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    Alomone Labs ryanodine
    Ca 2+ cooperativity for glutamatergic spontaneous release. (Aa) A representative image of hippocampal neurons in autaptic culture system labeled by the extracellular application of lipophilic fluorescent dyes, Dil. (Ab) Top. A representative trace of mEPSC in the presence of picrotoxin (PTX) and CNQX. Bottom. left: An enlarged trace of a single mEPSC. middle: A bar graph indicating rise and decay time constants of mEPSCs. Rise time constant was 0.53 ± 0.02 ms ( N = 62). right: A histogram representing number of cells by mEPSC frequency. (Ac) A representative trace of mEPSCs before (Ctrl) and after the application of 0.5 μM tetrodotoxin (TTX). (B) Ba-Bc. Top. Representative traces of mEPSCs in control (2 mM Ca 2+ ) and 0 mM [Ca 2+ ] e (0 Ca 2+ ) (Ba), and the presence of <t>ryanodine</t> (RYN) followed by 2-aminoethoxydiphenylborane (2-APB) (Bb), and 2-APB followed by RYN (Bc), respectively. Five 500 ms-long mEPSC traces were overlaid. Bottom. Average time courses of the normalized mEPSC frequency. In each time course plot, solid lines indicate the presence of 0 Ca 2+ , RYN, 2-APB, and RYN with 2-APB, respectively. The data were normalized by the mean mEPSC frequency of control. (Bd) A bar graph of average values of the normalized mEPSC frequency in 0 Ca 2+ ( N = 13, 0.42 ± 0.03, P
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    Images

    1) Product Images from "Voltage-gated calcium channels contribute to spontaneous glutamate release directly via nanodomain coupling or indirectly via calmodulin"

    Article Title: Voltage-gated calcium channels contribute to spontaneous glutamate release directly via nanodomain coupling or indirectly via calmodulin

    Journal: bioRxiv

    doi: 10.1101/2020.11.10.376111

    Ca 2+ cooperativity for glutamatergic spontaneous release. (Aa) A representative image of hippocampal neurons in autaptic culture system labeled by the extracellular application of lipophilic fluorescent dyes, Dil. (Ab) Top. A representative trace of mEPSC in the presence of picrotoxin (PTX) and CNQX. Bottom. left: An enlarged trace of a single mEPSC. middle: A bar graph indicating rise and decay time constants of mEPSCs. Rise time constant was 0.53 ± 0.02 ms ( N = 62). right: A histogram representing number of cells by mEPSC frequency. (Ac) A representative trace of mEPSCs before (Ctrl) and after the application of 0.5 μM tetrodotoxin (TTX). (B) Ba-Bc. Top. Representative traces of mEPSCs in control (2 mM Ca 2+ ) and 0 mM [Ca 2+ ] e (0 Ca 2+ ) (Ba), and the presence of ryanodine (RYN) followed by 2-aminoethoxydiphenylborane (2-APB) (Bb), and 2-APB followed by RYN (Bc), respectively. Five 500 ms-long mEPSC traces were overlaid. Bottom. Average time courses of the normalized mEPSC frequency. In each time course plot, solid lines indicate the presence of 0 Ca 2+ , RYN, 2-APB, and RYN with 2-APB, respectively. The data were normalized by the mean mEPSC frequency of control. (Bd) A bar graph of average values of the normalized mEPSC frequency in 0 Ca 2+ ( N = 13, 0.42 ± 0.03, P
    Figure Legend Snippet: Ca 2+ cooperativity for glutamatergic spontaneous release. (Aa) A representative image of hippocampal neurons in autaptic culture system labeled by the extracellular application of lipophilic fluorescent dyes, Dil. (Ab) Top. A representative trace of mEPSC in the presence of picrotoxin (PTX) and CNQX. Bottom. left: An enlarged trace of a single mEPSC. middle: A bar graph indicating rise and decay time constants of mEPSCs. Rise time constant was 0.53 ± 0.02 ms ( N = 62). right: A histogram representing number of cells by mEPSC frequency. (Ac) A representative trace of mEPSCs before (Ctrl) and after the application of 0.5 μM tetrodotoxin (TTX). (B) Ba-Bc. Top. Representative traces of mEPSCs in control (2 mM Ca 2+ ) and 0 mM [Ca 2+ ] e (0 Ca 2+ ) (Ba), and the presence of ryanodine (RYN) followed by 2-aminoethoxydiphenylborane (2-APB) (Bb), and 2-APB followed by RYN (Bc), respectively. Five 500 ms-long mEPSC traces were overlaid. Bottom. Average time courses of the normalized mEPSC frequency. In each time course plot, solid lines indicate the presence of 0 Ca 2+ , RYN, 2-APB, and RYN with 2-APB, respectively. The data were normalized by the mean mEPSC frequency of control. (Bd) A bar graph of average values of the normalized mEPSC frequency in 0 Ca 2+ ( N = 13, 0.42 ± 0.03, P

    Techniques Used: Labeling

    2) Product Images from "Double nanodomain coupling of calcium channels, ryanodine receptors and BK channels controls generation of burst firing"

