USA)); nerve growth factor and cyclosporin A (Sigma-Aldrich, St Louis, MO, USA); Semaphorin-3A and Netrin-1 (R & D Systems, Minneapolis, MN, USA); BDNF, thapsigargin, nifedipine and ω-conotoxin-MVIIC (Alomone Labs); SKF-96365 (TOCRIS, Bristol, UK); La3+ and Ni++ (Sigma).

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    Alomone Labs nifedipine
    Effect of ion channel blockers on L55P TTR-induced calcium influx and analysis of sensitivity to icilin and capsaicin , (A) L55P was applied to DRG growth cones in the presence of VGCC inhibitors <t>(nifedipine,</t> ω-agatoxin IVA, ω-conotoxin GIVA), Na V inhibitors (tetrodotoxin, ambroxol and carbamazepine) and TRP inhibitors (SKF-96365, BCTC). The resulting maximal calcium influx (max ΔF/F 0 ) calculated over the imaging period (7 min) was calculated. (B) Effect of capsaicin (1 μM) and icilin (100 μM) on cytosolic calcium in DRG growth cones in culture. When DRG cultures were pre-treated with ambroxol (5 μM), icilin-induced calcium fluorescence was significantly decreased. All graphs show maximal ΔF/F 0 ± SEM for n = 12-24 growth cones. Significant differences from control values are depicted as: * p
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    Effect of ion channel blockers on L55P TTR-induced calcium influx and analysis of sensitivity to icilin and capsaicin , (A) L55P was applied to DRG growth cones in the presence of VGCC inhibitors (nifedipine, ω-agatoxin IVA, ω-conotoxin GIVA), Na V inhibitors (tetrodotoxin, ambroxol and carbamazepine) and TRP inhibitors (SKF-96365, BCTC). The resulting maximal calcium influx (max ΔF/F 0 ) calculated over the imaging period (7 min) was calculated. (B) Effect of capsaicin (1 μM) and icilin (100 μM) on cytosolic calcium in DRG growth cones in culture. When DRG cultures were pre-treated with ambroxol (5 μM), icilin-induced calcium fluorescence was significantly decreased. All graphs show maximal ΔF/F 0 ± SEM for n = 12-24 growth cones. Significant differences from control values are depicted as: * p

    Journal: Molecular Neurodegeneration

    Article Title: TRPM8 and Nav1.8 sodium channels are required for transthyretin-induced calcium influx in growth cones of small-diameter TrkA-positive sensory neurons

    doi: 10.1186/1750-1326-6-19

    Figure Lengend Snippet: Effect of ion channel blockers on L55P TTR-induced calcium influx and analysis of sensitivity to icilin and capsaicin , (A) L55P was applied to DRG growth cones in the presence of VGCC inhibitors (nifedipine, ω-agatoxin IVA, ω-conotoxin GIVA), Na V inhibitors (tetrodotoxin, ambroxol and carbamazepine) and TRP inhibitors (SKF-96365, BCTC). The resulting maximal calcium influx (max ΔF/F 0 ) calculated over the imaging period (7 min) was calculated. (B) Effect of capsaicin (1 μM) and icilin (100 μM) on cytosolic calcium in DRG growth cones in culture. When DRG cultures were pre-treated with ambroxol (5 μM), icilin-induced calcium fluorescence was significantly decreased. All graphs show maximal ΔF/F 0 ± SEM for n = 12-24 growth cones. Significant differences from control values are depicted as: * p

    Article Snippet: Pharmacological compounds used in experiments were obtained from the following sources: nifedipine, ω-agatoxin IVA, ω-conotoxin GIVA (Alomone Labs, Israel), SKF-96365 (Tocris, Bristol, UK), [N-(4-tert-butylphenyl)-4-(3-chloropyridin-2-yl)piperazine-1-carboxamide] (BCTC), (ENZO, NY, USA), ambroxol and carbamazepine (Sigma-Aldrich, MO, USA).

