ryanodine  (Alomone Labs)


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    Structured Review

    Alomone Labs ryanodine
    <t>Ryanodine</t> inhibited Ca 2+ -sparks and oscillations. (A) Linescan and normalised fluorescence plots for 2 adjacent myocytes in an arteriole under control conditions and during superfusion with 100 μM ryanodine. Time-course data in the graph refers to the indicated regions of interest (R.O.I.). (B) Summary data from 17 cells for spark frequency and amplitude during the 20 s control period and 3 consecutive, 10 s periods of superfusion with ryanodine ( ** P
    Ryanodine, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Ca2+-sparks constitute elementary building blocks for global Ca2+-signals in myocytes of retinal arterioles"

    Article Title: Ca2+-sparks constitute elementary building blocks for global Ca2+-signals in myocytes of retinal arterioles

    Journal: Cell Calcium

    doi: 10.1016/j.ceca.2006.08.005

    Ryanodine inhibited Ca 2+ -sparks and oscillations. (A) Linescan and normalised fluorescence plots for 2 adjacent myocytes in an arteriole under control conditions and during superfusion with 100 μM ryanodine. Time-course data in the graph refers to the indicated regions of interest (R.O.I.). (B) Summary data from 17 cells for spark frequency and amplitude during the 20 s control period and 3 consecutive, 10 s periods of superfusion with ryanodine ( ** P
    Figure Legend Snippet: Ryanodine inhibited Ca 2+ -sparks and oscillations. (A) Linescan and normalised fluorescence plots for 2 adjacent myocytes in an arteriole under control conditions and during superfusion with 100 μM ryanodine. Time-course data in the graph refers to the indicated regions of interest (R.O.I.). (B) Summary data from 17 cells for spark frequency and amplitude during the 20 s control period and 3 consecutive, 10 s periods of superfusion with ryanodine ( ** P

    Techniques Used: Fluorescence

    2) Product Images from "Early and Simultaneous Emergence of Multiple Hippocampal Biomarkers of Aging Is Mediated by Ca2+-Induced Ca2+ Release"

    Article Title: Early and Simultaneous Emergence of Multiple Hippocampal Biomarkers of Aging Is Mediated by Ca2+-Induced Ca2+ Release

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.4171-05.2006

    Effect of ryanodine on kinetics of the [Ca 2+ ] i response. A , Examples of the effects of ryanodine in slowing the rising phase of somatic Ca 2+ at the onset of RSS in a 4-month-old (left) and 23-month-old (right) animal. B , Ryanodine did not significantly affect peak Ca 2+ levels measured during RSS. Grayscale bars, Preryanodine. White bars, Postryanodine. Aging effect persists after ryanodine (asterisks). C , Ryanodine eliminated the effect of aging on measures of the AUC. Although the rising ( D ) and decaying ( E ) time constants of Ca 2+ did not differ with aging, ryanodine treatment significantly lengthened both time constants. All aging comparisons are made within a treatment condition (i.e., preryanodine only or postryanodine only). Note that peak Ca 2+ levels are increased with aging in cells before the ryanodine treatment (asterisks above grayscale bars) and also after ryanodine treatment (asterisks above white bars). *Different from the 4-month-old group appropriate for preryanodine and postryanodine comparisons at p
    Figure Legend Snippet: Effect of ryanodine on kinetics of the [Ca 2+ ] i response. A , Examples of the effects of ryanodine in slowing the rising phase of somatic Ca 2+ at the onset of RSS in a 4-month-old (left) and 23-month-old (right) animal. B , Ryanodine did not significantly affect peak Ca 2+ levels measured during RSS. Grayscale bars, Preryanodine. White bars, Postryanodine. Aging effect persists after ryanodine (asterisks). C , Ryanodine eliminated the effect of aging on measures of the AUC. Although the rising ( D ) and decaying ( E ) time constants of Ca 2+ did not differ with aging, ryanodine treatment significantly lengthened both time constants. All aging comparisons are made within a treatment condition (i.e., preryanodine only or postryanodine only). Note that peak Ca 2+ levels are increased with aging in cells before the ryanodine treatment (asterisks above grayscale bars) and also after ryanodine treatment (asterisks above white bars). *Different from the 4-month-old group appropriate for preryanodine and postryanodine comparisons at 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 "Simultaneous recordings of action potentials and calcium transients from human induced pluripotent stem cell derived cardiomyocytes"

