penitrem a  (Alomone Labs)


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    Alomone Labs penitrem a
    Blocking BK channels enables calcium spikes evoked by current injection or climbing fiber activation to trigger DSE A , Dendritic calcium spikes evoked by dendritic current injection in control ACSF (black trace) and 100 nM <t>penitrem</t> A (red trace), recorded 130 µm from the soma. The amplitude of the injected dendritic current waveform (blue traces) was adjusted to evoke similar numbers of calcium spikes under the two conditions. B , Timecourse of PF synaptic strength before and after the calcium spikes evoked by current injection shown in panel A. The same number of calcium spikes, which were unable to trigger DSE in control ACSF, produced strong short-term depression of PF EPSPs when BK channels were blocked. C , The amount of DSE was plotted versus the number of calcium spikes evoked by current injection. An increasing amount of DSE was triggered with increasing number of calcium spikes, but only when BK channels were blocked by 100 nM penitrem A. Pooled data from 6 cells. D , The amount of DSE plotted against the number of synaptically evoked calcium spikes. Block of BK channels did not change the efficacy of synaptically evoked calcium spikes to evoke DSE. Pooled data from 4 cells. E , Timecourse of PF synaptic strength shows prominent DSE after 20 CF stimuli when BK channels were blocked, but not in control conditions. Single trials from the same cell. F , The amount of DSE was plotted versus the number of CF stimuli delivered during the induction. Pooled data from 5 cells. In C and F error bars show SEM and asterisks denote p
    Penitrem A, 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/penitrem a/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    penitrem a - by Bioz Stars, 2022-07
    93/100 stars

    Images

    1) Product Images from "Dendritic calcium spikes are tunable triggers of cannabinoid release and short-term synaptic plasticity in cerebellar Purkinje neurons"

    Article Title: Dendritic calcium spikes are tunable triggers of cannabinoid release and short-term synaptic plasticity in cerebellar Purkinje neurons

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

    doi: 10.1523/JNEUROSCI.5284-05.2006

    Blocking BK channels enables calcium spikes evoked by current injection or climbing fiber activation to trigger DSE A , Dendritic calcium spikes evoked by dendritic current injection in control ACSF (black trace) and 100 nM penitrem A (red trace), recorded 130 µm from the soma. The amplitude of the injected dendritic current waveform (blue traces) was adjusted to evoke similar numbers of calcium spikes under the two conditions. B , Timecourse of PF synaptic strength before and after the calcium spikes evoked by current injection shown in panel A. The same number of calcium spikes, which were unable to trigger DSE in control ACSF, produced strong short-term depression of PF EPSPs when BK channels were blocked. C , The amount of DSE was plotted versus the number of calcium spikes evoked by current injection. An increasing amount of DSE was triggered with increasing number of calcium spikes, but only when BK channels were blocked by 100 nM penitrem A. Pooled data from 6 cells. D , The amount of DSE plotted against the number of synaptically evoked calcium spikes. Block of BK channels did not change the efficacy of synaptically evoked calcium spikes to evoke DSE. Pooled data from 4 cells. E , Timecourse of PF synaptic strength shows prominent DSE after 20 CF stimuli when BK channels were blocked, but not in control conditions. Single trials from the same cell. F , The amount of DSE was plotted versus the number of CF stimuli delivered during the induction. Pooled data from 5 cells. In C and F error bars show SEM and asterisks denote p
    Figure Legend Snippet: Blocking BK channels enables calcium spikes evoked by current injection or climbing fiber activation to trigger DSE A , Dendritic calcium spikes evoked by dendritic current injection in control ACSF (black trace) and 100 nM penitrem A (red trace), recorded 130 µm from the soma. The amplitude of the injected dendritic current waveform (blue traces) was adjusted to evoke similar numbers of calcium spikes under the two conditions. B , Timecourse of PF synaptic strength before and after the calcium spikes evoked by current injection shown in panel A. The same number of calcium spikes, which were unable to trigger DSE in control ACSF, produced strong short-term depression of PF EPSPs when BK channels were blocked. C , The amount of DSE was plotted versus the number of calcium spikes evoked by current injection. An increasing amount of DSE was triggered with increasing number of calcium spikes, but only when BK channels were blocked by 100 nM penitrem A. Pooled data from 6 cells. D , The amount of DSE plotted against the number of synaptically evoked calcium spikes. Block of BK channels did not change the efficacy of synaptically evoked calcium spikes to evoke DSE. Pooled data from 4 cells. E , Timecourse of PF synaptic strength shows prominent DSE after 20 CF stimuli when BK channels were blocked, but not in control conditions. Single trials from the same cell. F , The amount of DSE was plotted versus the number of CF stimuli delivered during the induction. Pooled data from 5 cells. In C and F error bars show SEM and asterisks denote p