    Techniques: Imaging, Fluorescence

    Spontaneous calcium transients and growth cone turning are sensitive to blockage of store-operated channels . (A) Individual control morphant growth cones exhibited sparse spontaneous calcium transients, occurring at a rate of approximately one transient per three minutes. (B) Homer1 morphant growth cones exhibited significantly greater frequency, at a rate of at least one spontaneous transient per minute. (C) A trace from a single Homer1 morphant growth cone showed a decrease in spontaneous calcium transient frequency in the presence of bath applied SKF-96365. (D) Quantification of spontaneous calcium transient frequencies in Homer1 morphant growth cones. Removing calcium from the media (Ca free) or bath application of La 3+ (La) or SKF-96365 (SKF) reduced spontaneous transient frequencies in Homer1 morphant growth cones to control (ctrl) levels. Bath application of a voltage-gated calcium channel (VGCC) inhibitor cocktail or nifedipine alone had little effect on the frequency of spontaneous calcium transients in Homer1 morphant growth cones. (E) Calcium-dependent brain derived neurotrophic factor (BDNF)-induced turning is mediated through store-operated channels. BDNF attraction was abolished when TRPC channels were inactivated with bath application of SKF-96365 or La 3+ . Inhibition of VGCCs with nifedipine or ω-conotoxin-MVIIC had no effect on control and Homer1 morphant growth cone turning. (F) Inhibition of store-operated channels did not alter axon extension rates. Error bars indicate standard error of the mean. Cocktail = nifedipine, ω-conotoxin-MVIIC plus Ni ++ . The scale bar in (C) applies also to (A, B).

    Journal: Neural Development

    Article Title: Homer regulates calcium signalling in growth cone turning

    doi: 10.1186/1749-8104-4-29

    Figure Lengend Snippet: Spontaneous calcium transients and growth cone turning are sensitive to blockage of store-operated channels . (A) Individual control morphant growth cones exhibited sparse spontaneous calcium transients, occurring at a rate of approximately one transient per three minutes. (B) Homer1 morphant growth cones exhibited significantly greater frequency, at a rate of at least one spontaneous transient per minute. (C) A trace from a single Homer1 morphant growth cone showed a decrease in spontaneous calcium transient frequency in the presence of bath applied SKF-96365. (D) Quantification of spontaneous calcium transient frequencies in Homer1 morphant growth cones. Removing calcium from the media (Ca free) or bath application of La 3+ (La) or SKF-96365 (SKF) reduced spontaneous transient frequencies in Homer1 morphant growth cones to control (ctrl) levels. Bath application of a voltage-gated calcium channel (VGCC) inhibitor cocktail or nifedipine alone had little effect on the frequency of spontaneous calcium transients in Homer1 morphant growth cones. (E) Calcium-dependent brain derived neurotrophic factor (BDNF)-induced turning is mediated through store-operated channels. BDNF attraction was abolished when TRPC channels were inactivated with bath application of SKF-96365 or La 3+ . Inhibition of VGCCs with nifedipine or ω-conotoxin-MVIIC had no effect on control and Homer1 morphant growth cone turning. (F) Inhibition of store-operated channels did not alter axon extension rates. Error bars indicate standard error of the mean. Cocktail = nifedipine, ω-conotoxin-MVIIC plus Ni ++ . The scale bar in (C) applies also to (A, B).

    Article Snippet: Reagents Control (TGgTGAAcATAcGTTGTTgCCCgAT) and specific Homer1 (TGCTGAAGATAGTTGTTCCCCCAT) morpholine oligonucleotides labelled with either fluoro-isothiocyanate or biotin (designed by GeneTools, LLC, Philomath, OR, USA); KN-93 and KN-92 (Calbiochem, San Diego, CA, USA)); nerve growth factor and cyclosporin A (Sigma-Aldrich, St Louis, MO, USA); Semaphorin-3A and Netrin-1 (R & D Systems, Minneapolis, MN, USA); BDNF, thapsigargin, nifedipine and ω-conotoxin-MVIIC (Alomone Labs); SKF-96365 (TOCRIS, Bristol, UK); La3+ and Ni++ (Sigma).