    Article Title: Simultaneous recordings of action potentials and calcium transients from human induced pluripotent stem cell derived cardiomyocytes

    Journal: Biology Open

    doi: 10.1242/bio.035030

    Representative immunofluorescence images of hiPSC-CMs showing cardiac proteins. (Upper) 50 slices were combined from confocal immunofluorescence images of nucleus (DAPI, blue), cardiac troponin T (cTnT, green) and cardiac ryanodine receptors (RyR2, red). Final panel shows the former three merged. (Lower) 40 slices were combined from confocal immunoflurescence images of nucleus (DAPI, blue), cTnT (green), L-type calcium channels (Ca V 1.2, red). Final panel shows the former three merged. Scale bars: 10 µM.
    Figure Legend Snippet: Representative immunofluorescence images of hiPSC-CMs showing cardiac proteins. (Upper) 50 slices were combined from confocal immunofluorescence images of nucleus (DAPI, blue), cardiac troponin T (cTnT, green) and cardiac ryanodine receptors (RyR2, red). Final panel shows the former three merged. (Lower) 40 slices were combined from confocal immunoflurescence images of nucleus (DAPI, blue), cTnT (green), L-type calcium channels (Ca V 1.2, red). Final panel shows the former three merged. Scale bars: 10 µM.

    Techniques Used: Immunofluorescence

    5) Product Images from "Simultaneous recordings of action potentials and calcium transients from human induced pluripotent stem cell derived cardiomyocytes"

    Article Title: Simultaneous recordings of action potentials and calcium transients from human induced pluripotent stem cell derived cardiomyocytes

    Journal: Biology Open

    doi: 10.1242/bio.035030

    Representative immunofluorescence images of hiPSC-CMs showing cardiac proteins. (Upper) 50 slices were combined from confocal immunofluorescence images of nucleus (DAPI, blue), cardiac troponin T (cTnT, green) and cardiac ryanodine receptors (RyR2, red). Final panel shows the former three merged. (Lower) 40 slices were combined from confocal immunoflurescence images of nucleus (DAPI, blue), cTnT (green), L-type calcium channels (Ca V 1.2, red). Final panel shows the former three merged. Scale bars: 10 µM.
    Figure Legend Snippet: Representative immunofluorescence images of hiPSC-CMs showing cardiac proteins. (Upper) 50 slices were combined from confocal immunofluorescence images of nucleus (DAPI, blue), cardiac troponin T (cTnT, green) and cardiac ryanodine receptors (RyR2, red). Final panel shows the former three merged. (Lower) 40 slices were combined from confocal immunoflurescence images of nucleus (DAPI, blue), cTnT (green), L-type calcium channels (Ca V 1.2, red). Final panel shows the former three merged. Scale bars: 10 µM.

    Techniques Used: Immunofluorescence

    6) Product Images from "TRPML1 Channels Initiate Ca2+ Sparks in Vascular Smooth Muscle Cells"

    Article Title: TRPML1 Channels Initiate Ca2+ Sparks in Vascular Smooth Muscle Cells

