4 Aminopyridine, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Characterization of Voltage-Gated Potassium Channels in Human Neural Progenitor Cells"
Article Title: Characterization of Voltage-Gated Potassium Channels in Human Neural Progenitor Cells
Journal: PLoS ONE
Figure Legend Snippet: Influences of voltage-gated potassium (K v ) channel inhibition on progenitor c ell proliferation . Proliferation of hNPCs was analyzed via BrdU incorporation assay. (A): Progenitor cell proliferation was measured colorimetrically after 72 h of K v channel inhibition and normalized to control values without addition of inhibitor. Electrophysiologically determined inhibitory doses (IC 50 /IC 80 ) of 4-aminopyridine (4-AP), phrixotoxin-1 (PTX), ammonium chloride (NH 4 Cl), tetraethylammonium chloride (TEA), quinidine (QND) and α-dendrotoxin (DTX) were applied. Progenitor cell proliferation was significantly reduced by inhibition of I A with 4-AP, PTX, NH 4 Cl as well as by unspecific blockers like TEA and higher doses of QND. In contrast, the I K antagonist DTX increased proliferation of hNPCs (n≥4, 3 tissue preparations; one-way ANOVA, followed by Tukey's post-hoc test, *p
Techniques Used: Inhibition, BrdU Incorporation Assay
Figure Legend Snippet: Cell viability after inhibition of voltage-gated potassium (K v ) channels. Determination of cell viability in proliferating hNPCs via 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium salt (MTT) assay. (A): Cell viability was measured colorimetrically after 72 h of K v channel inhibition with different concentrations of 4-aminopyridine (4-AP), phrixotoxin-1 (PTX), ammonium chloride (NH 4 Cl), tetraethylammonium chloride (TEA), quinidine (QND) and α-dendrotoxin (DTX) and normalized to control values without addition of inhibitor. (B): Viability of hNPCs was significantly reduced by electrophysiologically determined inhibitory doses (IC 50 /IC 80 ) of 4-AP, PTX and NH 4 Cl, which specifically blocked I A , as well as by TEA and higher doses of QND, which inhibited both current components (n≥4, 3 tissue preparations; one-way ANOVA, followed by Tukey's post-hoc test, ***p
Techniques Used: Inhibition, MTT Assay
Figure Legend Snippet: Pharmacological inhibition of K v currents in hNPCs. Biophysically separated A-type (I A ) and delayed-rectifying (I K ) K v currents in proliferating hNPCs were differentially inhibited by the 4-aminopyridine (4-AP, i), phrixotoxin-1 (PTX, ii), ammonium chloride (NH 4 Cl, iii), tetraethylammonium chloride (TEA, iv), quinidine (QND, v) and α-dendrotoxin (DTX, vi). (A): Peak amplitudes of I A were measured during a depolarizing voltage step from −130 mV to 0 mV between 0 and 20 ms (inset). (B): I K was determined between 280 and 300 ms of a 100 mV depolarization step following a −40 mV prepulse during the application of different antagonist concentrations (insets). (C): Both current values were normalized to the non-inhibited peak amplitudes. Dose-response relationships were fitted with the Hill equation and IC 50 values were determined (see Tab. 2 ). Note that PTX selectively and 4-AP preferentially inhibited I A , while DTX selectively blocked I K .
Techniques Used: Inhibition, Mass Spectrometry
Figure Legend Snippet: Voltage-activated potassium (K v ) outward currents in hNPCs. (A): In whole-cell patch-clamp recordings human neural progenitor cells (hNPCs) expressed inactivating A-type (I A ) and non-inactivating delayed-rectifier-like potassium currents in activation (i) and inactivation protocols (ii, insets). (B): Pharmacological separation of current components was performed by application of 10 mM 4-aminopyridine (4-AP). I K was defined as 4-AP-insensitive component and I A as 4-AP-sensitive component. (C): Biophysical separation of I K was observed in activation protocols by a depolarizing prepulse to −40 mV (500 ms), which caused inactivation of I A . In inactivation protocols I A was revealed by a test pulse to 0 mV only since it activated at slightly more negative potentials than I K . During each voltage step peak values of the transient component were measured between 0 and 20 ms and sustained currents were determined between 280 and 300 ms. Chord conductances and current values respectively were normalized to their peak amplitudes and fitted to a Boltzmann distribution and current-voltage-relationships of control currents (A), pharmacologically (B) as well as biophysically (C) separated currents were calculated (iii, see Tab. 1 ). Note the similar I–V relations for both separation procedures.
Techniques Used: Patch Clamp, Activation Assay, Mass Spectrometry