    Techniques Used: Blocking Assay, Injection, Activation Assay, Produced

    BK channels control dendritic calcium spike propagation A ,  Dendritic recording from a Purkinje cell filled with Alexa 594 and Fluo-5F, 140 µm from the soma. The image was taken using the Alexa fluorescence. The stimulating electrode is drawn in blue. Calibration: 50 µm. Inset: high magnification image of the area of interest with 5 ROIs indicated.  B ,  Maximum intensity projections of image stacks acquired during synaptically or current injection-evoked calcium spikes in control ACSF and 100 nM penitrem A. Calibration: 20 µm.  C ,  Calcium transients recorded from the five respective ROIs in the inset of part A during synaptically evoked calcium spikes before (black) and after blocking BK channels (red).  D ,  The similarly selected 5 ROIs were averaged over 3 cells and normalized to the synaptic maximum in control ACSF.  E ,  Calcium transients recorded from the five respective ROIs in the inset of part A during current injection-evoked calcium spikes before (black) and after blocking BK channels (red).  F ,  The similarly selected 5 ROIs were averaged over several cells and normalized to the synaptic maximum in control ACSF. Blocking BK channels clearly improved the spatial spread of calcium spikes. Asterisks denote statistical significance (p
    Figure Legend Snippet: BK channels control dendritic calcium spike propagation A , Dendritic recording from a Purkinje cell filled with Alexa 594 and Fluo-5F, 140 µm from the soma. The image was taken using the Alexa fluorescence. The stimulating electrode is drawn in blue. Calibration: 50 µm. Inset: high magnification image of the area of interest with 5 ROIs indicated. B , Maximum intensity projections of image stacks acquired during synaptically or current injection-evoked calcium spikes in control ACSF and 100 nM penitrem A. Calibration: 20 µm. C , Calcium transients recorded from the five respective ROIs in the inset of part A during synaptically evoked calcium spikes before (black) and after blocking BK channels (red). D , The similarly selected 5 ROIs were averaged over 3 cells and normalized to the synaptic maximum in control ACSF. E , Calcium transients recorded from the five respective ROIs in the inset of part A during current injection-evoked calcium spikes before (black) and after blocking BK channels (red). F , The similarly selected 5 ROIs were averaged over several cells and normalized to the synaptic maximum in control ACSF. Blocking BK channels clearly improved the spatial spread of calcium spikes. Asterisks denote statistical significance (p

    Techniques Used: Fluorescence, Injection, Blocking Assay

    2) Product Images from "Essential Role of Somatic Kv2 Channels in High-Frequency Firing in Cartwheel Cells of the Dorsal Cochlear Nucleus"

    Article Title: Essential Role of Somatic Kv2 Channels in High-Frequency Firing in Cartwheel Cells of the Dorsal Cochlear Nucleus

