penitrem a (Alomone Labs)


Structured Review

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
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

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

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

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

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

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