    Techniques: Derivative Assay, Inhibition

    Effect of calcium channel inhibitors on basal and glucose-induced insulin secretion in adult beta cells. (A) Overall insulin secretory activity (insulin secretion index) of adult beta cells incubated with nifedipine (5 µM), mibefradil (1 µM), NiCl 2 (50 µM) and TTA-A 2 (50 µM), exposed at basal (5.6 mM glucose), and stimulating (15.6 mM glucose) conditions. Bars represent the mean ± SEM of three different experiments by duplicate. * p ≤ 0.05 denotes significant differences with respect to control cells at 5.6 and 15.5 mM glucose. Dunnet test (analysis of variance). (B,C) Frequency distribution of functional subpopulations of beta cells incubated with inhibitors of (A) observed in basal (B) and stimulating (C) glucose conditions.

    Journal: Frontiers in Endocrinology

    Article Title: Calcium Channels in Postnatal Development of Rat Pancreatic Beta Cells and Their Role in Insulin Secretion

    doi: 10.3389/fendo.2018.00040

    Figure Lengend Snippet: Effect of calcium channel inhibitors on basal and glucose-induced insulin secretion in adult beta cells. (A) Overall insulin secretory activity (insulin secretion index) of adult beta cells incubated with nifedipine (5 µM), mibefradil (1 µM), NiCl 2 (50 µM) and TTA-A 2 (50 µM), exposed at basal (5.6 mM glucose), and stimulating (15.6 mM glucose) conditions. Bars represent the mean ± SEM of three different experiments by duplicate. * p ≤ 0.05 denotes significant differences with respect to control cells at 5.6 and 15.5 mM glucose. Dunnet test (analysis of variance). (B,C) Frequency distribution of functional subpopulations of beta cells incubated with inhibitors of (A) observed in basal (B) and stimulating (C) glucose conditions.

    Article Snippet: Reagents were obtained from the following sources: collagenase P, bovine serum albumin (BSA), Ficoll 400, trypan blue, 4-(2-hydroxyethyl)-1 piperazineethanesulfonic acid (HEPES), poly-L-lysine, Staphylococcus aureus protein A, trypsin, insulin, guinea-pig complement, nickel chloride (II), and all salts of electrophysiological recordings from Sigma-Aldrich (St. Louis, MO, USA); mibefradil, nifedipine, anti-VGCC rabbit polyclonal IgG from Alomone Labs (Jerusalem, Israel); FITC-conjugated anti-guinea pig, and Alexa Fluor 647-conjugated anti-rabbit IgG from Jackson ImmunoResearch (West Grove, USA).

    Techniques: Activity Assay, Incubation, Functional Assay

    Effect of calcium channel inhibitors on low-voltage-activated (LVA) and high-voltage-activated (HVA) calcium currents in adult beta cells. (A–F) Representative recordings of global calcium currents observed in adult beta cells before and after of calcium channel inhibitors: mibefradil (1 and 10 µM), NiCl 2 (50 µM), TTA-A 2 (5 and 50 µM), and nifedipine (5 µM), respectively. Protocol: voltage ramp from −80 to +60 mV, 500 ms duration, and 0.5 mV/ms slope. (G) Normalized calcium current after of calcium channel inhibitors: 1 µM mibefradil ( n = 5), 10 µM mibefradil ( n = 6), NiCl 2 ( n = 6), 5 µM TTA-A 2 ( n = 5), 50 µM TTA-A 2 ( n = 3), and nifedipine ( n = 6). * p ≤ 0.05 denotes significant differences compared with cells without inhibitors, paired t -test.