    Journal: eNeuro

    doi: 10.1523/ENEURO.0515-20.2021

    Biophysical properties of GxTX-sensitive Kv2 current in cartwheel cells. A , Outward current evoked by voltage steps. Pulse protocol is indicated at the bottom of A . The recordings were made at room temperature (23–24°C) using ACSF supplemented with NBQX, MK-801, strychnine, picrotoxin, TTX, apamin (a SK channel blocker), and penitrem A (a BK channel blocker). To remove inward current by voltage-gated calcium channels, CaCl 2 in the ACSF was excluded and replaced with equimolar MgCl 2 , and 0.25 m m EGTA-Na was added. GxTX-sensitive current was obtained by subtraction. B , The current–voltage relationship of the outward current in the absence (control) or presence of 100 n m GxTX (GxTX). The amplitude of steady-state was used for the plotting. Here and the following figures, error bars indicate SEM, numbers in parentheses indicate the number of replications (cells). Statistical significance was tested using two-way repeated measure ANOVA and Bonferroni post hoc tests (significance at p
    Figure Legend Snippet: Biophysical properties of GxTX-sensitive Kv2 current in cartwheel cells. A , Outward current evoked by voltage steps. Pulse protocol is indicated at the bottom of A . The recordings were made at room temperature (23–24°C) using ACSF supplemented with NBQX, MK-801, strychnine, picrotoxin, TTX, apamin (a SK channel blocker), and penitrem A (a BK channel blocker). To remove inward current by voltage-gated calcium channels, CaCl 2 in the ACSF was excluded and replaced with equimolar MgCl 2 , and 0.25 m m EGTA-Na was added. GxTX-sensitive current was obtained by subtraction. B , The current–voltage relationship of the outward current in the absence (control) or presence of 100 n m GxTX (GxTX). The amplitude of steady-state was used for the plotting. Here and the following figures, error bars indicate SEM, numbers in parentheses indicate the number of replications (cells). Statistical significance was tested using two-way repeated measure ANOVA and Bonferroni post hoc tests (significance at p

    Techniques Used:

    3) Product Images from "Hypoxia and metabolic inhibitors alter the intracellular ATP:ADP ratio and membrane potential in human coronary artery smooth muscle cells"

    Article Title: Hypoxia and metabolic inhibitors alter the intracellular ATP:ADP ratio and membrane potential in human coronary artery smooth muscle cells

    Journal: PeerJ

    doi: 10.7717/peerj.10344

    The identification of K + channels in setting HCASMC resting membrane potential. (A–F) The change in the fractional fluorescence of DiBAC 4 (3) treated with 10 µM glibenclamide (A), 200 nM penitrem A (B), 1 µM tram34 (C), 200 nM apamin (D), 25 µM BaCl 2 (E), and 10 µM XE991 (F). (G) A summary of percentchange in fractional fluorescence of DiBAC 4 (3) after application of K + channel inhibitors: glibenclamide ( p
    Figure Legend Snippet: The identification of K + channels in setting HCASMC resting membrane potential. (A–F) The change in the fractional fluorescence of DiBAC 4 (3) treated with 10 µM glibenclamide (A), 200 nM penitrem A (B), 1 µM tram34 (C), 200 nM apamin (D), 25 µM BaCl 2 (E), and 10 µM XE991 (F). (G) A summary of percentchange in fractional fluorescence of DiBAC 4 (3) after application of K + channel inhibitors: glibenclamide ( p

    Techniques Used: Fluorescence

    4) Product Images from "Hypoxia and metabolic inhibitors alter the intracellular ATP:ADP ratio and membrane potential in human coronary artery smooth muscle cells"

    Article Title: Hypoxia and metabolic inhibitors alter the intracellular ATP:ADP ratio and membrane potential in human coronary artery smooth muscle cells

    Journal: PeerJ

    doi: 10.7717/peerj.10344

    The identification of K + channels in setting HCASMC resting membrane potential. (A–F) The change in the fractional fluorescence of DiBAC 4 (3) treated with 10 µM glibenclamide (A), 200 nM penitrem A (B), 1 µM tram34 (C), 200 nM apamin (D), 25 µM BaCl 2 (E), and 10 µM XE991 (F). (G) A summary of percentchange in fractional fluorescence of DiBAC 4 (3) after application of K + channel inhibitors: glibenclamide ( p
    Figure Legend Snippet: The identification of K + channels in setting HCASMC resting membrane potential. (A–F) The change in the fractional fluorescence of DiBAC 4 (3) treated with 10 µM glibenclamide (A), 200 nM penitrem A (B), 1 µM tram34 (C), 200 nM apamin (D), 25 µM BaCl 2 (E), and 10 µM XE991 (F). (G) A summary of percentchange in fractional fluorescence of DiBAC 4 (3) after application of K + channel inhibitors: glibenclamide ( p