    Journal: Science signaling

    doi: 10.1126/scisignal.aba1015

    Super-resolution imaging demonstrates nanoscale colocalization of TRPML1 and RyR2 in native SMCs. A–C) Representative super-resolution localization maps of native, contractile cerebral artery SMCs co-immunolabeled for Lamp-1 and TRPML1 (A), Lamp-1 and RyR2 (B), or TRPML1 and RyR2 (C). Scale bars = 3 μm. Representative of n= 8–10 cells isolated from N = 3 animals. The second column of images shows a magnified view of the region enclosed in the white boxes. Scale bars = 1 μm. Insets show magnified views of the indicated regions of interest. Scale bars = 0.1 μm. D and E) Histograms showing the distribution of the surface areas of individual protein clusters for TRPML1 (D) and RyR2 (E) (TRPML1, n = 6143 clusters; RyR2, n = 35432 clusters). F) TRPML1 and RyR2 protein cluster density (n = 19 cells from N = 6 animals/group; *P ≤ 0.05) G) Histogram showing the area distribution of Lamp-1–positive LELs (n = 216 ovoids). H) Nearest neighbor analysis showing the distance between the center of RyR2 protein clusters and the edge of Lamp-1–positive LELs (n = 1409 RyR2 protein clusters). I) Object-based analysis comparing the fraction of TRPML1 and RyR2 co-localizing clusters with the fraction of clusters that co-localize in a simulated random distribution of RyR2 protein clusters (TRPML1-RyR2, 1.51 ± 0.12 %; Random, 0.44 ± 0.07 %; n = 10 cells from 3 animals; *P ≤ 0.05). All data are shown as mean ± SEM.
    Figure Legend Snippet: Super-resolution imaging demonstrates nanoscale colocalization of TRPML1 and RyR2 in native SMCs. A–C) Representative super-resolution localization maps of native, contractile cerebral artery SMCs co-immunolabeled for Lamp-1 and TRPML1 (A), Lamp-1 and RyR2 (B), or TRPML1 and RyR2 (C). Scale bars = 3 μm. Representative of n= 8–10 cells isolated from N = 3 animals. The second column of images shows a magnified view of the region enclosed in the white boxes. Scale bars = 1 μm. Insets show magnified views of the indicated regions of interest. Scale bars = 0.1 μm. D and E) Histograms showing the distribution of the surface areas of individual protein clusters for TRPML1 (D) and RyR2 (E) (TRPML1, n = 6143 clusters; RyR2, n = 35432 clusters). F) TRPML1 and RyR2 protein cluster density (n = 19 cells from N = 6 animals/group; *P ≤ 0.05) G) Histogram showing the area distribution of Lamp-1–positive LELs (n = 216 ovoids). H) Nearest neighbor analysis showing the distance between the center of RyR2 protein clusters and the edge of Lamp-1–positive LELs (n = 1409 RyR2 protein clusters). I) Object-based analysis comparing the fraction of TRPML1 and RyR2 co-localizing clusters with the fraction of clusters that co-localize in a simulated random distribution of RyR2 protein clusters (TRPML1-RyR2, 1.51 ± 0.12 %; Random, 0.44 ± 0.07 %; n = 10 cells from 3 animals; *P ≤ 0.05). All data are shown as mean ± SEM.

    Techniques Used: Imaging, Immunolabeling, Isolation

    7) Product Images from "Ca2+-Dependent Regulation of Rho GTPases Triggers Turning of Nerve Growth Cones"

    Article Title: Ca2+-Dependent Regulation of Rho GTPases Triggers Turning of Nerve Growth Cones

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.4889-04.2005

    PKC mediates Ca 2+ signaling to Rho GTPases. a , b , Western blots showing the active form of PKC and CaMKII in HEK293T cells or cultured cerebellar granule cells treated with ryanodine (10 n m ) at different times. Western blots using antibody against actin
    Figure Legend Snippet: PKC mediates Ca 2+ signaling to Rho GTPases. a , b , Western blots showing the active form of PKC and CaMKII in HEK293T cells or cultured cerebellar granule cells treated with ryanodine (10 n m ) at different times. Western blots using antibody against actin

    Techniques Used: Western Blot, Cell Culture

    Ryanodine-induced attractive turning response depends on both Ca 2+ and Rho GTPases. a , Distribution of growth cone turning angles (left) for control neurons and neurons treated with BAPTA-AM (BAPTA; 10 μ m ), thapsigargin (Thaps; 10 μ m ),
    Figure Legend Snippet: Ryanodine-induced attractive turning response depends on both Ca 2+ and Rho GTPases. a , Distribution of growth cone turning angles (left) for control neurons and neurons treated with BAPTA-AM (BAPTA; 10 μ m ), thapsigargin (Thaps; 10 μ m ),

    Techniques Used:

    Ca 2+ elevation regulates the activity of Rho GTPases in transfected HEK293T cells. a , b , Representative Western blots showing the dose-response and time course of the activation of Cdc42 and Rac and inactivation of RhoA by bath-applied ryanodine in HEK293T
    Figure Legend Snippet: Ca 2+ elevation regulates the activity of Rho GTPases in transfected HEK293T cells. a , b , Representative Western blots showing the dose-response and time course of the activation of Cdc42 and Rac and inactivation of RhoA by bath-applied ryanodine in HEK293T

    Techniques Used: Activity Assay, Transfection, Western Blot, Activation Assay

    Ryanodine-induced attraction depends on CaMKII and PKC. Distribution of turning angles in a gradient of ryanodine ( a , c , 10 μ m in the pipette) or netrin-1 ( b , 5 μg/ml in the pipette) for cultured Xenopus spinal neurons in control condition
    Figure Legend Snippet: Ryanodine-induced attraction depends on CaMKII and PKC. Distribution of turning angles in a gradient of ryanodine ( a , c , 10 μ m in the pipette) or netrin-1 ( b , 5 μg/ml in the pipette) for cultured Xenopus spinal neurons in control condition

    Techniques Used: Transferring, Cell Culture

    Ca 2+ -dependent regulation of Rho GTPase activity in cultured neurons. a , Activation of Cdc42 and inactivation of RhoA by bath-applied ryanodine (10 n m . The effects
    Figure Legend Snippet: Ca 2+ -dependent regulation of Rho GTPase activity in cultured neurons. a , Activation of Cdc42 and inactivation of RhoA by bath-applied ryanodine (10 n m . The effects

    Techniques Used: Activity Assay, Cell Culture, Activation Assay

    Growth cone turning and local [Ca 2+ ] i elevation induced by ryanodine gradient. a , Microscopic images of a cultured Xenopus spinal neuron at the beginning (0 min) and the end (60 min) at a 1 hexposure to a ryanodine gradient created by pulsatile application
    Figure Legend Snippet: Growth cone turning and local [Ca 2+ ] i elevation induced by ryanodine gradient. a , Microscopic images of a cultured Xenopus spinal neuron at the beginning (0 min) and the end (60 min) at a 1 hexposure to a ryanodine gradient created by pulsatile application

    Techniques Used: Cell Culture

    Regulation of the activities of Rho GTPases by ryanodine requires CaMKII and PKC. a , b , Regulation of Rho GTPases by bath-applied ryanodine (10 n m for 3 min) in HEK293T cells transfected with wild-type Rho GTPases was abolished by specific inhibitors
    Figure Legend Snippet: Regulation of the activities of Rho GTPases by ryanodine requires CaMKII and PKC. a , b , Regulation of Rho GTPases by bath-applied ryanodine (10 n m for 3 min) in HEK293T cells transfected with wild-type Rho GTPases was abolished by specific inhibitors

    Techniques Used: Transfection

    8) 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

    9) 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:

    10) 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

    11) 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

    12) 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

    13) Product Images from "Upregulation of the CaV 1.1-ryanodine receptor complex in a rat model of critical illness myopathy"

    Article Title: Upregulation of the CaV 1.1-ryanodine receptor complex in a rat model of critical illness myopathy

    Journal: American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

    doi: 10.1152/ajpregu.00032.2011

    Fibers with elevated RYR1 contain fast myosin. Shown is a field from a tibialis anterior muscle double labeled for myosin II and RYR1. All 3 fibers in the field are positive for fast myosin. In the lower center of the field is a small fiber that stains
    Figure Legend Snippet: Fibers with elevated RYR1 contain fast myosin. Shown is a field from a tibialis anterior muscle double labeled for myosin II and RYR1. All 3 fibers in the field are positive for fast myosin. In the lower center of the field is a small fiber that stains

    Techniques Used: Labeling

    Marked elevation of RYR1 in a subset of fibers. A : RYR1 staining in 2 fibers from the tibialis anterior muscle in a control rat. The staining is well organized into parallel stripes running perpendicular to the length of the fiber. B : RYR1 staining in
    Figure Legend Snippet: Marked elevation of RYR1 in a subset of fibers. A : RYR1 staining in 2 fibers from the tibialis anterior muscle in a control rat. The staining is well organized into parallel stripes running perpendicular to the length of the fiber. B : RYR1 staining in

    Techniques Used: Staining

    Expression of the ryanodine receptor (RYR) increases in critical illness myopathy (CIM).  A : skeletal muscle membranes prepared from individual control (Con) or CIM animals were analyzed in Western blot analysis using a monoclonal antibody to RYR. There
    Figure Legend Snippet: Expression of the ryanodine receptor (RYR) increases in critical illness myopathy (CIM). A : skeletal muscle membranes prepared from individual control (Con) or CIM animals were analyzed in Western blot analysis using a monoclonal antibody to RYR. There

    Techniques Used: Expressing, Western Blot

    Voltage-gated calcium channel type 1.1 (Ca V 1.1) and RYR1 are upregulated in the same fibers in CIM. Two fields from an individual tibialis anterior muscle double labeled for Ca V 1.1 and RYR1 are shown. In the field at the top , a severely atrophied muscle
    Figure Legend Snippet: Voltage-gated calcium channel type 1.1 (Ca V 1.1) and RYR1 are upregulated in the same fibers in CIM. Two fields from an individual tibialis anterior muscle double labeled for Ca V 1.1 and RYR1 are shown. In the field at the top , a severely atrophied muscle

    Techniques Used: Labeling

    Calpain II is elevated in fibers with elevated RYR1. Shown is a field from a tibialis anterior muscle double labeled for calpain II and RYR1. In the field are two atrophied fibers that have elevated levels of both calpain II and RYR1. The normal fibers
    Figure Legend Snippet: Calpain II is elevated in fibers with elevated RYR1. Shown is a field from a tibialis anterior muscle double labeled for calpain II and RYR1. In the field are two atrophied fibers that have elevated levels of both calpain II and RYR1. The normal fibers

    Techniques Used: Labeling

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    Alomone Labs ryanodine
    <t>Ryanodine</t> inhibited Ca 2+ -sparks and oscillations. (A) Linescan and normalised fluorescence plots for 2 adjacent myocytes in an arteriole under control conditions and during superfusion with 100 μM ryanodine. Time-course data in the graph refers to the indicated regions of interest (R.O.I.). (B) Summary data from 17 cells for spark frequency and amplitude during the 20 s control period and 3 consecutive, 10 s periods of superfusion with ryanodine ( ** P
    Ryanodine, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ryanodine/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
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    Alomone Labs snx 482
    Effects of CTX alone and of a cocktail of toxins (CTX, ATX and SNX 482) on physostigmine (Physo)- and EFS (10 Hz)-induced contractions in isolated muscle strips of the guinea pig bladder. (A) Averaged data from six guinea pigs shows the lack of effect of CTX (0.3 µmol·L −1 ) on physostigmine (1 µmol·L −1 )-induced contractions in the presence of TTX (1 µmol·L −1 ). (B) Averaged data ( N = 7) of the effect of CTX (0.3 µmol·L −1 ) on EFS (10 Hz)-induced contractions. (C) Averaged data from five guinea pigs of the effects of the cocktail of toxins [CTX (0.3 µmol·L −1 ), ATX (0.1 µmol·L −1 ) and <t>SNX</t> 482 (0.3 µmol·L −1 )] on physostigmine (1 µmol·L −1 )-induced contractions, in the presence of TTX (1 µmol·L −1 ). (D) Averaged data ( N = 5) of the effect of the same cocktail of toxins on EFS (10 Hz)-induced contractions revealing significant, but incomplete blockade. (E) Averaged data ( N = 6) of the corresponding time control for the effect of 1 µmol·L −1 physostigmine (physo 1 = 25–30 min and physo 2 = 45–50 min) alone. *, significant difference from TTX, P
    Snx 482, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Ryanodine inhibited Ca 2+ -sparks and oscillations. (A) Linescan and normalised fluorescence plots for 2 adjacent myocytes in an arteriole under control conditions and during superfusion with 100 μM ryanodine. Time-course data in the graph refers to the indicated regions of interest (R.O.I.). (B) Summary data from 17 cells for spark frequency and amplitude during the 20 s control period and 3 consecutive, 10 s periods of superfusion with ryanodine ( ** P

    Journal: Cell Calcium

    Article Title: Ca2+-sparks constitute elementary building blocks for global Ca2+-signals in myocytes of retinal arterioles

    doi: 10.1016/j.ceca.2006.08.005

    Figure Lengend Snippet: Ryanodine inhibited Ca 2+ -sparks and oscillations. (A) Linescan and normalised fluorescence plots for 2 adjacent myocytes in an arteriole under control conditions and during superfusion with 100 μM ryanodine. Time-course data in the graph refers to the indicated regions of interest (R.O.I.). (B) Summary data from 17 cells for spark frequency and amplitude during the 20 s control period and 3 consecutive, 10 s periods of superfusion with ryanodine ( ** P

    Article Snippet: The drug suppliers and bath concentrations of vehicle (%v/v) were as follows: cyclopiazonic acid (Alexis; 0.05% DMSO); ryanodine (Alomone; 0.1% ethanol), tetracaine (Sigma–Aldrich; 0.01% H2O), nifedipine (Sigma–Aldrich; 0.01% ethanol), EGTA (Lancaster; dissolved directly in bath solution).

    Techniques: Fluorescence

    Effect of ryanodine on kinetics of the [Ca 2+ ] i response. A , Examples of the effects of ryanodine in slowing the rising phase of somatic Ca 2+ at the onset of RSS in a 4-month-old (left) and 23-month-old (right) animal. B , Ryanodine did not significantly affect peak Ca 2+ levels measured during RSS. Grayscale bars, Preryanodine. White bars, Postryanodine. Aging effect persists after ryanodine (asterisks). C , Ryanodine eliminated the effect of aging on measures of the AUC. Although the rising ( D ) and decaying ( E ) time constants of Ca 2+ did not differ with aging, ryanodine treatment significantly lengthened both time constants. All aging comparisons are made within a treatment condition (i.e., preryanodine only or postryanodine only). Note that peak Ca 2+ levels are increased with aging in cells before the ryanodine treatment (asterisks above grayscale bars) and also after ryanodine treatment (asterisks above white bars). *Different from the 4-month-old group appropriate for preryanodine and postryanodine comparisons at p

    Journal: The Journal of Neuroscience

    Article Title: Early and Simultaneous Emergence of Multiple Hippocampal Biomarkers of Aging Is Mediated by Ca2+-Induced Ca2+ Release

    doi: 10.1523/JNEUROSCI.4171-05.2006

    Figure Lengend Snippet: Effect of ryanodine on kinetics of the [Ca 2+ ] i response. A , Examples of the effects of ryanodine in slowing the rising phase of somatic Ca 2+ at the onset of RSS in a 4-month-old (left) and 23-month-old (right) animal. B , Ryanodine did not significantly affect peak Ca 2+ levels measured during RSS. Grayscale bars, Preryanodine. White bars, Postryanodine. Aging effect persists after ryanodine (asterisks). C , Ryanodine eliminated the effect of aging on measures of the AUC. Although the rising ( D ) and decaying ( E ) time constants of Ca 2+ did not differ with aging, ryanodine treatment significantly lengthened both time constants. All aging comparisons are made within a treatment condition (i.e., preryanodine only or postryanodine only). Note that peak Ca 2+ levels are increased with aging in cells before the ryanodine treatment (asterisks above grayscale bars) and also after ryanodine treatment (asterisks above white bars). *Different from the 4-month-old group appropriate for preryanodine and postryanodine comparisons at p

    Article Snippet: Ryanodine (Alomone Labs, Jerusalem, Israel) is a plant alkaloid with high specificity and potency at RyRs, and at > 10 μ m selectively blocks the receptors, eliminating CICR without influencing Ca2+ influx from other sources ( ; ; ; ).

    Techniques:

    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

    Journal: Nature Communications

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

    doi: 10.1038/s41467-017-00044-2

    Figure Lengend 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

    Article Snippet: In some experiments, the following reagents were applied to the culture medium at least 30 min before the application of the NT-3 gradients as previouslydescribed : 2 μM xestospongin C, 20 μM dantrolene, 3 μM SKF96365, 100 μM ryanodine (Alomone Labs), 5 μM BAPTA-AM (Invitrogen), 1 μM KN-93 or 5 μM STO-609.

    Techniques: Generated, Concentration Assay, Fluorescence

    Effects of CTX alone and of a cocktail of toxins (CTX, ATX and SNX 482) on physostigmine (Physo)- and EFS (10 Hz)-induced contractions in isolated muscle strips of the guinea pig bladder. (A) Averaged data from six guinea pigs shows the lack of effect of CTX (0.3 µmol·L −1 ) on physostigmine (1 µmol·L −1 )-induced contractions in the presence of TTX (1 µmol·L −1 ). (B) Averaged data ( N = 7) of the effect of CTX (0.3 µmol·L −1 ) on EFS (10 Hz)-induced contractions. (C) Averaged data from five guinea pigs of the effects of the cocktail of toxins [CTX (0.3 µmol·L −1 ), ATX (0.1 µmol·L −1 ) and SNX 482 (0.3 µmol·L −1 )] on physostigmine (1 µmol·L −1 )-induced contractions, in the presence of TTX (1 µmol·L −1 ). (D) Averaged data ( N = 5) of the effect of the same cocktail of toxins on EFS (10 Hz)-induced contractions revealing significant, but incomplete blockade. (E) Averaged data ( N = 6) of the corresponding time control for the effect of 1 µmol·L −1 physostigmine (physo 1 = 25–30 min and physo 2 = 45–50 min) alone. *, significant difference from TTX, P

    Journal: British Journal of Pharmacology

    Article Title: Spontaneous release of acetylcholine from autonomic nerves in the bladder

    doi: 10.1111/j.1476-5381.2009.00166.x

    Figure Lengend Snippet: Effects of CTX alone and of a cocktail of toxins (CTX, ATX and SNX 482) on physostigmine (Physo)- and EFS (10 Hz)-induced contractions in isolated muscle strips of the guinea pig bladder. (A) Averaged data from six guinea pigs shows the lack of effect of CTX (0.3 µmol·L −1 ) on physostigmine (1 µmol·L −1 )-induced contractions in the presence of TTX (1 µmol·L −1 ). (B) Averaged data ( N = 7) of the effect of CTX (0.3 µmol·L −1 ) on EFS (10 Hz)-induced contractions. (C) Averaged data from five guinea pigs of the effects of the cocktail of toxins [CTX (0.3 µmol·L −1 ), ATX (0.1 µmol·L −1 ) and SNX 482 (0.3 µmol·L −1 )] on physostigmine (1 µmol·L −1 )-induced contractions, in the presence of TTX (1 µmol·L −1 ). (D) Averaged data ( N = 5) of the effect of the same cocktail of toxins on EFS (10 Hz)-induced contractions revealing significant, but incomplete blockade. (E) Averaged data ( N = 6) of the corresponding time control for the effect of 1 µmol·L −1 physostigmine (physo 1 = 25–30 min and physo 2 = 45–50 min) alone. *, significant difference from TTX, P

    Article Snippet: In order to investigate which neuronal Ca2+ channel is responsible for spontaneous acetylcholine release, we studied the effects of selective Ca2+ channels blockers, such as CTX (for N type), ATX (for P/Q type) or by SNX 482 (for R-type).

    Techniques: Isolation