    Article Title: Double nanodomain coupling of calcium channels, ryanodine receptors and BK channels controls generation of burst firing

    Journal: Neuron

    doi: 10.1016/j.neuron.2017.10.014

    Action potential-induced CICR at somatic plasma membrane but not AIS or dendrites (A) Two-photon Ca 2+ imaging at somatic plasma membrane. (Ai) Maximum intensity projection of Alexa-594-filled cartwheel cell. The red boxed region is enlarged in Ai, inset. Regions of interest for segmented line scans are indicated by red lines. C: cytosolic side. M: membrane side. (Aii, top and middle panels) Spike trains evoked by current injection (top) elicited an increase of Fluo-5F fluorescence with no change in Alexa-594. (Aii, bottom) Ca 2+ transients induced by spike trains (6 simple spikes at 50 Hz). The transients are expressed as ΔG/R (change in Fluo-5F intensity divided by Alexa-594 intensity). Black, control; blue, in ryanodine. (Aiii) Averaged Ca 2+ transients from 10 regions of interest of 5 cells. Single spike or trains of simple spikes (6 spikes at 50 Hz) evoked by current injection. (Aiv) Summary of the changes in Ca 2+ transients. *** p
    Figure Legend Snippet: Action potential-induced CICR at somatic plasma membrane but not AIS or dendrites (A) Two-photon Ca 2+ imaging at somatic plasma membrane. (Ai) Maximum intensity projection of Alexa-594-filled cartwheel cell. The red boxed region is enlarged in Ai, inset. Regions of interest for segmented line scans are indicated by red lines. C: cytosolic side. M: membrane side. (Aii, top and middle panels) Spike trains evoked by current injection (top) elicited an increase of Fluo-5F fluorescence with no change in Alexa-594. (Aii, bottom) Ca 2+ transients induced by spike trains (6 simple spikes at 50 Hz). The transients are expressed as ΔG/R (change in Fluo-5F intensity divided by Alexa-594 intensity). Black, control; blue, in ryanodine. (Aiii) Averaged Ca 2+ transients from 10 regions of interest of 5 cells. Single spike or trains of simple spikes (6 spikes at 50 Hz) evoked by current injection. (Aiv) Summary of the changes in Ca 2+ transients. *** p

    Techniques Used: Imaging, Injection, Fluorescence

    The effects of ryanodine and IbTX on action potential properties (A and B) Evoked action potentials recorded in perforated patch mode. Resting potential was slightly hyperpolarized by injecting negative current to suppress spontaneous firing (A). Traces recorded in control (black) and ryanodine (gray) are superimposed. Injected currents in (Ai) and (Aii) were 500 and 900 pA, respectively. Duration: 5 ms. Asterisk indicates fAHP between 1st and 2nd spikelets. The region surrounded with box in (Ai) was expanded in the inset. The inset in (Aii) includes a longer segment of the recording to illustrate the slow afterpotential. (Aiii) Summary of the change of burst firing probability by ryanodine. Three to four successive trials were used to obtain averaged probability in each experiment. (B) The effect of ryanodine was occluded by IbTX. Bath application of IbTX (100 nM) alone broadened 1st action potentials (Bi and Bii, gray traces) and made the fAHP less negative (Bii,, asterisk). Subsequent application of ryanodine in the presence of IbTX did not affect the waveform (Bi’ and Bii’, black traces). Inset in (Bii) is the same sweep but displayed with longer time base, with spikes truncated. (Biii) Summary of the change of burst firing probabilities by IbTX. Statistical significance was tested between control and IbTX.
    Figure Legend Snippet: The effects of ryanodine and IbTX on action potential properties (A and B) Evoked action potentials recorded in perforated patch mode. Resting potential was slightly hyperpolarized by injecting negative current to suppress spontaneous firing (A). Traces recorded in control (black) and ryanodine (gray) are superimposed. Injected currents in (Ai) and (Aii) were 500 and 900 pA, respectively. Duration: 5 ms. Asterisk indicates fAHP between 1st and 2nd spikelets. The region surrounded with box in (Ai) was expanded in the inset. The inset in (Aii) includes a longer segment of the recording to illustrate the slow afterpotential. (Aiii) Summary of the change of burst firing probability by ryanodine. Three to four successive trials were used to obtain averaged probability in each experiment. (B) The effect of ryanodine was occluded by IbTX. Bath application of IbTX (100 nM) alone broadened 1st action potentials (Bi and Bii, gray traces) and made the fAHP less negative (Bii,, asterisk). Subsequent application of ryanodine in the presence of IbTX did not affect the waveform (Bi’ and Bii’, black traces). Inset in (Bii) is the same sweep but displayed with longer time base, with spikes truncated. (Biii) Summary of the change of burst firing probabilities by IbTX. Statistical significance was tested between control and IbTX.

    Techniques Used: Injection, Mass Spectrometry

    CICR triggers BK channel-mediated transient outward currents (A) IbTX-sensitive transient outward currents. (Ai) In control, transient currents followed by sustained currents were evoked by depolarizing voltage steps (−30 to −10 mV from −70 mV holding potential, 10-mV increment). All transient current was inhibited by 100 nM IbTX (traces in IbTX and subtraction). IbTX-sensitive currents were obtained by subtracting traces in IbTX from control traces. (Aii) Summary of the peak current densities (left panel), and rise time and decay time constant of IbTX-sensitive currents (right panel). In (A) and (B), capacitive artifacts were blanked for clarity. Here and in following figures, dashed lines in current traces indicate zero current levels. (B) RyRs are involved in the transient outward currents. Same voltage protocol as in (A). (Bi) Note that some transient outward currents remain in ryanodine (Bi, ryanodine). (Bii) Summary of peak current densities (left panel) and rise time and decay time constant of ryanodine-sensitive currents (right panel). (Ci) Most of the transient current is suppressed by ω-Agatoxin-IVA (Aga-IVA, a P/Q-type blocker, 200 nM; trace in Aga-IVA and Aga-IVA-sensitive). Subsequent application of nonspecific Ca v channel blockers (200 µM CdCl 2 and 500 µM NiCl 2 ) blocked transient currents almost completely (traces in lower panel in Ci). Data in (C) were recorded in the presence of TTX, synaptic blockers, and 1 mM 4-AP. (Cii) Summary of peak current densities (left panel), and the rise time and decay time constant of Aga-VIA-sensitive currents (right panel). (Ciii) Summary of effects of subtype-specific Ca v blockers on transient currents. Aga-VIA inhibited transient currents more potently than nimodipine or TTA-P2. Effects are expressed as 100 × (selective blocker-sensitive current)/(nonspecific Ca v blockers-sensitive current). ***p
    Figure Legend Snippet: CICR triggers BK channel-mediated transient outward currents (A) IbTX-sensitive transient outward currents. (Ai) In control, transient currents followed by sustained currents were evoked by depolarizing voltage steps (−30 to −10 mV from −70 mV holding potential, 10-mV increment). All transient current was inhibited by 100 nM IbTX (traces in IbTX and subtraction). IbTX-sensitive currents were obtained by subtracting traces in IbTX from control traces. (Aii) Summary of the peak current densities (left panel), and rise time and decay time constant of IbTX-sensitive currents (right panel). In (A) and (B), capacitive artifacts were blanked for clarity. Here and in following figures, dashed lines in current traces indicate zero current levels. (B) RyRs are involved in the transient outward currents. Same voltage protocol as in (A). (Bi) Note that some transient outward currents remain in ryanodine (Bi, ryanodine). (Bii) Summary of peak current densities (left panel) and rise time and decay time constant of ryanodine-sensitive currents (right panel). (Ci) Most of the transient current is suppressed by ω-Agatoxin-IVA (Aga-IVA, a P/Q-type blocker, 200 nM; trace in Aga-IVA and Aga-IVA-sensitive). Subsequent application of nonspecific Ca v channel blockers (200 µM CdCl 2 and 500 µM NiCl 2 ) blocked transient currents almost completely (traces in lower panel in Ci). Data in (C) were recorded in the presence of TTX, synaptic blockers, and 1 mM 4-AP. (Cii) Summary of peak current densities (left panel), and the rise time and decay time constant of Aga-VIA-sensitive currents (right panel). (Ciii) Summary of effects of subtype-specific Ca v blockers on transient currents. Aga-VIA inhibited transient currents more potently than nimodipine or TTA-P2. Effects are expressed as 100 × (selective blocker-sensitive current)/(nonspecific Ca v blockers-sensitive current). ***p

    Techniques Used:

    SMOCs are induced by CICR triggered by P/Q-type Ca 2+ channels (A–C) Representative current traces containing SMOCs evoked by 10-mV depolarization from −70 mV in the presence of TTX and synaptic blockers. SMOCs were blocked completely by IbTX (A), ryanodine (B), and Aga-IVA (P/Q-type Ca 2+ blocker, 200 nM). (D) Summary of change of SMOC frequency (Di) and amplitude (Dii). Frequencies and amplitudes were normalized by using control data obtained before drug application. ** p
    Figure Legend Snippet: SMOCs are induced by CICR triggered by P/Q-type Ca 2+ channels (A–C) Representative current traces containing SMOCs evoked by 10-mV depolarization from −70 mV in the presence of TTX and synaptic blockers. SMOCs were blocked completely by IbTX (A), ryanodine (B), and Aga-IVA (P/Q-type Ca 2+ blocker, 200 nM). (D) Summary of change of SMOC frequency (Di) and amplitude (Dii). Frequencies and amplitudes were normalized by using control data obtained before drug application. ** p

    Techniques Used:

    Blockade of CICR induces spontaneous spike bursts (A) Loose cell-attached recordings of a spontaneously firing cell in the presence of synaptic blockers. (Ai, left) Control, all action potentials are simple spikes. (Ai, right) The boxed region in (Ai, left) with expanded time base. (Aii, left) Bursting (*) observed in the presence of 20 µM ryanodine. (Aii, right) The boxed region (Aii, left), showing one burst of 5 spikelets. (B) Instantaneous firing frequency over time. The data were obtained from the same cell in (A). Ryanodine was bath-applied during time marked by gray box. (C) Summarized data of instantaneous frequencies in ryanodine or CPA (10 µM). Simple: data from spontaneous simple spike-firing cells; Burst: data from spontaneous burst-firing cells; Simple+Burst: pooled data from both firing types of cells. Here and elsewhere, error bars indicate SEM, and statistical significance was tested using paired t -test unless otherwise stated (significance, p
    Figure Legend Snippet: Blockade of CICR induces spontaneous spike bursts (A) Loose cell-attached recordings of a spontaneously firing cell in the presence of synaptic blockers. (Ai, left) Control, all action potentials are simple spikes. (Ai, right) The boxed region in (Ai, left) with expanded time base. (Aii, left) Bursting (*) observed in the presence of 20 µM ryanodine. (Aii, right) The boxed region (Aii, left), showing one burst of 5 spikelets. (B) Instantaneous firing frequency over time. The data were obtained from the same cell in (A). Ryanodine was bath-applied during time marked by gray box. (C) Summarized data of instantaneous frequencies in ryanodine or CPA (10 µM). Simple: data from spontaneous simple spike-firing cells; Burst: data from spontaneous burst-firing cells; Simple+Burst: pooled data from both firing types of cells. Here and elsewhere, error bars indicate SEM, and statistical significance was tested using paired t -test unless otherwise stated (significance, p

    Techniques Used:

    3) Product Images from "Discovery of long-range inhibitory signaling to ensure single axon formation"

    Article Title: Discovery of long-range inhibitory signaling to ensure single axon formation

    Journal: Nature Communications

    doi: 10.1038/s41467-017-00044-2

    NT-3 generated long-range Ca 2+ signaling from the axon to the cell body. a Long-range Ca 2+ wave. The relative change in the Cal-520 emission ratio (defined as R) was used as a measure of changes in Ca 2+ concentration. The pseudocolored images represent R after local application of PBS ( top ) or NT-3 ( bottom ) to the axon ( arrow ). Scale bars, 50 μm. b The mean amplitude of R treat / R 0 for 90 s during local application of NT-3 in the presence of the indicated inhibitors (PBS = 10, NT-3 = 16, xestospongin C = 9, ryanodine = 15, dantrolene = 18, SKF96365 = 12 neurons from three independent experiments). c , d The axon was exposed to NT-3 in the presence of the indicated inhibitors, and then minor neurite outgrowth (PBS = 21, NT-3 = 21, xestospongin C = 26, ryanodine = 25, dantrolene = 25, SKF96365 = 24 neurites from three independent experiments) c and axonal outgrowth (PBS = 7, NT-3 = 9, xestospongin C = 9, ryanodine = 9, dantrolene = 8, SKF96365 = 8 neurons from three independent experiments) d were measured. e Local application of NT-3 increased the quantity of phospho-CaMKI in the cell body. After local application of PBS ( top ) or NT-3 ( bottom ), hippocampal neurons were immunostained with antibodies against CaMKI ( green ) and phospho-Thr177 of CaMKI ( magenta ). The merged images ( right panels ) are shown. The graph plots the fluorescence intensities of total CaMKI ( green ) and CaMKI phosphorylated at Thr177 ( magenta ) and in the line. Scale bars, 20 μm. f NT-3-induced minor neurite retraction was abolished by Ca 2+ signaling inhibitors. The axon was exposed to NT-3 in the presence of the indicated inhibitors, and minor neurite outgrowth was measured (PBS = 27, NT-3 = 31, BAPTA = 47, STO-609 = 45, KN-93 = 40 neurites from three independent experiments). g , h Local application of indicated inhibitors to the axon. Minor neurite outgrowth (DMSO = 42, xestospongin C = 32, ryanodine = 37, dantrolene = 35, SKF96365 = 32 neurons from three independent experiments) g and axonal outgrowth (DMSO = 14, xestospongin C = 11, ryanodine = 13, dantrolene = 13, SKF96365 = 12 neurons from three independent experiments) h were measured. Error bars represent SEM. * P
    Figure Legend Snippet: NT-3 generated long-range Ca 2+ signaling from the axon to the cell body. a Long-range Ca 2+ wave. The relative change in the Cal-520 emission ratio (defined as R) was used as a measure of changes in Ca 2+ concentration. The pseudocolored images represent R after local application of PBS ( top ) or NT-3 ( bottom ) to the axon ( arrow ). Scale bars, 50 μm. b The mean amplitude of R treat / R 0 for 90 s during local application of NT-3 in the presence of the indicated inhibitors (PBS = 10, NT-3 = 16, xestospongin C = 9, ryanodine = 15, dantrolene = 18, SKF96365 = 12 neurons from three independent experiments). c , d The axon was exposed to NT-3 in the presence of the indicated inhibitors, and then minor neurite outgrowth (PBS = 21, NT-3 = 21, xestospongin C = 26, ryanodine = 25, dantrolene = 25, SKF96365 = 24 neurites from three independent experiments) c and axonal outgrowth (PBS = 7, NT-3 = 9, xestospongin C = 9, ryanodine = 9, dantrolene = 8, SKF96365 = 8 neurons from three independent experiments) d were measured. e Local application of NT-3 increased the quantity of phospho-CaMKI in the cell body. After local application of PBS ( top ) or NT-3 ( bottom ), hippocampal neurons were immunostained with antibodies against CaMKI ( green ) and phospho-Thr177 of CaMKI ( magenta ). The merged images ( right panels ) are shown. The graph plots the fluorescence intensities of total CaMKI ( green ) and CaMKI phosphorylated at Thr177 ( magenta ) and in the line. Scale bars, 20 μm. f NT-3-induced minor neurite retraction was abolished by Ca 2+ signaling inhibitors. The axon was exposed to NT-3 in the presence of the indicated inhibitors, and minor neurite outgrowth was measured (PBS = 27, NT-3 = 31, BAPTA = 47, STO-609 = 45, KN-93 = 40 neurites from three independent experiments). g , h Local application of indicated inhibitors to the axon. Minor neurite outgrowth (DMSO = 42, xestospongin C = 32, ryanodine = 37, dantrolene = 35, SKF96365 = 32 neurons from three independent experiments) g and axonal outgrowth (DMSO = 14, xestospongin C = 11, ryanodine = 13, dantrolene = 13, SKF96365 = 12 neurons from three independent experiments) h were measured. Error bars represent SEM. * P

    Techniques Used: Generated, Concentration Assay, Fluorescence

    4) Product Images from "Staphylococcal leukotoxins trigger free intracellular Ca2+ rise in neurones, signalling through acidic stores and activation of store-operated channels"

    Article Title: Staphylococcal leukotoxins trigger free intracellular Ca2+ rise in neurones, signalling through acidic stores and activation of store-operated channels

    Journal: Cellular Microbiology

    doi: 10.1111/cmi.12069

    Disruption of the Store-Operated Ca 2+ entry complex strongly inhibits the effect of leukotoxin HlgC/HlgB in cerebellar neurones. A. Mean traces of cells recorded in the presence of 5 μM econazole (24 cells) and 100 μM gadolinium (38 cells). The control experiment corresponds to the mean of 35 cells. B. Mean traces of cells recorded in the presence of drugs that target SOCE by also interfering with Ins(1,4,5)-P3 Ca 2+ mobilization (2-APB, 100 μM) or ryanodine receptors (dentrolene, 90 μM). Pre-treatment with these agents significantly reduced the effect of γ-leukotoxin HlgC/HlgB. Control experiment, 38 cells; 2-APB, 13 cells; dentrolene, 49 cells. This experiment was reproduced three times. C. incubation of neurones in the presence of LY-294002 (50 μM), which inactivates phosphatidylinositol 3 and 4 kinase and modifies membrane PIP2 content, thus strongly affecting the cellular response to leukotoxin action. Control boxes present the median of 110 recorded cells and LY-294002 (red lines) recordings are the mean of 52 and 63 treated cells. The boxes in the three panels correspond to the values of control recordings. Addition of the toxins is indicated by a vertical stroke in all panels.
    Figure Legend Snippet: Disruption of the Store-Operated Ca 2+ entry complex strongly inhibits the effect of leukotoxin HlgC/HlgB in cerebellar neurones. A. Mean traces of cells recorded in the presence of 5 μM econazole (24 cells) and 100 μM gadolinium (38 cells). The control experiment corresponds to the mean of 35 cells. B. Mean traces of cells recorded in the presence of drugs that target SOCE by also interfering with Ins(1,4,5)-P3 Ca 2+ mobilization (2-APB, 100 μM) or ryanodine receptors (dentrolene, 90 μM). Pre-treatment with these agents significantly reduced the effect of γ-leukotoxin HlgC/HlgB. Control experiment, 38 cells; 2-APB, 13 cells; dentrolene, 49 cells. This experiment was reproduced three times. C. incubation of neurones in the presence of LY-294002 (50 μM), which inactivates phosphatidylinositol 3 and 4 kinase and modifies membrane PIP2 content, thus strongly affecting the cellular response to leukotoxin action. Control boxes present the median of 110 recorded cells and LY-294002 (red lines) recordings are the mean of 52 and 63 treated cells. The boxes in the three panels correspond to the values of control recordings. Addition of the toxins is indicated by a vertical stroke in all panels.