    Techniques Used: Fluorescence

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    Alomone Labs penitrem a
    Blocking BK channels enables calcium spikes evoked by current injection or climbing fiber activation to trigger DSE A , Dendritic calcium spikes evoked by dendritic current injection in control ACSF (black trace) and 100 nM <t>penitrem</t> A (red trace), recorded 130 µm from the soma. The amplitude of the injected dendritic current waveform (blue traces) was adjusted to evoke similar numbers of calcium spikes under the two conditions. B , Timecourse of PF synaptic strength before and after the calcium spikes evoked by current injection shown in panel A. The same number of calcium spikes, which were unable to trigger DSE in control ACSF, produced strong short-term depression of PF EPSPs when BK channels were blocked. C , The amount of DSE was plotted versus the number of calcium spikes evoked by current injection. An increasing amount of DSE was triggered with increasing number of calcium spikes, but only when BK channels were blocked by 100 nM penitrem A. Pooled data from 6 cells. D , The amount of DSE plotted against the number of synaptically evoked calcium spikes. Block of BK channels did not change the efficacy of synaptically evoked calcium spikes to evoke DSE. Pooled data from 4 cells. E , Timecourse of PF synaptic strength shows prominent DSE after 20 CF stimuli when BK channels were blocked, but not in control conditions. Single trials from the same cell. F , The amount of DSE was plotted versus the number of CF stimuli delivered during the induction. Pooled data from 5 cells. In C and F error bars show SEM and asterisks denote p
    Penitrem A, 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/penitrem a/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    penitrem a - by Bioz Stars, 2022-07
    93/100 stars
      Buy from Supplier

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    Blocking BK channels enables calcium spikes evoked by current injection or climbing fiber activation to trigger DSE A , Dendritic calcium spikes evoked by dendritic current injection in control ACSF (black trace) and 100 nM penitrem A (red trace), recorded 130 µm from the soma. The amplitude of the injected dendritic current waveform (blue traces) was adjusted to evoke similar numbers of calcium spikes under the two conditions. B , Timecourse of PF synaptic strength before and after the calcium spikes evoked by current injection shown in panel A. The same number of calcium spikes, which were unable to trigger DSE in control ACSF, produced strong short-term depression of PF EPSPs when BK channels were blocked. C , The amount of DSE was plotted versus the number of calcium spikes evoked by current injection. An increasing amount of DSE was triggered with increasing number of calcium spikes, but only when BK channels were blocked by 100 nM penitrem A. Pooled data from 6 cells. D , The amount of DSE plotted against the number of synaptically evoked calcium spikes. Block of BK channels did not change the efficacy of synaptically evoked calcium spikes to evoke DSE. Pooled data from 4 cells. E , Timecourse of PF synaptic strength shows prominent DSE after 20 CF stimuli when BK channels were blocked, but not in control conditions. Single trials from the same cell. F , The amount of DSE was plotted versus the number of CF stimuli delivered during the induction. Pooled data from 5 cells. In C and F error bars show SEM and asterisks denote p

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

    Article Title: Dendritic calcium spikes are tunable triggers of cannabinoid release and short-term synaptic plasticity in cerebellar Purkinje neurons

