Review

mgtx (Alomone Labs)

Alomone Labs is a verified supplier

Alomone Labs manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Alomone Labs mgtx

( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin <t>(MgTx;</t> Kv1.3 channel blocker) or <t>dendrotoxin</t> <t>(DTx;</t> Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.

Mgtx, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 35 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/stm-325/pmc12187130-208-86-92?v=Alomone+Labs
Average 93 stars, based on 35 article reviews

mgtx - by Bioz Stars, 2026-07

93/100 stars

Images

1) Product Images from "Striatal cholinergic interneuron pause response requires Kv1 channels, is absent in dyskinetic mice, and is restored by dopamine D5 receptor inverse agonism"

Article Title: Striatal cholinergic interneuron pause response requires Kv1 channels, is absent in dyskinetic mice, and is restored by dopamine D5 receptor inverse agonism

Journal: eLife

doi: 10.7554/eLife.102184

Figure Legend Snippet: ( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin (MgTx; Kv1.3 channel blocker) or dendrotoxin (DTx; Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.

Techniques Used: Activation Assay, Control, Concentration Assay

Image Search Results

Journal: eLife

Article Title: Striatal cholinergic interneuron pause response requires Kv1 channels, is absent in dyskinetic mice, and is restored by dopamine D5 receptor inverse agonism

doi: 10.7554/eLife.102184

Figure Lengend Snippet: ( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin (MgTx; Kv1.3 channel blocker) or dendrotoxin (DTx; Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.

Article Snippet: The following stock solvents and final concentrations were used: distilled H 2 O for BaCl (10 μM), ZD7288 (30 μM), mecamylamine (10 μM, RBI), methiothepin (10 μM), quinpirole (1 μM, 10 μM), and sumanirole (10 μM); DMSO for CNQX (40 μM, Tocris), PIC (100 μM), SKF81297 (2 μM), SCH23390 (10 μM), sulpiride (10 μM, Santa Cruz Biotechnology), XE991 (10 μM), and clozapine (10 μM, Rospaw Laboratory); and the manufacturer’s recommended storage buffer (0.1% BSA, 100 mM NaCl, 10 mM Tris pH 7.5, 1 mM EDTA) for MgTx (3 nM and 30 nM, Alomone Labs) and g-DTx (100 nM, Alomone Labs).

Techniques: Activation Assay, Control, Concentration Assay

Journal: bioRxiv

Article Title: Striatal cholinergic interneuron pause response requires Kv1 channels, is absent in dyskinetic mice, and is restored by dopamine D5 receptor inverse agonism

doi: 10.1101/2024.05.31.596877

Figure Lengend Snippet: A. Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. B. Representative recordings of SCIN in response to optogenetic activation of thalamic terminals, with or without Margatoxin (MgTx; Kv1.3 channel blocker) or dendrotoxin (DTx; Kv1.1 and Kv1.6 channels blocker) in the bath. C. Pause duration/Baseline ISI of SCIN that responded with 1, 2, 3 or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3nM, 30 nM, or DTx 100 nM, in the bath (Two-way RM ANOVA interaction ns, treatment *p=0.0051; Control-MgTx 30nM: *p=0.0005; Control-MgTx 3nM: ns; Control-DTX: *p=0.0462; MgTx 30nM-MgTx 3nM: *p<0.0001; MgTx 30nM-DTX: ns; MgTx 3nM-DTX: *p=0.0027). D. Baseline ISI of SCIN recorded with or without MgTx 3nM, 30 nM, or DTx (One-way ANOVA, ns). E. Burst duration of SCIN that responded with 2, 3 or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3nM, 30 nM or DTx 100 nM, in the bath (Two-way RM ANOVA, ns). F. Representative recordings of SCIN in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 uM; Kir2.2 channel blocker at this concentration) or XE 991 (10 uM; Kv7 channel blocker) in the bath. G. Pause duration/Baseline ISI of SCIN that responded with 1, 2, 3 or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 uM XE 991 or 10 uM Ba 2+ (Two-way RM ANOVA, ns). H. Baseline ISI of SCIN recorded with or without Ba 2+ or XE 991 (One-way ANOVA, ns). I. Burst duration of SCIN that responded with 2, 3 or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (Two-way RM ANOVA, ns). Mean +/- SEM; n=7-16 cells per group, from >5 mice.

Article Snippet: The following stock solvents and final concentrations were used: distilled H 2 O for BaCl (10μM), ZD7288 (30μM); DMSO for CNQX (40μM, Tocris), picrotoxin (100μM), SKF81297 (2μM), SCH23390 (10μM), Sulpiride (10μM, Santa Cruz Biotechnology), XE991 (10μM) and clozapine (10μM, Rospaw Laboratory); and the manufacturer’s recommended storage buffer (0.1% BSA, 100mM NaCl, 10mM Tris pH 7.5, 1mM EDTA) for margatoxin (MgTx 3nM and 30nM, Alomone Labs) and g-Dendrotoxin (100nM, Alomone labs).

Techniques: Activation Assay, Control, Concentration Assay

A. Experimental design. B. Micrographs showing TH immunostaining at the level of the substantia nigra. C-E. Rotation index (C), forelimb asymmetry (D) and latency to fall from the rotarod (E) for sham and 6-OHDA mice (C-D: unpaired t test, **p<0.0001; E: Two-way RM ANOVA, interaction: *p=0.0284, n=5 sham and 22 6-OHDA mice). F. Abnormal involuntary movement (AIM) score of chronically L-DOPA-treated 6-OHDA mice. (Two-way RM ANOVA, interaction: p=0.0081; post-hoc: Day 1 vs Day 4 *p<0.03). G. Representative cell-attached recordings of the pause response of SCIN to optogenetic stimulation of thalamic terminals, in a sham and a dyskinetic mouse in the OFF L-DOPA condition, with or without MgTx 30 nM in the bath. H. Pause duration/Baseline ISI of SCIN that responded with 1, 2, 3 or 4 spikes to optogenetic activation of thalamic terminals (Two-way RM ANOVA, interaction ns, treatment *p=0.0227; Sham vs OFF L-DOPA: *p=0.0301; OFF L-DOPA vs OFF L-DOPA+MgTx: ns; Sham vs OFF L-DOPA+MgTx: *p=0.0032). I. Baseline ISI of SCIN that responded with 1, 2, 3 or 4 spikes to optogenetic activation of thalamic terminals under the above conditions (One-way ANOVA, *p=0.0254; Sham vs OFF L-DOPA: *p=0.0201; OFF L-DOPA vs OFF L-DOPA+MgTx: ns; Sham vs OFF L-DOPA+MgTx: ns). J. Burst duration of SCIN that responded with 2, 3 or 4 spikes to optogenetic activation of thalamic terminals under the above conditions (Two-way RM ANOVA, ns). Mean +/- SEM; n=14-27 cells per group, from >5 mice.

Journal: bioRxiv

Article Title: Striatal cholinergic interneuron pause response requires Kv1 channels, is absent in dyskinetic mice, and is restored by dopamine D5 receptor inverse agonism

doi: 10.1101/2024.05.31.596877

Figure Lengend Snippet: A. Experimental design. B. Micrographs showing TH immunostaining at the level of the substantia nigra. C-E. Rotation index (C), forelimb asymmetry (D) and latency to fall from the rotarod (E) for sham and 6-OHDA mice (C-D: unpaired t test, **p<0.0001; E: Two-way RM ANOVA, interaction: *p=0.0284, n=5 sham and 22 6-OHDA mice). F. Abnormal involuntary movement (AIM) score of chronically L-DOPA-treated 6-OHDA mice. (Two-way RM ANOVA, interaction: p=0.0081; post-hoc: Day 1 vs Day 4 *p<0.03). G. Representative cell-attached recordings of the pause response of SCIN to optogenetic stimulation of thalamic terminals, in a sham and a dyskinetic mouse in the OFF L-DOPA condition, with or without MgTx 30 nM in the bath. H. Pause duration/Baseline ISI of SCIN that responded with 1, 2, 3 or 4 spikes to optogenetic activation of thalamic terminals (Two-way RM ANOVA, interaction ns, treatment *p=0.0227; Sham vs OFF L-DOPA: *p=0.0301; OFF L-DOPA vs OFF L-DOPA+MgTx: ns; Sham vs OFF L-DOPA+MgTx: *p=0.0032). I. Baseline ISI of SCIN that responded with 1, 2, 3 or 4 spikes to optogenetic activation of thalamic terminals under the above conditions (One-way ANOVA, *p=0.0254; Sham vs OFF L-DOPA: *p=0.0201; OFF L-DOPA vs OFF L-DOPA+MgTx: ns; Sham vs OFF L-DOPA+MgTx: ns). J. Burst duration of SCIN that responded with 2, 3 or 4 spikes to optogenetic activation of thalamic terminals under the above conditions (Two-way RM ANOVA, ns). Mean +/- SEM; n=14-27 cells per group, from >5 mice.

Techniques: Immunostaining, Activation Assay

A. Schematic representation of the tested hypothesis. B. Representative responses of SCIN from OFF L-DOPA dyskinetic mice to optogenetic activation of thalamic terminals, with or without SKF81297, Clozapine (10 uM; D1/D5 receptor inverse agonist), SCH23390 (10 uM; D1/D5 selective antagonist), Clozapine + SCH23390 or Clozapine + MgTx, in the bath. C. Pause duration/Baseline ISI of SCIN from OFF L-DOPA dyskinetic mice that responded with 1, 2, 3 or 4 spikes to optogenetic activation of thalamic terminals (Two-way RM ANOVA, interaction *p=0.0489, Dunnett’s multiple comparisons test: 4 elicited spikes: OFF L-DOPA vs Clozapine: *p=0.0181). D. Baseline ISI of SCIN that responded with 1, 2, 3 or 4 spikes to optogenetic activation of thalamic terminals, under the above conditions (One-way ANOVA, ns). E. Burst duration of SCIN from dyskinetic mice OFF L-DOPA that responded with 2, 3 or 4 spikes to optogenetic activation of thalamic terminals, under the above conditions (Two-way RM ANOVA, interaction ns, treatment ns). Mean +/- SEM; n=6-17 cells per group, from >5 mice. F. Schematic representation of conclusion. Left, in physiologic conditions the balance of D2 versus D5 activation emerges as a determinant of the Kv1-dependent pause expression; right, in parkinsonian mice an imbalance towards D5 signaling abolishes the pause (top), which can be reset with D5 inverse agonism (bottom).

Journal: bioRxiv

Article Title: Striatal cholinergic interneuron pause response requires Kv1 channels, is absent in dyskinetic mice, and is restored by dopamine D5 receptor inverse agonism

doi: 10.1101/2024.05.31.596877

Figure Lengend Snippet: A. Schematic representation of the tested hypothesis. B. Representative responses of SCIN from OFF L-DOPA dyskinetic mice to optogenetic activation of thalamic terminals, with or without SKF81297, Clozapine (10 uM; D1/D5 receptor inverse agonist), SCH23390 (10 uM; D1/D5 selective antagonist), Clozapine + SCH23390 or Clozapine + MgTx, in the bath. C. Pause duration/Baseline ISI of SCIN from OFF L-DOPA dyskinetic mice that responded with 1, 2, 3 or 4 spikes to optogenetic activation of thalamic terminals (Two-way RM ANOVA, interaction *p=0.0489, Dunnett’s multiple comparisons test: 4 elicited spikes: OFF L-DOPA vs Clozapine: *p=0.0181). D. Baseline ISI of SCIN that responded with 1, 2, 3 or 4 spikes to optogenetic activation of thalamic terminals, under the above conditions (One-way ANOVA, ns). E. Burst duration of SCIN from dyskinetic mice OFF L-DOPA that responded with 2, 3 or 4 spikes to optogenetic activation of thalamic terminals, under the above conditions (Two-way RM ANOVA, interaction ns, treatment ns). Mean +/- SEM; n=6-17 cells per group, from >5 mice. F. Schematic representation of conclusion. Left, in physiologic conditions the balance of D2 versus D5 activation emerges as a determinant of the Kv1-dependent pause expression; right, in parkinsonian mice an imbalance towards D5 signaling abolishes the pause (top), which can be reset with D5 inverse agonism (bottom).

Techniques: Activation Assay, Expressing

Review

Structured Review

Images

1) Product Images from "Striatal cholinergic interneuron pause response requires Kv1 channels, is absent in dyskinetic mice, and is restored by dopamine D5 receptor inverse agonism"

Similar Products

Image Search Results