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positive allosteric modulator pnu120596  (Tocris)


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    Structured Review

    Tocris positive allosteric modulator pnu120596
    Positive Allosteric Modulator Pnu120596, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 115 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/position+module/PNU+120596/pm42012794-258-16-22
    Average 93 stars, based on 115 article reviews
    positive allosteric modulator pnu120596 - by Bioz Stars, 2026-09
    93/100 stars

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    Related Articles

    other:

    Article Title: Novel nicotinic acetylcholine receptor inhibitors derived from oleoylcholine analogs
    Article Snippet: Через 24 ч к клеткам добавляли исследуемые вещества Ol-Chol+I-, Ol-Chol+Mes-, DOGG-Chol+I -, DOTAP+Mes - в концентрации 6.25–100 мкМ, а также лиганды нАХР: 100 мкМ никотин (Nic, Sigma-Aldrich, Германия), мекамиламин (Mec), d-тубокурарин (d-TC), метилликаконитин (MLA); 10 мкМ PNU 120596, PNU 282987 (Tocris, Великобритания); 1 мкМ α-кобратоксин CTX.

    Calcium Assay:

    Article Title: Novel nicotinic acetylcholine receptor inhibitors derived from oleoylcholine analogs
    Article Snippet: .. Использовали следующие реактивы: Fluo-4 Direct Calcium Assay Kit (ThermoFisher Scientific, США), резазурин (Macklin Inc., Шанхай, Китай), а также ряд лигандов нАХР: никотин Nic (Sigma-Aldrich), мекамиламин Mec, d-тубокурарин d-TC, метилликаконитин MLA, PNU120596, PNU282987 (Tocris, Великобритания), линию клеток нейробластомы человека SH-SY5Y (Sigma-Aldrich). ..

    Saline:

    Article Title: A positive allosteric modulator of α7 nicotinic receptor reduces levodopa-induced dyskinesias in hemi-parkinsonian mice.
    Article Snippet: Parkinson’s disease is a prevalent neurodegenerative disorder characterized by motor impairments including rigidity, bradykinesia and tremor.. L-3,4-dihydroxyphenylalanine (L-DOPA) keeps being the standard treatment for Parkinson’s disease.. But long-term treatment often leads to L-DOPA induced dyskinesias (LIDs): abnormal involuntary movements (AIMs) that significantly impact patients’ quality of life.

    Injection:

    Article Title: A positive allosteric modulator of α7 nicotinic receptor reduces levodopa-induced dyskinesias in hemi-parkinsonian mice.
    Article Snippet: Parkinson’s disease is a prevalent neurodegenerative disorder characterized by motor impairments including rigidity, bradykinesia and tremor.. L-3,4-dihydroxyphenylalanine (L-DOPA) keeps being the standard treatment for Parkinson’s disease.. But long-term treatment often leads to L-DOPA induced dyskinesias (LIDs): abnormal involuntary movements (AIMs) that significantly impact patients’ quality of life.

    Isolation:

    Article Title: Nicotinic Acetylcholine Receptor of α7 Subtype is Linked to Glioblastoma Cholinergic Heterogeneity.
    Article Snippet: 1 Department of molecular neuroimmune signaling, Shemyakin-Ovchinnikov Institute of bioorganic chemistry of Russian academy of sciences, Moscow, Russian Federation 2 Department of functioning of living systems, ShemyakinOvchinnikov Institute of bioorganic chemistry of Russian academy of sciences, Moscow, Russian Federation 3 Department of Microbiology & Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA 4 Laboratory of systems biology, Institute of biomedical chemistry of Russian academy of sciences, Moscow, Russian Federation 5 Department of biology and general genetics, Sechenov University, Moscow, Russian Federation Abstract Glioblastoma multiforme (GBM) shows tremendous heterogeneity in terms of morphology and gene expression.. One of the diagnostically significant characteristics of GBM is the choline peak that can be found in patients’ NMR.. Choline derivatives are distributed unevenly throughout the tumor and concentrated, in particular, at the leading edge and infiltrating GBM tumour zones as well as gene transcripts of α7 nicotinic acetylcholine receptor (nAChR), known for its ability to become activated upon choline binding.



