w conotoxin mviic 2  (Alomone Labs)


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    Structured Review

    Alomone Labs w conotoxin mviic 2
    Effects of HVACC blockade by <t>ω-conotoxin</t> <t>MVIIC</t> (CTX, 1 μM) on spontaneous activity. ( A ) Representative experiment showing voltage-clamp recordings (+10 mV) from a mitral cell in the presence of DNI (control, top trace), upon addition of CTX (middle trace) and further wash-in of BCC (50 µM; bottom trace). ( B ) sIPSCs in control and in presence of CTX (n = 7 MCs). Left: Frequency. Right: Amplitude. sIPSCs were abolished in BCC (analysis not shown) ( C ) Linear regression between the CTX effect on sIPSC frequency vs urIPSC amplitude (n = 7 MCs). No significant correlation.
    W Conotoxin Mviic 2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/w conotoxin mviic 2/product/Alomone Labs
    Average 94 stars, based on 40 article reviews
    Price from $9.99 to $1999.99
    w conotoxin mviic 2 - by Bioz Stars, 2022-12
    94/100 stars

    Images

    1) Product Images from "Presynaptic NMDARs cooperate with local spikes toward GABA release from the reciprocal olfactory bulb granule cell spine"

    Article Title: Presynaptic NMDARs cooperate with local spikes toward GABA release from the reciprocal olfactory bulb granule cell spine

    Journal: eLife

    doi: 10.7554/eLife.63737

    Effects of HVACC blockade by ω-conotoxin MVIIC (CTX, 1 μM) on spontaneous activity. ( A ) Representative experiment showing voltage-clamp recordings (+10 mV) from a mitral cell in the presence of DNI (control, top trace), upon addition of CTX (middle trace) and further wash-in of BCC (50 µM; bottom trace). ( B ) sIPSCs in control and in presence of CTX (n = 7 MCs). Left: Frequency. Right: Amplitude. sIPSCs were abolished in BCC (analysis not shown) ( C ) Linear regression between the CTX effect on sIPSC frequency vs urIPSC amplitude (n = 7 MCs). No significant correlation.
    Figure Legend Snippet: Effects of HVACC blockade by ω-conotoxin MVIIC (CTX, 1 μM) on spontaneous activity. ( A ) Representative experiment showing voltage-clamp recordings (+10 mV) from a mitral cell in the presence of DNI (control, top trace), upon addition of CTX (middle trace) and further wash-in of BCC (50 µM; bottom trace). ( B ) sIPSCs in control and in presence of CTX (n = 7 MCs). Left: Frequency. Right: Amplitude. sIPSCs were abolished in BCC (analysis not shown) ( C ) Linear regression between the CTX effect on sIPSC frequency vs urIPSC amplitude (n = 7 MCs). No significant correlation.

    Techniques Used: Activity Assay

    2) Product Images from "Functional microstructure of CaV-mediated calcium signaling in the axon initial segment"

    Article Title: Functional microstructure of CaV-mediated calcium signaling in the axon initial segment

    Journal: bioRxiv

    doi: 10.1101/2020.11.13.382374

    Ca V 2.1/2.2 contribute to AIS calcium in the somatosensory cortex. A. Representative effect of ω-conotoxin MVIIC application on AIS calcium in L5b pyramidal cells in the somatosensory cortex. Left: example time-locked control cell. Black, baseline; gray, post. Right: example of the effect of ω-conotoxin MVIIC. Black, baseline; green, ω-conotoxin MVIIC. Linescan data are plotted as mean ± standard error. B. Summary of the effects of ω-conotoxin MVIIC on AIS calcium in somatosensory L5b pyramidal neurons. Black, time-locked control cells; green, ω-conotoxin MVIIC. C. Decreases in EPSP amplitude confirm the presence of ω-conotoxin MVIIC at the slice. Top: representative examples ofPSPs in ω-conotoxin MVIIC (right) or in time-locked control cells (left). Bottom: Summary of the effects of ω-conotoxin MVIIC on EPSP amplitude in somatosensory cortex. Black, baseline; gray, time-locked control; green, ω-conotoxin MVIIC.
    Figure Legend Snippet: Ca V 2.1/2.2 contribute to AIS calcium in the somatosensory cortex. A. Representative effect of ω-conotoxin MVIIC application on AIS calcium in L5b pyramidal cells in the somatosensory cortex. Left: example time-locked control cell. Black, baseline; gray, post. Right: example of the effect of ω-conotoxin MVIIC. Black, baseline; green, ω-conotoxin MVIIC. Linescan data are plotted as mean ± standard error. B. Summary of the effects of ω-conotoxin MVIIC on AIS calcium in somatosensory L5b pyramidal neurons. Black, time-locked control cells; green, ω-conotoxin MVIIC. C. Decreases in EPSP amplitude confirm the presence of ω-conotoxin MVIIC at the slice. Top: representative examples ofPSPs in ω-conotoxin MVIIC (right) or in time-locked control cells (left). Bottom: Summary of the effects of ω-conotoxin MVIIC on EPSP amplitude in somatosensory cortex. Black, baseline; gray, time-locked control; green, ω-conotoxin MVIIC.