    Techniques Used: Incubation

    5) Product Images from "Disrupting Function of FK506-Binding Protein 1b/12.6 Induces the Ca2+-Dysregulation Aging Phenotype in Hippocampal Neurons"

    Article Title: Disrupting Function of FK506-Binding Protein 1b/12.6 Induces the Ca2+-Dysregulation Aging Phenotype in Hippocampal Neurons

    Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

    doi: 10.1523/JNEUROSCI.4805-10.2011

    Rapamycin (Rap) enhanced the ryanodine (Rya)-sensitive AHP in hippocampal slices. A , Representative intracellular recording traces of AHPs, shown at high magnification to illustrate the enhancing effect of rapamycin on the AHP and its reversal by ryanodine,
    Figure Legend Snippet: Rapamycin (Rap) enhanced the ryanodine (Rya)-sensitive AHP in hippocampal slices. A , Representative intracellular recording traces of AHPs, shown at high magnification to illustrate the enhancing effect of rapamycin on the AHP and its reversal by ryanodine,

    Techniques Used:

    Rapamycin enhanced the ryanodine-sensitive component (CICR) of stimulated Ca 2+ transients in hippocampal slice neurons. Representative traces showing Ca 2+ indicator fluorescence responses during 7 Hz RSS in a control ( A1 ) and a rapamycin-treated ( A2 ) neuron,
    Figure Legend Snippet: Rapamycin enhanced the ryanodine-sensitive component (CICR) of stimulated Ca 2+ transients in hippocampal slice neurons. Representative traces showing Ca 2+ indicator fluorescence responses during 7 Hz RSS in a control ( A1 ) and a rapamycin-treated ( A2 ) neuron,

    Techniques Used: Fluorescence

    6) Product Images from "Alteration of Sarcoplasmic Reticulum Ca2+ Release in Skeletal Muscle from Calpain 3-Deficient Mice"

    Article Title: Alteration of Sarcoplasmic Reticulum Ca2+ Release in Skeletal Muscle from Calpain 3-Deficient Mice

    Journal: International Journal of Cell Biology

    doi: 10.1155/2009/340346

    Morphological and molecular features of skeletal muscle cells used throughout this study. (a) Phase contrast and fluorescence micrographs of murine skeletal muscle cells in primary culture. Typical morphology of the living cells (left upper panel: myoblasts; right upper panel: myotubes) used for calcium measurements observed by phase contrast microscopy. Circles indicate the region of drug application and monitoring of [Ca 2+ ] i . Immunological staining of myogenin on myoblasts (left middle panel) and myotubes (right middle panel) was visualized by confocal microscopy using a FITC-labelled secondary antibody (green fluorescence). Myosine Heavy Chain (MHC) was similarly observed in myoblasts (left lower panel) and myotubes (right lower panel) using a TRITC-labelled secondary antibody (red fluorescence). Myoblasts and myotubes were obtained after 6 or 11 days in culture, respectively. (b) Detection of calpain 3-mRNA in wild type (+/+) myoblasts and myotubes by RT-PCR. Gel electrophoresis of the RT-PCR reactions obtained using the primer pairs p94sys3, p94sys5 and p94sys6 (see Section 2 ) on murine myoblast (MB) or myotube (MT) mRNA. (c) Detection of the ryanodine receptor in skeletal muscle from normal and capn3 -deficient mice. Muscle from normal (Lane 3) and capn3 -deficient mice (Lane 2) were extracted and left 30 min at room temperature to allow the cleavage of RyR and were then subjected to SDS-PAGE. Human muscle was used as control (Lane1). No difference in the cleavage pattern was observed, indicating that the partial cleavage of RyR also occurs in the absence of calpain 3 in this biochemical assay. (d) Measurement of caspase 3 activity in wild type and capn3 -deficient myoblasts. The graph displays the levels of substrate cleavage expressed as means ± S.D. in arbitrary units. The results are based on 4 different experiments. The differences in the median values among the two groups are greater than would be expected by chance; there is a statistically significant difference ( P = 0.029), as indicated by a Mann-Whitney Rank Sum test.
    Figure Legend Snippet: Morphological and molecular features of skeletal muscle cells used throughout this study. (a) Phase contrast and fluorescence micrographs of murine skeletal muscle cells in primary culture. Typical morphology of the living cells (left upper panel: myoblasts; right upper panel: myotubes) used for calcium measurements observed by phase contrast microscopy. Circles indicate the region of drug application and monitoring of [Ca 2+ ] i . Immunological staining of myogenin on myoblasts (left middle panel) and myotubes (right middle panel) was visualized by confocal microscopy using a FITC-labelled secondary antibody (green fluorescence). Myosine Heavy Chain (MHC) was similarly observed in myoblasts (left lower panel) and myotubes (right lower panel) using a TRITC-labelled secondary antibody (red fluorescence). Myoblasts and myotubes were obtained after 6 or 11 days in culture, respectively. (b) Detection of calpain 3-mRNA in wild type (+/+) myoblasts and myotubes by RT-PCR. Gel electrophoresis of the RT-PCR reactions obtained using the primer pairs p94sys3, p94sys5 and p94sys6 (see Section 2 ) on murine myoblast (MB) or myotube (MT) mRNA. (c) Detection of the ryanodine receptor in skeletal muscle from normal and capn3 -deficient mice. Muscle from normal (Lane 3) and capn3 -deficient mice (Lane 2) were extracted and left 30 min at room temperature to allow the cleavage of RyR and were then subjected to SDS-PAGE. Human muscle was used as control (Lane1). No difference in the cleavage pattern was observed, indicating that the partial cleavage of RyR also occurs in the absence of calpain 3 in this biochemical assay. (d) Measurement of caspase 3 activity in wild type and capn3 -deficient myoblasts. The graph displays the levels of substrate cleavage expressed as means ± S.D. in arbitrary units. The results are based on 4 different experiments. The differences in the median values among the two groups are greater than would be expected by chance; there is a statistically significant difference ( P = 0.029), as indicated by a Mann-Whitney Rank Sum test.

    Techniques Used: Fluorescence, Microscopy, Staining, Confocal Microscopy, Reverse Transcription Polymerase Chain Reaction, Nucleic Acid Electrophoresis, Mouse Assay, SDS Page, Activity Assay, MANN-WHITNEY

    7) Product Images from "Uniform Action Potential Repolarization within the Sarcolemma of In Situ Ventricular Cardiomyocytes"

    Article Title: Uniform Action Potential Repolarization within the Sarcolemma of In Situ Ventricular Cardiomyocytes

    Journal:

    doi: 10.1016/j.bpj.2008.12.3896

    Confocal imaging of the cardiomyocyte action potential in Langendorff-perfused mouse hearts in the presence of 50 μ M cytochalasin D and 1 μ M ryanodine. ( A ) Full-frame mode ( XY ) image obtained from a heart loaded with ANNINE-6. The green
    Figure Legend Snippet: Confocal imaging of the cardiomyocyte action potential in Langendorff-perfused mouse hearts in the presence of 50 μ M cytochalasin D and 1 μ M ryanodine. ( A ) Full-frame mode ( XY ) image obtained from a heart loaded with ANNINE-6. The green

    Techniques Used: Imaging

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    Alomone Labs mambalgin 3
    Pharmacology of endogenous proton-activated currents in HEK cells. (A) Individual % inhibition values plotted against concentration of PcTx1 applied during QPatch 48 recordings, with mean shown by horizontal black lines. Data was obtained from cumulative IC 50 assays where each cell was exposed to three concentrations of PcTx1, typically in half log unit increments. (B) Potency of <t>Mambalgin-3</t> to inhibit pH-activated currents plotted as a cumulative concentration-response IC 50 curve. Symbols are mean ± S.D ( n = 2 or 3). (C) Exemplar current traces from a HEK cell in response to pH 6.5 activation before and after pre-incubation in increasing concentrations of Mambalgin-3. Scale bar is 500 pA and 1 s. (D) Inhibition of proton-activated currents in HEK cells by Amiloride. Data was obtained in a similar fashion to C, with each cell stimulated by pH 6.5 solution and then pre-incubated in increasing concentrations of Amiloride to construct a cumulative mini-IC 50 curve. Symbols are mean ± S.D ( n = 3). (E) Endogenous proton-activated currents are insensitive to Ruthenium Red (RR, 1 μM) but completely inhibited by a non-selective concentration of the ASIC/ENaC/Degenerin antagonist Amiloride (100 μM). The HEK cell was stimulated by pH 6.5 solution and then pre-incubated (at pH 7.4) in RR or Amiloride followed by consecutive stimulation with pH 6.5 solution containing RR or Amiloride.
    Mambalgin 3, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Alomone Labs low dose of ryanodine
    Pharmacology of endogenous proton-activated currents in HEK cells. (A) Individual % inhibition values plotted against concentration of PcTx1 applied during QPatch 48 recordings, with mean shown by horizontal black lines. Data was obtained from cumulative IC 50 assays where each cell was exposed to three concentrations of PcTx1, typically in half log unit increments. (B) Potency of <t>Mambalgin-3</t> to inhibit pH-activated currents plotted as a cumulative concentration-response IC 50 curve. Symbols are mean ± S.D ( n = 2 or 3). (C) Exemplar current traces from a HEK cell in response to pH 6.5 activation before and after pre-incubation in increasing concentrations of Mambalgin-3. Scale bar is 500 pA and 1 s. (D) Inhibition of proton-activated currents in HEK cells by Amiloride. Data was obtained in a similar fashion to C, with each cell stimulated by pH 6.5 solution and then pre-incubated in increasing concentrations of Amiloride to construct a cumulative mini-IC 50 curve. Symbols are mean ± S.D ( n = 3). (E) Endogenous proton-activated currents are insensitive to Ruthenium Red (RR, 1 μM) but completely inhibited by a non-selective concentration of the ASIC/ENaC/Degenerin antagonist Amiloride (100 μM). The HEK cell was stimulated by pH 6.5 solution and then pre-incubated (at pH 7.4) in RR or Amiloride followed by consecutive stimulation with pH 6.5 solution containing RR or Amiloride.
    Low Dose Of Ryanodine, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/low dose of ryanodine/product/Alomone Labs
    Average 94 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    low dose of ryanodine - by Bioz Stars, 2022-12
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    Pharmacology of endogenous proton-activated currents in HEK cells. (A) Individual % inhibition values plotted against concentration of PcTx1 applied during QPatch 48 recordings, with mean shown by horizontal black lines. Data was obtained from cumulative IC 50 assays where each cell was exposed to three concentrations of PcTx1, typically in half log unit increments. (B) Potency of Mambalgin-3 to inhibit pH-activated currents plotted as a cumulative concentration-response IC 50 curve. Symbols are mean ± S.D ( n = 2 or 3). (C) Exemplar current traces from a HEK cell in response to pH 6.5 activation before and after pre-incubation in increasing concentrations of Mambalgin-3. Scale bar is 500 pA and 1 s. (D) Inhibition of proton-activated currents in HEK cells by Amiloride. Data was obtained in a similar fashion to C, with each cell stimulated by pH 6.5 solution and then pre-incubated in increasing concentrations of Amiloride to construct a cumulative mini-IC 50 curve. Symbols are mean ± S.D ( n = 3). (E) Endogenous proton-activated currents are insensitive to Ruthenium Red (RR, 1 μM) but completely inhibited by a non-selective concentration of the ASIC/ENaC/Degenerin antagonist Amiloride (100 μM). The HEK cell was stimulated by pH 6.5 solution and then pre-incubated (at pH 7.4) in RR or Amiloride followed by consecutive stimulation with pH 6.5 solution containing RR or Amiloride.

    Journal: Frontiers in Molecular Neuroscience

    Article Title: Development of ASIC1a ligand-gated ion channel drug screening assays across multiple automated patch clamp platforms

    doi: 10.3389/fnmol.2022.982689

    Figure Lengend Snippet: Pharmacology of endogenous proton-activated currents in HEK cells. (A) Individual % inhibition values plotted against concentration of PcTx1 applied during QPatch 48 recordings, with mean shown by horizontal black lines. Data was obtained from cumulative IC 50 assays where each cell was exposed to three concentrations of PcTx1, typically in half log unit increments. (B) Potency of Mambalgin-3 to inhibit pH-activated currents plotted as a cumulative concentration-response IC 50 curve. Symbols are mean ± S.D ( n = 2 or 3). (C) Exemplar current traces from a HEK cell in response to pH 6.5 activation before and after pre-incubation in increasing concentrations of Mambalgin-3. Scale bar is 500 pA and 1 s. (D) Inhibition of proton-activated currents in HEK cells by Amiloride. Data was obtained in a similar fashion to C, with each cell stimulated by pH 6.5 solution and then pre-incubated in increasing concentrations of Amiloride to construct a cumulative mini-IC 50 curve. Symbols are mean ± S.D ( n = 3). (E) Endogenous proton-activated currents are insensitive to Ruthenium Red (RR, 1 μM) but completely inhibited by a non-selective concentration of the ASIC/ENaC/Degenerin antagonist Amiloride (100 μM). The HEK cell was stimulated by pH 6.5 solution and then pre-incubated (at pH 7.4) in RR or Amiloride followed by consecutive stimulation with pH 6.5 solution containing RR or Amiloride.

    Article Snippet: As our pharmacology data faithfully replicates the known potency of Mambalgin-3 and PcTx1 against human ASIC1a responses in CHO cells on the same APC platform , this suggests that the relative potency and efficacy of non-selective vs. selective ASIC1a ligands in HEK cells is evidence for functional expression of an atypical pH-gated receptor complex in this parental cell line.

    Techniques: Inhibition, Concentration Assay, Activation Assay, Incubation, Construct

    Validation of a multi-hole ASIC1a assay on QPatch 48. (A) Comparison of efficiency and success rate of single vs. multi-hole QPlate assay format. Mean (± S.D) data for the percentage of wells that passed various quality control (QC) criteria during and after whole-cell recordings in single hole ( n = 4 plates, black squares) or multi-hole mode ( n = 5 plates, filled circles). (B) ASIC1a assay pharmacology in multi-hole mode. Mean (± S.D) concentration-response data for inhibition of ASIC1a currents by Mambalgin-3 ( n = 12), Amiloride ( n = 8) and Benzamil ( n = 4) in multi-hole recordings, with indicated IC 50 and Hill slope values.

    Journal: Frontiers in Molecular Neuroscience

    Article Title: Development of ASIC1a ligand-gated ion channel drug screening assays across multiple automated patch clamp platforms

    doi: 10.3389/fnmol.2022.982689

    Figure Lengend Snippet: Validation of a multi-hole ASIC1a assay on QPatch 48. (A) Comparison of efficiency and success rate of single vs. multi-hole QPlate assay format. Mean (± S.D) data for the percentage of wells that passed various quality control (QC) criteria during and after whole-cell recordings in single hole ( n = 4 plates, black squares) or multi-hole mode ( n = 5 plates, filled circles). (B) ASIC1a assay pharmacology in multi-hole mode. Mean (± S.D) concentration-response data for inhibition of ASIC1a currents by Mambalgin-3 ( n = 12), Amiloride ( n = 8) and Benzamil ( n = 4) in multi-hole recordings, with indicated IC 50 and Hill slope values.

    Article Snippet: As our pharmacology data faithfully replicates the known potency of Mambalgin-3 and PcTx1 against human ASIC1a responses in CHO cells on the same APC platform , this suggests that the relative potency and efficacy of non-selective vs. selective ASIC1a ligands in HEK cells is evidence for functional expression of an atypical pH-gated receptor complex in this parental cell line.

    Techniques: Concentration Assay, Inhibition