    doi: 10.1523/JNEUROSCI.5284-05.2006

    Figure Lengend Snippet: Blocking BK channels enables calcium spikes evoked by current injection or climbing fiber activation to trigger DSE A , Dendritic calcium spikes evoked by dendritic current injection in control ACSF (black trace) and 100 nM penitrem A (red trace), recorded 130 µm from the soma. The amplitude of the injected dendritic current waveform (blue traces) was adjusted to evoke similar numbers of calcium spikes under the two conditions. B , Timecourse of PF synaptic strength before and after the calcium spikes evoked by current injection shown in panel A. The same number of calcium spikes, which were unable to trigger DSE in control ACSF, produced strong short-term depression of PF EPSPs when BK channels were blocked. C , The amount of DSE was plotted versus the number of calcium spikes evoked by current injection. An increasing amount of DSE was triggered with increasing number of calcium spikes, but only when BK channels were blocked by 100 nM penitrem A. Pooled data from 6 cells. D , The amount of DSE plotted against the number of synaptically evoked calcium spikes. Block of BK channels did not change the efficacy of synaptically evoked calcium spikes to evoke DSE. Pooled data from 4 cells. E , Timecourse of PF synaptic strength shows prominent DSE after 20 CF stimuli when BK channels were blocked, but not in control conditions. Single trials from the same cell. F , The amount of DSE was plotted versus the number of CF stimuli delivered during the induction. Pooled data from 5 cells. In C and F error bars show SEM and asterisks denote p

    Article Snippet: Methanesulfonic acid was obtained from Fluka (Ronkonkoma, New York), penitrem A was obtained from Alomone Laboratories (Jerusalem, Israel), and other chemicals were obtained from Sigma or Tocris.

    Techniques: Blocking Assay, Injection, Activation Assay, Produced

    BK channels control dendritic calcium spike propagation A ,  Dendritic recording from a Purkinje cell filled with Alexa 594 and Fluo-5F, 140 µm from the soma. The image was taken using the Alexa fluorescence. The stimulating electrode is drawn in blue. Calibration: 50 µm. Inset: high magnification image of the area of interest with 5 ROIs indicated.  B ,  Maximum intensity projections of image stacks acquired during synaptically or current injection-evoked calcium spikes in control ACSF and 100 nM penitrem A. Calibration: 20 µm.  C ,  Calcium transients recorded from the five respective ROIs in the inset of part A during synaptically evoked calcium spikes before (black) and after blocking BK channels (red).  D ,  The similarly selected 5 ROIs were averaged over 3 cells and normalized to the synaptic maximum in control ACSF.  E ,  Calcium transients recorded from the five respective ROIs in the inset of part A during current injection-evoked calcium spikes before (black) and after blocking BK channels (red).  F ,  The similarly selected 5 ROIs were averaged over several cells and normalized to the synaptic maximum in control ACSF. Blocking BK channels clearly improved the spatial spread of calcium spikes. Asterisks denote statistical significance (p

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

    Article Title: Dendritic calcium spikes are tunable triggers of cannabinoid release and short-term synaptic plasticity in cerebellar Purkinje neurons

    doi: 10.1523/JNEUROSCI.5284-05.2006

    Figure Lengend Snippet: BK channels control dendritic calcium spike propagation A , Dendritic recording from a Purkinje cell filled with Alexa 594 and Fluo-5F, 140 µm from the soma. The image was taken using the Alexa fluorescence. The stimulating electrode is drawn in blue. Calibration: 50 µm. Inset: high magnification image of the area of interest with 5 ROIs indicated. B , Maximum intensity projections of image stacks acquired during synaptically or current injection-evoked calcium spikes in control ACSF and 100 nM penitrem A. Calibration: 20 µm. C , Calcium transients recorded from the five respective ROIs in the inset of part A during synaptically evoked calcium spikes before (black) and after blocking BK channels (red). D , The similarly selected 5 ROIs were averaged over 3 cells and normalized to the synaptic maximum in control ACSF. E , Calcium transients recorded from the five respective ROIs in the inset of part A during current injection-evoked calcium spikes before (black) and after blocking BK channels (red). F , The similarly selected 5 ROIs were averaged over several cells and normalized to the synaptic maximum in control ACSF. Blocking BK channels clearly improved the spatial spread of calcium spikes. Asterisks denote statistical significance (p

    Article Snippet: Methanesulfonic acid was obtained from Fluka (Ronkonkoma, New York), penitrem A was obtained from Alomone Laboratories (Jerusalem, Israel), and other chemicals were obtained from Sigma or Tocris.

    Techniques: Fluorescence, Injection, Blocking Assay

    Biophysical properties of GxTX-sensitive Kv2 current in cartwheel cells. A , Outward current evoked by voltage steps. Pulse protocol is indicated at the bottom of A . The recordings were made at room temperature (23–24°C) using ACSF supplemented with NBQX, MK-801, strychnine, picrotoxin, TTX, apamin (a SK channel blocker), and penitrem A (a BK channel blocker). To remove inward current by voltage-gated calcium channels, CaCl 2 in the ACSF was excluded and replaced with equimolar MgCl 2 , and 0.25 m m EGTA-Na was added. GxTX-sensitive current was obtained by subtraction. B , The current–voltage relationship of the outward current in the absence (control) or presence of 100 n m GxTX (GxTX). The amplitude of steady-state was used for the plotting. Here and the following figures, error bars indicate SEM, numbers in parentheses indicate the number of replications (cells). Statistical significance was tested using two-way repeated measure ANOVA and Bonferroni post hoc tests (significance at p

    Journal: eNeuro

    Article Title: Essential Role of Somatic Kv2 Channels in High-Frequency Firing in Cartwheel Cells of the Dorsal Cochlear Nucleus

    doi: 10.1523/ENEURO.0515-20.2021

    Figure Lengend Snippet: Biophysical properties of GxTX-sensitive Kv2 current in cartwheel cells. A , Outward current evoked by voltage steps. Pulse protocol is indicated at the bottom of A . The recordings were made at room temperature (23–24°C) using ACSF supplemented with NBQX, MK-801, strychnine, picrotoxin, TTX, apamin (a SK channel blocker), and penitrem A (a BK channel blocker). To remove inward current by voltage-gated calcium channels, CaCl 2 in the ACSF was excluded and replaced with equimolar MgCl 2 , and 0.25 m m EGTA-Na was added. GxTX-sensitive current was obtained by subtraction. B , The current–voltage relationship of the outward current in the absence (control) or presence of 100 n m GxTX (GxTX). The amplitude of steady-state was used for the plotting. Here and the following figures, error bars indicate SEM, numbers in parentheses indicate the number of replications (cells). Statistical significance was tested using two-way repeated measure ANOVA and Bonferroni post hoc tests (significance at p

    Article Snippet: The ACSF for outward current was further supplemented with 0.5 μm TTX (Alomone Labs), 100 nm apamin (a SK channel blocker, Alomone Labs), and 1 mm penitrem A (a BK channel blocker, Alomone Labs).

    Techniques:

    The identification of K + channels in setting HCASMC resting membrane potential. (A–F) The change in the fractional fluorescence of DiBAC 4 (3) treated with 10 µM glibenclamide (A), 200 nM penitrem A (B), 1 µM tram34 (C), 200 nM apamin (D), 25 µM BaCl 2 (E), and 10 µM XE991 (F). (G) A summary of percentchange in fractional fluorescence of DiBAC 4 (3) after application of K + channel inhibitors: glibenclamide ( p

    Journal: PeerJ

    Article Title: Hypoxia and metabolic inhibitors alter the intracellular ATP:ADP ratio and membrane potential in human coronary artery smooth muscle cells

    doi: 10.7717/peerj.10344

    Figure Lengend Snippet: The identification of K + channels in setting HCASMC resting membrane potential. (A–F) The change in the fractional fluorescence of DiBAC 4 (3) treated with 10 µM glibenclamide (A), 200 nM penitrem A (B), 1 µM tram34 (C), 200 nM apamin (D), 25 µM BaCl 2 (E), and 10 µM XE991 (F). (G) A summary of percentchange in fractional fluorescence of DiBAC 4 (3) after application of K + channel inhibitors: glibenclamide ( p

    Article Snippet: K+ channels inhibitors, glibenclamide (Sigma-Aldrich), penitrem A (Alomone labs, Jerusalem, Israel), tram34 (Sigma-Aldrich), apamin (Tocris Bioscience, Abingdon, UK) and XE991 (Tocris Bioscience) were also prepared in DMSO as 10, 1, 10, 1 and 10 mM stock solutions, respectively.

    Techniques: Fluorescence