    Techniques Used:

    Ca V 3 channels and Ca V 2.1/2.2 exhibit distinct functional distributions. A. Schematic of 2PLSM point scan imaging protocol. Points were imaged in sets of 5, with each point separated by 0.5 µm. The laser was parked at a single diffraction-limited point for 25 ms preceding and 100 ms following an AP and calcium influx was measured with OGB-5N. Points were scanned in the sequence 2, 4, 1, 3, 5 and each point sampled a single AP. Data was averaged over 20-50 repetitions. B. Isochronal calcium peaks from neighboring point sets. Calcium influx at each point is color-coded as in panel A. B1 shows a point set with a hotspot at point 5. B2 is the point set immediately adjacent to B1 and shows equivalent calcium influx across all points. Gray bar indicates the calcium transient onset and offset. C. Distribution of point sets containing hotspots. Peak calcium influx at the brightest point was divided by the isochronal calcium influx at the point(s) 1 µm away. 46 of 59 sites imaged fell within a normal distribution, while 13 sites exhibited higher relative calcium influx. Black, point sets containing a local hotspot; gray, point sets with no local hotspot. Red line indicates the fit of a normal distribution. Total distribution fit for normality (Shapiro Wilk test p = 0.0016). D. Calcium influx at hotspots was approximately 2x higher than calcium influx at non-hotspot points. Black, point sets containing a local hotspot; gray, point sets with no local hotspot. Data are plotted as mean ± standard deviation. E. Comparison of the flanks of point sets with a local hotspot and those without. Black, point sets containing a local hotspot; gray, point sets with no local hotspot. Data are plotted as mean ± standard deviation for each 0.5 µm increment from the brightest point of the set. F.Influence of selective Ca V antagonists or store depletion on peak calcium influx during point scan imaging. Circles represent single point sets. Black, control; pink, TTA-P2; green, ω-conotoxin MVIIC; orange, CPA. G. Influence of selective Ca V antagonists or store depletion on calcium hotspots. Hotspots were classified as points > 1.5 times brighter than the point(s) 1 µm away. Dotted gray line represents the distinction between point sets with a local hotspot (above) and those without (below). Color code as in panel F.
    Figure Legend Snippet: Ca V 3 channels and Ca V 2.1/2.2 exhibit distinct functional distributions. A. Schematic of 2PLSM point scan imaging protocol. Points were imaged in sets of 5, with each point separated by 0.5 µm. The laser was parked at a single diffraction-limited point for 25 ms preceding and 100 ms following an AP and calcium influx was measured with OGB-5N. Points were scanned in the sequence 2, 4, 1, 3, 5 and each point sampled a single AP. Data was averaged over 20-50 repetitions. B. Isochronal calcium peaks from neighboring point sets. Calcium influx at each point is color-coded as in panel A. B1 shows a point set with a hotspot at point 5. B2 is the point set immediately adjacent to B1 and shows equivalent calcium influx across all points. Gray bar indicates the calcium transient onset and offset. C. Distribution of point sets containing hotspots. Peak calcium influx at the brightest point was divided by the isochronal calcium influx at the point(s) 1 µm away. 46 of 59 sites imaged fell within a normal distribution, while 13 sites exhibited higher relative calcium influx. Black, point sets containing a local hotspot; gray, point sets with no local hotspot. Red line indicates the fit of a normal distribution. Total distribution fit for normality (Shapiro Wilk test p = 0.0016). D. Calcium influx at hotspots was approximately 2x higher than calcium influx at non-hotspot points. Black, point sets containing a local hotspot; gray, point sets with no local hotspot. Data are plotted as mean ± standard deviation. E. Comparison of the flanks of point sets with a local hotspot and those without. Black, point sets containing a local hotspot; gray, point sets with no local hotspot. Data are plotted as mean ± standard deviation for each 0.5 µm increment from the brightest point of the set. F.Influence of selective Ca V antagonists or store depletion on peak calcium influx during point scan imaging. Circles represent single point sets. Black, control; pink, TTA-P2; green, ω-conotoxin MVIIC; orange, CPA. G. Influence of selective Ca V antagonists or store depletion on calcium hotspots. Hotspots were classified as points > 1.5 times brighter than the point(s) 1 µm away. Dotted gray line represents the distinction between point sets with a local hotspot (above) and those without (below). Color code as in panel F.

    Techniques Used: Functional Assay, Imaging, Sequencing, Standard Deviation

    Sodium and calcium influx occur on the rising and falling phases of the AP at physiological temperatures, respectively. A. Pointscan imaging protocol was performed as in Figure 4A . OGB-5N was replaced with the sodium indicator ING-2, and Alexa-594 was excluded from the internal recording solution. B. Representative ING-2 sodium imaging pointset. Points are color-coded as in Panel A. Gray bar indicates the sodium transient onset and offset. C. Distribution of sodium imaging point sets calculated as in Fig 4C . Red line represents the fit of a normal distribution to the data. D. Sodium and calcium transients from pointscan imaging temporally-aligned to AP threshold and peak. Left: Sodium and calcium influx onset relative to AP threshold. Right: Sodium and calcium influx onset relative to AP peak. Transient onset time was measured for the brightest point in a point set. Circles are individual point sets. Gray dashed line shows AP threshold (left) or peak (right) timing. Red, ING-2 sodium imaging; black, OGB-5N calcium imaging in control conditions; blue, calcium imaging in the presence of TTA-P2; green, calcium imaging in the presence of ω-conotoxin MVIIC; orange, calcium imaging in the presence of cyclopiazonic acid.
    Figure Legend Snippet: Sodium and calcium influx occur on the rising and falling phases of the AP at physiological temperatures, respectively. A. Pointscan imaging protocol was performed as in Figure 4A . OGB-5N was replaced with the sodium indicator ING-2, and Alexa-594 was excluded from the internal recording solution. B. Representative ING-2 sodium imaging pointset. Points are color-coded as in Panel A. Gray bar indicates the sodium transient onset and offset. C. Distribution of sodium imaging point sets calculated as in Fig 4C . Red line represents the fit of a normal distribution to the data. D. Sodium and calcium transients from pointscan imaging temporally-aligned to AP threshold and peak. Left: Sodium and calcium influx onset relative to AP threshold. Right: Sodium and calcium influx onset relative to AP peak. Transient onset time was measured for the brightest point in a point set. Circles are individual point sets. Gray dashed line shows AP threshold (left) or peak (right) timing. Red, ING-2 sodium imaging; black, OGB-5N calcium imaging in control conditions; blue, calcium imaging in the presence of TTA-P2; green, calcium imaging in the presence of ω-conotoxin MVIIC; orange, calcium imaging in the presence of cyclopiazonic acid.

    Techniques Used: Imaging

    3) Product Images from "Functional microstructure of CaV-mediated calcium signaling in the axon initial segment"

    Article Title: Functional microstructure of CaV-mediated calcium signaling in the axon initial segment

    Journal: bioRxiv

    doi: 10.1101/2020.11.13.382374

    Ca V 2.1/2.2 contribute to AIS calcium in the somatosensory cortex. A. Representative effect of ω-conotoxin MVIIC application on AIS calcium in L5b pyramidal cells in the somatosensory cortex. Left: example time-locked control cell. Black, baseline; gray, post. Right: example of the effect of ω-conotoxin MVIIC. Black, baseline; green, ω-conotoxin MVIIC. Linescan data are plotted as mean ± standard error. B. Summary of the effects of ω-conotoxin MVIIC on AIS calcium in somatosensory L5b pyramidal neurons. Black, time-locked control cells; green, ω-conotoxin MVIIC. C. Decreases in EPSP amplitude confirm the presence of ω-conotoxin MVIIC at the slice. Top: representative examples ofPSPs in ω-conotoxin MVIIC (right) or in time-locked control cells (left). Bottom: Summary of the effects of ω-conotoxin MVIIC on EPSP amplitude in somatosensory cortex. Black, baseline; gray, time-locked control; green, ω-conotoxin MVIIC.
    Figure Legend Snippet: Ca V 2.1/2.2 contribute to AIS calcium in the somatosensory cortex. A. Representative effect of ω-conotoxin MVIIC application on AIS calcium in L5b pyramidal cells in the somatosensory cortex. Left: example time-locked control cell. Black, baseline; gray, post. Right: example of the effect of ω-conotoxin MVIIC. Black, baseline; green, ω-conotoxin MVIIC. Linescan data are plotted as mean ± standard error. B. Summary of the effects of ω-conotoxin MVIIC on AIS calcium in somatosensory L5b pyramidal neurons. Black, time-locked control cells; green, ω-conotoxin MVIIC. C. Decreases in EPSP amplitude confirm the presence of ω-conotoxin MVIIC at the slice. Top: representative examples ofPSPs in ω-conotoxin MVIIC (right) or in time-locked control cells (left). Bottom: Summary of the effects of ω-conotoxin MVIIC on EPSP amplitude in somatosensory cortex. Black, baseline; gray, time-locked control; green, ω-conotoxin MVIIC.

    Techniques Used:

    Ca V 3 channels and Ca V 2.1/2.2 exhibit distinct functional distributions. A. Schematic of 2PLSM point scan imaging protocol. Points were imaged in sets of 5, with each point separated by 0.5 µm. The laser was parked at a single diffraction-limited point for 25 ms preceding and 100 ms following an AP and calcium influx was measured with OGB-5N. Points were scanned in the sequence 2, 4, 1, 3, 5 and each point sampled a single AP. Data was averaged over 20-50 repetitions. B. Isochronal calcium peaks from neighboring point sets. Calcium influx at each point is color-coded as in panel A. B1 shows a point set with a hotspot at point 5. B2 is the point set immediately adjacent to B1 and shows equivalent calcium influx across all points. Gray bar indicates the calcium transient onset and offset. C. Distribution of point sets containing hotspots. Peak calcium influx at the brightest point was divided by the isochronal calcium influx at the point(s) 1 µm away. 46 of 59 sites imaged fell within a normal distribution, while 13 sites exhibited higher relative calcium influx. Black, point sets containing a local hotspot; gray, point sets with no local hotspot. Red line indicates the fit of a normal distribution. Total distribution fit for normality (Shapiro Wilk test p = 0.0016). D. Calcium influx at hotspots was approximately 2x higher than calcium influx at non-hotspot points. Black, point sets containing a local hotspot; gray, point sets with no local hotspot. Data are plotted as mean ± standard deviation. E. Comparison of the flanks of point sets with a local hotspot and those without. Black, point sets containing a local hotspot; gray, point sets with no local hotspot. Data are plotted as mean ± standard deviation for each 0.5 µm increment from the brightest point of the set. F.Influence of selective Ca V antagonists or store depletion on peak calcium influx during point scan imaging. Circles represent single point sets. Black, control; pink, TTA-P2; green, ω-conotoxin MVIIC; orange, CPA. G. Influence of selective Ca V antagonists or store depletion on calcium hotspots. Hotspots were classified as points > 1.5 times brighter than the point(s) 1 µm away. Dotted gray line represents the distinction between point sets with a local hotspot (above) and those without (below). Color code as in panel F.
    Figure Legend Snippet: Ca V 3 channels and Ca V 2.1/2.2 exhibit distinct functional distributions. A. Schematic of 2PLSM point scan imaging protocol. Points were imaged in sets of 5, with each point separated by 0.5 µm. The laser was parked at a single diffraction-limited point for 25 ms preceding and 100 ms following an AP and calcium influx was measured with OGB-5N. Points were scanned in the sequence 2, 4, 1, 3, 5 and each point sampled a single AP. Data was averaged over 20-50 repetitions. B. Isochronal calcium peaks from neighboring point sets. Calcium influx at each point is color-coded as in panel A. B1 shows a point set with a hotspot at point 5. B2 is the point set immediately adjacent to B1 and shows equivalent calcium influx across all points. Gray bar indicates the calcium transient onset and offset. C. Distribution of point sets containing hotspots. Peak calcium influx at the brightest point was divided by the isochronal calcium influx at the point(s) 1 µm away. 46 of 59 sites imaged fell within a normal distribution, while 13 sites exhibited higher relative calcium influx. Black, point sets containing a local hotspot; gray, point sets with no local hotspot. Red line indicates the fit of a normal distribution. Total distribution fit for normality (Shapiro Wilk test p = 0.0016). D. Calcium influx at hotspots was approximately 2x higher than calcium influx at non-hotspot points. Black, point sets containing a local hotspot; gray, point sets with no local hotspot. Data are plotted as mean ± standard deviation. E. Comparison of the flanks of point sets with a local hotspot and those without. Black, point sets containing a local hotspot; gray, point sets with no local hotspot. Data are plotted as mean ± standard deviation for each 0.5 µm increment from the brightest point of the set. F.Influence of selective Ca V antagonists or store depletion on peak calcium influx during point scan imaging. Circles represent single point sets. Black, control; pink, TTA-P2; green, ω-conotoxin MVIIC; orange, CPA. G. Influence of selective Ca V antagonists or store depletion on calcium hotspots. Hotspots were classified as points > 1.5 times brighter than the point(s) 1 µm away. Dotted gray line represents the distinction between point sets with a local hotspot (above) and those without (below). Color code as in panel F.

    Techniques Used: Functional Assay, Imaging, Sequencing, Standard Deviation

    Sodium and calcium influx occur on the rising and falling phases of the AP at physiological temperatures, respectively. A. Pointscan imaging protocol was performed as in Figure 4A . OGB-5N was replaced with the sodium indicator ING-2, and Alexa-594 was excluded from the internal recording solution. B. Representative ING-2 sodium imaging pointset. Points are color-coded as in Panel A. Gray bar indicates the sodium transient onset and offset. C. Distribution of sodium imaging point sets calculated as in Fig 4C . Red line represents the fit of a normal distribution to the data. D. Sodium and calcium transients from pointscan imaging temporally-aligned to AP threshold and peak. Left: Sodium and calcium influx onset relative to AP threshold. Right: Sodium and calcium influx onset relative to AP peak. Transient onset time was measured for the brightest point in a point set. Circles are individual point sets. Gray dashed line shows AP threshold (left) or peak (right) timing. Red, ING-2 sodium imaging; black, OGB-5N calcium imaging in control conditions; blue, calcium imaging in the presence of TTA-P2; green, calcium imaging in the presence of ω-conotoxin MVIIC; orange, calcium imaging in the presence of cyclopiazonic acid.
    Figure Legend Snippet: Sodium and calcium influx occur on the rising and falling phases of the AP at physiological temperatures, respectively. A. Pointscan imaging protocol was performed as in Figure 4A . OGB-5N was replaced with the sodium indicator ING-2, and Alexa-594 was excluded from the internal recording solution. B. Representative ING-2 sodium imaging pointset. Points are color-coded as in Panel A. Gray bar indicates the sodium transient onset and offset. C. Distribution of sodium imaging point sets calculated as in Fig 4C . Red line represents the fit of a normal distribution to the data. D. Sodium and calcium transients from pointscan imaging temporally-aligned to AP threshold and peak. Left: Sodium and calcium influx onset relative to AP threshold. Right: Sodium and calcium influx onset relative to AP peak. Transient onset time was measured for the brightest point in a point set. Circles are individual point sets. Gray dashed line shows AP threshold (left) or peak (right) timing. Red, ING-2 sodium imaging; black, OGB-5N calcium imaging in control conditions; blue, calcium imaging in the presence of TTA-P2; green, calcium imaging in the presence of ω-conotoxin MVIIC; orange, calcium imaging in the presence of cyclopiazonic acid.

    Techniques Used: Imaging

    4) Product Images from "Presynaptic NMDA receptors cooperate with local action potentials to implement activity-dependent GABA release from the reciprocal olfactory bulb granule cell spine"

    Article Title: Presynaptic NMDA receptors cooperate with local action potentials to implement activity-dependent GABA release from the reciprocal olfactory bulb granule cell spine

    Journal: bioRxiv

    doi: 10.1101/440198

    Blockade of high voltage activated Ca 2+ -channels by ω-conotoxin MVIIC (CTX, 1 μM) causes a prominent reduction of urIPSC amplitudes. ( A, B ) Two representative experiments in brain slices from VGAT-Venus rat with the corresponding MC (red), the site of TPU (blue star) and the uncaging traces according to the condition (individual traces : grey, average control: red, average CTX: green). The average traces contain all recordings, both with and without detected responses. Left: same cell as in Fig. 1B . ( C ) Magnified illustration of traces in B (for control individual traces with urIPSC responses and their average, for CTX only average, color coding as above). ( D ) Left: Summary of effects of CTX on average normalized urIPSC amplitude (n = 8 MCs). Diamonds indicate the experiments with no detectable response in the presence of the drug. Right: Comparison of delta urIPSC areas normalized to control versus in the presence of CTX (n = 9 MCs).
    Figure Legend Snippet: Blockade of high voltage activated Ca 2+ -channels by ω-conotoxin MVIIC (CTX, 1 μM) causes a prominent reduction of urIPSC amplitudes. ( A, B ) Two representative experiments in brain slices from VGAT-Venus rat with the corresponding MC (red), the site of TPU (blue star) and the uncaging traces according to the condition (individual traces : grey, average control: red, average CTX: green). The average traces contain all recordings, both with and without detected responses. Left: same cell as in Fig. 1B . ( C ) Magnified illustration of traces in B (for control individual traces with urIPSC responses and their average, for CTX only average, color coding as above). ( D ) Left: Summary of effects of CTX on average normalized urIPSC amplitude (n = 8 MCs). Diamonds indicate the experiments with no detectable response in the presence of the drug. Right: Comparison of delta urIPSC areas normalized to control versus in the presence of CTX (n = 9 MCs).

    Techniques Used:

    5) Product Images from "Use-dependent potentiation of voltage-gated calcium channels rescues neurotransmission in nerve terminals intoxicated by botulinum neurotoxin serotype A"

    Article Title: Use-dependent potentiation of voltage-gated calcium channels rescues neurotransmission in nerve terminals intoxicated by botulinum neurotoxin serotype A

    Journal: Scientific Reports

    doi: 10.1038/s41598-017-16064-3

    Rescue of spontaneous synaptic activity in BoNT/A-silenced synapses by elevated extracellular Ca 2+ requires VGCCs. ( A ) Representative whole-cell recordings and mean mEPSC frequencies from non-intoxicated cultures in the presence of 2, 4, 8, or 16 mM Ca 2+ . Representative whole-cell recordings and mean mEPSC frequencies from BoNT/A-intoxicated cultures, in the presence of 2, 4, 8, or 16 mM Ca 2+ as well in 16 mM Ca 2+ with VGCC antagonists (10 µM nimodipine, 0.5 µM ω-agatoxin IVA and 0.5 µM ω-conotoxin MVIIC). ( C ) Representative whole-cell recordings and mean mEPSC frequencies from neurons intoxicated by BoNT/D or BoNT/E and incubated in 2 or 16 mM Ca 2+ . mEPSC frequencies are normalized to recordings from age-matched, non-intoxicated control cultures. Scale bars represent 5 s (x-axis) and 40 pA (y-axis). All data presented as mean ± SEM and n ≥ 10 neurons for all conditions. **Indicates p
    Figure Legend Snippet: Rescue of spontaneous synaptic activity in BoNT/A-silenced synapses by elevated extracellular Ca 2+ requires VGCCs. ( A ) Representative whole-cell recordings and mean mEPSC frequencies from non-intoxicated cultures in the presence of 2, 4, 8, or 16 mM Ca 2+ . Representative whole-cell recordings and mean mEPSC frequencies from BoNT/A-intoxicated cultures, in the presence of 2, 4, 8, or 16 mM Ca 2+ as well in 16 mM Ca 2+ with VGCC antagonists (10 µM nimodipine, 0.5 µM ω-agatoxin IVA and 0.5 µM ω-conotoxin MVIIC). ( C ) Representative whole-cell recordings and mean mEPSC frequencies from neurons intoxicated by BoNT/D or BoNT/E and incubated in 2 or 16 mM Ca 2+ . mEPSC frequencies are normalized to recordings from age-matched, non-intoxicated control cultures. Scale bars represent 5 s (x-axis) and 40 pA (y-axis). All data presented as mean ± SEM and n ≥ 10 neurons for all conditions. **Indicates p

    Techniques Used: Activity Assay, Incubation

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

    Article Title: Homer regulates calcium signalling in growth cone turning

    Journal: Neural Development

    doi: 10.1186/1749-8104-4-29

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

    Techniques Used: Derivative Assay, Inhibition

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    Alomone Labs w conotoxin mviic 2
    Effects of HVACC blockade by <t>ω-conotoxin</t> <t>MVIIC</t> (CTX, 1 μM) on spontaneous activity. ( A ) Representative experiment showing voltage-clamp recordings (+10 mV) from a mitral cell in the presence of DNI (control, top trace), upon addition of CTX (middle trace) and further wash-in of BCC (50 µM; bottom trace). ( B ) sIPSCs in control and in presence of CTX (n = 7 MCs). Left: Frequency. Right: Amplitude. sIPSCs were abolished in BCC (analysis not shown) ( C ) Linear regression between the CTX effect on sIPSC frequency vs urIPSC amplitude (n = 7 MCs). No significant correlation.
    W Conotoxin Mviic 2, 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
    https://www.bioz.com/result/w conotoxin mviic 2/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    w conotoxin mviic 2 - by Bioz Stars, 2022-12
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    Effects of HVACC blockade by ω-conotoxin MVIIC (CTX, 1 μM) on spontaneous activity. ( A ) Representative experiment showing voltage-clamp recordings (+10 mV) from a mitral cell in the presence of DNI (control, top trace), upon addition of CTX (middle trace) and further wash-in of BCC (50 µM; bottom trace). ( B ) sIPSCs in control and in presence of CTX (n = 7 MCs). Left: Frequency. Right: Amplitude. sIPSCs were abolished in BCC (analysis not shown) ( C ) Linear regression between the CTX effect on sIPSC frequency vs urIPSC amplitude (n = 7 MCs). No significant correlation.

    Journal: eLife

    Article Title: Presynaptic NMDARs cooperate with local spikes toward GABA release from the reciprocal olfactory bulb granule cell spine

    doi: 10.7554/eLife.63737

    Figure Lengend Snippet: Effects of HVACC blockade by ω-conotoxin MVIIC (CTX, 1 μM) on spontaneous activity. ( A ) Representative experiment showing voltage-clamp recordings (+10 mV) from a mitral cell in the presence of DNI (control, top trace), upon addition of CTX (middle trace) and further wash-in of BCC (50 µM; bottom trace). ( B ) sIPSCs in control and in presence of CTX (n = 7 MCs). Left: Frequency. Right: Amplitude. sIPSCs were abolished in BCC (analysis not shown) ( C ) Linear regression between the CTX effect on sIPSC frequency vs urIPSC amplitude (n = 7 MCs). No significant correlation.

    Article Snippet: The following pharmacological agents were bath-applied in some experiments: bicuculline (BCC, 50 µM, Sigma-Aldrich), ω-conotoxin MVIIC (CTX, 1 µM, Alomone, Jerusalem, Israel), TTX (500 nM, Alomone), D-APV (25 µM, Tocris), gabazine (GBZ, 20 µM, Tocris).

    Techniques: Activity Assay