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    Potentiating SK channels restores normal NMDAR integration in Grin1 Y647S +/− mice (A) Schematic of potential mechanism showing impaired negative feedback in Y647S +/− neurons due to insufficient Ca 2+ influx compared to WT and the effect of <t>NS309</t> in boosting SK channel Ca 2+ sensitivity, thereby restoring negative feedback in Y647S +/− neurons. (B) Average NMDAR plateau potential in Y647S +/− neurons at 70 μA with extended tail indicated by red arrow. Application of 10 μM NS309 to the slice restores normal duration and terminates the NMDAR plateau potential in Y647S +/− (Y647S +/− + NS309). (Inset) Restoration of plateau potential duration by NS309 at increasing stimulus intensities in a Y647S +/− neuron. (C) Total width of the NMDAR plateau potential in WT, Y647S +/− , and Y647S +/− + NS309 neurons (∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 10 −4 , Tukey’s post hoc. Black stars: WT vs. Y647S +/− , purple stars: Y647S +/− vs. Y647S +/− + NS309). (D) SK2 channel blocker (Leidab7, 100 nM) prevents NS309 from reducing plateau potential duration in Y647S +/− neurons. (E) Normalized NMDAR plateau width in Y647S +/− neurons with the addition of NS309 and NS309+SK2 blockers (∗ p < 0.05, Sidak’s post hoc).
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    Potentiating SK channels restores normal NMDAR integration in Grin1 Y647S +/− mice (A) Schematic of potential mechanism showing impaired negative feedback in Y647S +/− neurons due to insufficient Ca 2+ influx compared to WT and the effect of <t>NS309</t> in boosting SK channel Ca 2+ sensitivity, thereby restoring negative feedback in Y647S +/− neurons. (B) Average NMDAR plateau potential in Y647S +/− neurons at 70 μA with extended tail indicated by red arrow. Application of 10 μM NS309 to the slice restores normal duration and terminates the NMDAR plateau potential in Y647S +/− (Y647S +/− + NS309). (Inset) Restoration of plateau potential duration by NS309 at increasing stimulus intensities in a Y647S +/− neuron. (C) Total width of the NMDAR plateau potential in WT, Y647S +/− , and Y647S +/− + NS309 neurons (∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 10 −4 , Tukey’s post hoc. Black stars: WT vs. Y647S +/− , purple stars: Y647S +/− vs. Y647S +/− + NS309). (D) SK2 channel blocker (Leidab7, 100 nM) prevents NS309 from reducing plateau potential duration in Y647S +/− neurons. (E) Normalized NMDAR plateau width in Y647S +/− neurons with the addition of NS309 and NS309+SK2 blockers (∗ p < 0.05, Sidak’s post hoc).
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    Potentiating SK channels restores normal NMDAR integration in Grin1 Y647S +/− mice (A) Schematic of potential mechanism showing impaired negative feedback in Y647S +/− neurons due to insufficient Ca 2+ influx compared to WT and the effect of <t>NS309</t> in boosting SK channel Ca 2+ sensitivity, thereby restoring negative feedback in Y647S +/− neurons. (B) Average NMDAR plateau potential in Y647S +/− neurons at 70 μA with extended tail indicated by red arrow. Application of 10 μM NS309 to the slice restores normal duration and terminates the NMDAR plateau potential in Y647S +/− (Y647S +/− + NS309). (Inset) Restoration of plateau potential duration by NS309 at increasing stimulus intensities in a Y647S +/− neuron. (C) Total width of the NMDAR plateau potential in WT, Y647S +/− , and Y647S +/− + NS309 neurons (∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 10 −4 , Tukey’s post hoc. Black stars: WT vs. Y647S +/− , purple stars: Y647S +/− vs. Y647S +/− + NS309). (D) SK2 channel blocker (Leidab7, 100 nM) prevents NS309 from reducing plateau potential duration in Y647S +/− neurons. (E) Normalized NMDAR plateau width in Y647S +/− neurons with the addition of NS309 and NS309+SK2 blockers (∗ p < 0.05, Sidak’s post hoc).
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    Potentiating SK channels restores normal NMDAR integration in Grin1 Y647S +/− mice (A) Schematic of potential mechanism showing impaired negative feedback in Y647S +/− neurons due to insufficient Ca 2+ influx compared to WT and the effect of <t>NS309</t> in boosting SK channel Ca 2+ sensitivity, thereby restoring negative feedback in Y647S +/− neurons. (B) Average NMDAR plateau potential in Y647S +/− neurons at 70 μA with extended tail indicated by red arrow. Application of 10 μM NS309 to the slice restores normal duration and terminates the NMDAR plateau potential in Y647S +/− (Y647S +/− + NS309). (Inset) Restoration of plateau potential duration by NS309 at increasing stimulus intensities in a Y647S +/− neuron. (C) Total width of the NMDAR plateau potential in WT, Y647S +/− , and Y647S +/− + NS309 neurons (∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 10 −4 , Tukey’s post hoc. Black stars: WT vs. Y647S +/− , purple stars: Y647S +/− vs. Y647S +/− + NS309). (D) SK2 channel blocker (Leidab7, 100 nM) prevents NS309 from reducing plateau potential duration in Y647S +/− neurons. (E) Normalized NMDAR plateau width in Y647S +/− neurons with the addition of NS309 and NS309+SK2 blockers (∗ p < 0.05, Sidak’s post hoc).
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    Potentiating SK channels restores normal NMDAR integration in Grin1 Y647S +/− mice (A) Schematic of potential mechanism showing impaired negative feedback in Y647S +/− neurons due to insufficient Ca 2+ influx compared to WT and the effect of <t>NS309</t> in boosting SK channel Ca 2+ sensitivity, thereby restoring negative feedback in Y647S +/− neurons. (B) Average NMDAR plateau potential in Y647S +/− neurons at 70 μA with extended tail indicated by red arrow. Application of 10 μM NS309 to the slice restores normal duration and terminates the NMDAR plateau potential in Y647S +/− (Y647S +/− + NS309). (Inset) Restoration of plateau potential duration by NS309 at increasing stimulus intensities in a Y647S +/− neuron. (C) Total width of the NMDAR plateau potential in WT, Y647S +/− , and Y647S +/− + NS309 neurons (∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 10 −4 , Tukey’s post hoc. Black stars: WT vs. Y647S +/− , purple stars: Y647S +/− vs. Y647S +/− + NS309). (D) SK2 channel blocker (Leidab7, 100 nM) prevents NS309 from reducing plateau potential duration in Y647S +/− neurons. (E) Normalized NMDAR plateau width in Y647S +/− neurons with the addition of NS309 and NS309+SK2 blockers (∗ p < 0.05, Sidak’s post hoc).
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    Image Search Results