    Journal: Frontiers in Endocrinology

    Article Title: Calcium Channels in Postnatal Development of Rat Pancreatic Beta Cells and Their Role in Insulin Secretion

    doi: 10.3389/fendo.2018.00040

    Figure Lengend Snippet: Effect of calcium channel inhibitors on low-voltage-activated (LVA) and high-voltage-activated (HVA) calcium currents in adult beta cells. (A–F) Representative recordings of global calcium currents observed in adult beta cells before and after of calcium channel inhibitors: mibefradil (1 and 10 µM), NiCl 2 (50 µM), TTA-A 2 (5 and 50 µM), and nifedipine (5 µM), respectively. Protocol: voltage ramp from −80 to +60 mV, 500 ms duration, and 0.5 mV/ms slope. (G) Normalized calcium current after of calcium channel inhibitors: 1 µM mibefradil ( n = 5), 10 µM mibefradil ( n = 6), NiCl 2 ( n = 6), 5 µM TTA-A 2 ( n = 5), 50 µM TTA-A 2 ( n = 3), and nifedipine ( n = 6). * p ≤ 0.05 denotes significant differences compared with cells without inhibitors, paired t -test.

    Article Snippet: Chemical and Reagents Reagents were obtained from the following sources: collagenase P, bovine serum albumin (BSA), Ficoll 400, trypan blue, 4-(2-hydroxyethyl)-1 piperazineethanesulfonic acid (HEPES), poly-L-lysine, Staphylococcus aureus protein A, trypsin, insulin, guinea-pig complement, nickel chloride (II), and all salts of electrophysiological recordings from Sigma-Aldrich (St. Louis, MO, USA); mibefradil, nifedipine, anti-VGCC rabbit polyclonal IgG from Alomone Labs (Jerusalem, Israel); FITC-conjugated anti-guinea pig, and Alexa Fluor 647-conjugated anti-rabbit IgG from Jackson ImmunoResearch (West Grove, USA).

    Techniques: Mass Spectrometry

    Effect of calcium channel inhibitors on basal and glucose-induced insulin secretion in adult beta cells. (A) Overall insulin secretory activity (insulin secretion index) of adult beta cells incubated with nifedipine (5 µM), mibefradil (1 µM), NiCl 2 (50 µM) and TTA-A 2 (50 µM), exposed at basal (5.6 mM glucose), and stimulating (15.6 mM glucose) conditions. Bars represent the mean ± SEM of three different experiments by duplicate. * p ≤ 0.05 denotes significant differences with respect to control cells at 5.6 and 15.5 mM glucose. Dunnet test (analysis of variance). (B,C) Frequency distribution of functional subpopulations of beta cells incubated with inhibitors of (A) observed in basal (B) and stimulating (C) glucose conditions.

    Journal: Frontiers in Endocrinology

    Article Title: Calcium Channels in Postnatal Development of Rat Pancreatic Beta Cells and Their Role in Insulin Secretion

    doi: 10.3389/fendo.2018.00040

    Figure Lengend Snippet: Effect of calcium channel inhibitors on basal and glucose-induced insulin secretion in adult beta cells. (A) Overall insulin secretory activity (insulin secretion index) of adult beta cells incubated with nifedipine (5 µM), mibefradil (1 µM), NiCl 2 (50 µM) and TTA-A 2 (50 µM), exposed at basal (5.6 mM glucose), and stimulating (15.6 mM glucose) conditions. Bars represent the mean ± SEM of three different experiments by duplicate. * p ≤ 0.05 denotes significant differences with respect to control cells at 5.6 and 15.5 mM glucose. Dunnet test (analysis of variance). (B,C) Frequency distribution of functional subpopulations of beta cells incubated with inhibitors of (A) observed in basal (B) and stimulating (C) glucose conditions.

    Article Snippet: Chemical and Reagents Reagents were obtained from the following sources: collagenase P, bovine serum albumin (BSA), Ficoll 400, trypan blue, 4-(2-hydroxyethyl)-1 piperazineethanesulfonic acid (HEPES), poly-L-lysine, Staphylococcus aureus protein A, trypsin, insulin, guinea-pig complement, nickel chloride (II), and all salts of electrophysiological recordings from Sigma-Aldrich (St. Louis, MO, USA); mibefradil, nifedipine, anti-VGCC rabbit polyclonal IgG from Alomone Labs (Jerusalem, Israel); FITC-conjugated anti-guinea pig, and Alexa Fluor 647-conjugated anti-rabbit IgG from Jackson ImmunoResearch (West Grove, USA).

    Techniques: Activity Assay, Incubation, Functional Assay