    Potentiating SK channels restores normal NMDAR integration in Grin1 Y647S +/− mice (A) Schematic of potential mechanism showing impaired negative feedback in Y647S +/− neurons due to insufficient Ca 2+ influx compared to WT and the effect of NS309 in boosting SK channel Ca 2+ sensitivity, thereby restoring negative feedback in Y647S +/− neurons. (B) Average NMDAR plateau potential in Y647S +/− neurons at 70 μA with extended tail indicated by red arrow. Application of 10 μM NS309 to the slice restores normal duration and terminates the NMDAR plateau potential in Y647S +/− (Y647S +/− + NS309). (Inset) Restoration of plateau potential duration by NS309 at increasing stimulus intensities in a Y647S +/− neuron. (C) Total width of the NMDAR plateau potential in WT, Y647S +/− , and Y647S +/− + NS309 neurons (∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 10 −4 , Tukey’s post hoc. Black stars: WT vs. Y647S +/− , purple stars: Y647S +/− vs. Y647S +/− + NS309). (D) SK2 channel blocker (Leidab7, 100 nM) prevents NS309 from reducing plateau potential duration in Y647S +/− neurons. (E) Normalized NMDAR plateau width in Y647S +/− neurons with the addition of NS309 and NS309+SK2 blockers (∗ p < 0.05, Sidak’s post hoc).

    Journal: iScience

    Article Title: Context-dependent NMDA receptor dysfunction predicts seizure treatment in mice with human GluN1 variant

    doi: 10.1016/j.isci.2025.114301

    Figure Lengend Snippet: Potentiating SK channels restores normal NMDAR integration in Grin1 Y647S +/− mice (A) Schematic of potential mechanism showing impaired negative feedback in Y647S +/− neurons due to insufficient Ca 2+ influx compared to WT and the effect of NS309 in boosting SK channel Ca 2+ sensitivity, thereby restoring negative feedback in Y647S +/− neurons. (B) Average NMDAR plateau potential in Y647S +/− neurons at 70 μA with extended tail indicated by red arrow. Application of 10 μM NS309 to the slice restores normal duration and terminates the NMDAR plateau potential in Y647S +/− (Y647S +/− + NS309). (Inset) Restoration of plateau potential duration by NS309 at increasing stimulus intensities in a Y647S +/− neuron. (C) Total width of the NMDAR plateau potential in WT, Y647S +/− , and Y647S +/− + NS309 neurons (∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 10 −4 , Tukey’s post hoc. Black stars: WT vs. Y647S +/− , purple stars: Y647S +/− vs. Y647S +/− + NS309). (D) SK2 channel blocker (Leidab7, 100 nM) prevents NS309 from reducing plateau potential duration in Y647S +/− neurons. (E) Normalized NMDAR plateau width in Y647S +/− neurons with the addition of NS309 and NS309+SK2 blockers (∗ p < 0.05, Sidak’s post hoc).

    Article Snippet: SK channel positive allosteric modulator NS309 (10 μM, Tocris ) was included in a subset of experiments to restore appropriate duration of dendritic integration in Y647S +/− mice.

    Techniques: