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k252a  (Tocris)


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    Tocris k252a
    K252a, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 109 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/k-252a/K+252a/pm41942002-57-9-22
    Average 93 stars, based on 109 article reviews
    k252a - by Bioz Stars, 2026-10
    93/100 stars

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    other:

    Article Title: Hippocampal SENP3 mediates chronic stress-induced depression-like behaviors by impairing the CREB-BDNF signaling.
    Article Snippet: Impaired signaling between cyclic adenosine monophosphate response element binding protein (CREB) and brain-derived neurotrophic factor (BDNF) in the hippocampus is generally considered to be the cause of depression.. The mechanisms underlying the impairment of CREB-BDNF signaling under stress conditions are largely unclear.. Small ubiquitin-like modifier (SUMO) specific peptidase 3 (SENP3) is a molecule that can regulate SUMOylation of target proteins related to synaptic plasticity.

    Article Title: Cannabinoid overrides triggers of GABAergic plasticity in vestibular circuits and distorts the development of navigation
    Article Snippet: K252a ((9S,10R,12R)-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3′,2',1′-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester) , Tocris Bioscience 1683/200U , .

    Incubation:

    Article Title: PLC-γ-Ca 2+ pathway regulates axonal TrkB endocytosis and is required for long-distance propagation of BDNF signaling
    Article Snippet: .. The next day (DIV 7), the neurons were incubated with neurobasal medium containing TrkB-Fc (100 ng/ml) in the cell body compartment, and the AC was pre-incubated for 1 h with vehicle or 0.2 μM K252a (Tocris cat# 1683) ( ). ..



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    k252a  (MedChemExpress)
    95
    MedChemExpress k252a
    Suppression of the BDNF/TrkB signaling pathway by <t>K252a</t> can partly reverse the KCC2 downregulation and dysfunction after hypoxia injury. (A) NeuN and KCC2 immunolabeling in the hippocampal CA1 region of MCAO‐R mice, and those pretreated with K252a are depicted in confocal scanning images. Scale bars: 50 μm. (B) Quantitative assessment of membrane KCC2 labeling density in fluorescently labeled cells relative to NeuN (Sham: N = 4, MCAO‐R N = 7, MCAO‐ R + K252a: N = 7). (C) Confocal microscopy images illustrate KCC2 (green) and NeuN (blue‐violet) expression in cultured hippocampal neurons exposed to OGD/R with or without K252a. (Control: N = 23 cells; OGD/R: N = 21 cells; OGD/ R + K252a: N = 32 cells, all from N = 5 cultures). Scale bar: 5 μm. (D) Quantitative assessment of membrane KCC2 in cultured hippocampal neurons. (E) Experimental determination of E GABA recorded by a small‐tip whole‐cell patch clamp is depicted in I‐V plots. (F) Statistical analysis indicates a significant positive shift in E GABA after MCAO‐R, which is partially reversed by K252a (MCAO‐ R + K252a: −55.0 ± 4.2 mV, N = 3, n = 21 vs. MCAO‐R: −52.1 ± 3.8 mV, N = 3, n = 15, p = 0.08; MCAO‐ R + K252a vs. Sham: −57.5 ± 3.6 mV, N = 4, n = 19, p = 0.12). (G) Patch clamp recordings using a low‐chloride electrode solution demonstrate that both the amplitude (H) and frequency (I) of mIPSCs, which are KCC2‐dependent, are significantly reduced by MCAO‐R, with only the amplitude being partially rescued by pretreatment with K252a (MCAO‐R: 17.0 ± 3.4 pA, N = 3, n = 17 vs. MCAO‐ R + K252a:19.3 ± 2.8 pA, N = 3, n = 18, p = 0.13; MCAO‐R + K252a vs. Sham:21.3 ± 3.3 pA, N = 3, n = 15). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the Sham group; ## p < 0.01 and ### p < 0.001 compared to the MCAO‐R group or OGD/R group.
    K252a, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/k-252a/K-252a/pmc12905008-59-7-12
    Average 95 stars, based on 1 article reviews
    k252a - by Bioz Stars, 2026-10
    95/100 stars
    		  Buy from Supplier
    k252a  (Tocris)
    93
    Tocris k252a
    Suppression of the BDNF/TrkB signaling pathway by <t>K252a</t> can partly reverse the KCC2 downregulation and dysfunction after hypoxia injury. (A) NeuN and KCC2 immunolabeling in the hippocampal CA1 region of MCAO‐R mice, and those pretreated with K252a are depicted in confocal scanning images. Scale bars: 50 μm. (B) Quantitative assessment of membrane KCC2 labeling density in fluorescently labeled cells relative to NeuN (Sham: N = 4, MCAO‐R N = 7, MCAO‐ R + K252a: N = 7). (C) Confocal microscopy images illustrate KCC2 (green) and NeuN (blue‐violet) expression in cultured hippocampal neurons exposed to OGD/R with or without K252a. (Control: N = 23 cells; OGD/R: N = 21 cells; OGD/ R + K252a: N = 32 cells, all from N = 5 cultures). Scale bar: 5 μm. (D) Quantitative assessment of membrane KCC2 in cultured hippocampal neurons. (E) Experimental determination of E GABA recorded by a small‐tip whole‐cell patch clamp is depicted in I‐V plots. (F) Statistical analysis indicates a significant positive shift in E GABA after MCAO‐R, which is partially reversed by K252a (MCAO‐ R + K252a: −55.0 ± 4.2 mV, N = 3, n = 21 vs. MCAO‐R: −52.1 ± 3.8 mV, N = 3, n = 15, p = 0.08; MCAO‐ R + K252a vs. Sham: −57.5 ± 3.6 mV, N = 4, n = 19, p = 0.12). (G) Patch clamp recordings using a low‐chloride electrode solution demonstrate that both the amplitude (H) and frequency (I) of mIPSCs, which are KCC2‐dependent, are significantly reduced by MCAO‐R, with only the amplitude being partially rescued by pretreatment with K252a (MCAO‐R: 17.0 ± 3.4 pA, N = 3, n = 17 vs. MCAO‐ R + K252a:19.3 ± 2.8 pA, N = 3, n = 18, p = 0.13; MCAO‐R + K252a vs. Sham:21.3 ± 3.3 pA, N = 3, n = 15). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the Sham group; ## p < 0.01 and ### p < 0.001 compared to the MCAO‐R group or OGD/R group.
    K252a, supplied by Tocris, 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/product/k-252a/K+252a/pm41942002-57-9-22
    Average 93 stars, based on 1 article reviews
    k252a - by Bioz Stars, 2026-10
    93/100 stars
    		  Buy from Supplier
    agents k252a  (MedChemExpress)
    95
    MedChemExpress agents k252a
    Suppression of the BDNF/TrkB signaling pathway by <t>K252a</t> can partly reverse the KCC2 downregulation and dysfunction after hypoxia injury. (A) NeuN and KCC2 immunolabeling in the hippocampal CA1 region of MCAO‐R mice, and those pretreated with K252a are depicted in confocal scanning images. Scale bars: 50 μm. (B) Quantitative assessment of membrane KCC2 labeling density in fluorescently labeled cells relative to NeuN (Sham: N = 4, MCAO‐R N = 7, MCAO‐ R + K252a: N = 7). (C) Confocal microscopy images illustrate KCC2 (green) and NeuN (blue‐violet) expression in cultured hippocampal neurons exposed to OGD/R with or without K252a. (Control: N = 23 cells; OGD/R: N = 21 cells; OGD/ R + K252a: N = 32 cells, all from N = 5 cultures). Scale bar: 5 μm. (D) Quantitative assessment of membrane KCC2 in cultured hippocampal neurons. (E) Experimental determination of E GABA recorded by a small‐tip whole‐cell patch clamp is depicted in I‐V plots. (F) Statistical analysis indicates a significant positive shift in E GABA after MCAO‐R, which is partially reversed by K252a (MCAO‐ R + K252a: −55.0 ± 4.2 mV, N = 3, n = 21 vs. MCAO‐R: −52.1 ± 3.8 mV, N = 3, n = 15, p = 0.08; MCAO‐ R + K252a vs. Sham: −57.5 ± 3.6 mV, N = 4, n = 19, p = 0.12). (G) Patch clamp recordings using a low‐chloride electrode solution demonstrate that both the amplitude (H) and frequency (I) of mIPSCs, which are KCC2‐dependent, are significantly reduced by MCAO‐R, with only the amplitude being partially rescued by pretreatment with K252a (MCAO‐R: 17.0 ± 3.4 pA, N = 3, n = 17 vs. MCAO‐ R + K252a:19.3 ± 2.8 pA, N = 3, n = 18, p = 0.13; MCAO‐R + K252a vs. Sham:21.3 ± 3.3 pA, N = 3, n = 15). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the Sham group; ## p < 0.01 and ### p < 0.001 compared to the MCAO‐R group or OGD/R group.
    Agents K252a, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/k-252a/K-252a/pm41872517-54-2-16
    Average 95 stars, based on 1 article reviews
    agents k252a - by Bioz Stars, 2026-10
    95/100 stars
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    k252a hy n6732  (MedChemExpress)
    95
    MedChemExpress k252a hy n6732
    Suppression of the BDNF/TrkB signaling pathway by <t>K252a</t> can partly reverse the KCC2 downregulation and dysfunction after hypoxia injury. (A) NeuN and KCC2 immunolabeling in the hippocampal CA1 region of MCAO‐R mice, and those pretreated with K252a are depicted in confocal scanning images. Scale bars: 50 μm. (B) Quantitative assessment of membrane KCC2 labeling density in fluorescently labeled cells relative to NeuN (Sham: N = 4, MCAO‐R N = 7, MCAO‐ R + K252a: N = 7). (C) Confocal microscopy images illustrate KCC2 (green) and NeuN (blue‐violet) expression in cultured hippocampal neurons exposed to OGD/R with or without K252a. (Control: N = 23 cells; OGD/R: N = 21 cells; OGD/ R + K252a: N = 32 cells, all from N = 5 cultures). Scale bar: 5 μm. (D) Quantitative assessment of membrane KCC2 in cultured hippocampal neurons. (E) Experimental determination of E GABA recorded by a small‐tip whole‐cell patch clamp is depicted in I‐V plots. (F) Statistical analysis indicates a significant positive shift in E GABA after MCAO‐R, which is partially reversed by K252a (MCAO‐ R + K252a: −55.0 ± 4.2 mV, N = 3, n = 21 vs. MCAO‐R: −52.1 ± 3.8 mV, N = 3, n = 15, p = 0.08; MCAO‐ R + K252a vs. Sham: −57.5 ± 3.6 mV, N = 4, n = 19, p = 0.12). (G) Patch clamp recordings using a low‐chloride electrode solution demonstrate that both the amplitude (H) and frequency (I) of mIPSCs, which are KCC2‐dependent, are significantly reduced by MCAO‐R, with only the amplitude being partially rescued by pretreatment with K252a (MCAO‐R: 17.0 ± 3.4 pA, N = 3, n = 17 vs. MCAO‐ R + K252a:19.3 ± 2.8 pA, N = 3, n = 18, p = 0.13; MCAO‐R + K252a vs. Sham:21.3 ± 3.3 pA, N = 3, n = 15). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the Sham group; ## p < 0.01 and ### p < 0.001 compared to the MCAO‐R group or OGD/R group.
    K252a Hy N6732, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/k-252a/K-252a/10__1016_slash_j__jfutfo__2025__08__027-96-1-23
    Average 95 stars, based on 1 article reviews
    k252a hy n6732 - by Bioz Stars, 2026-10
    95/100 stars
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    Image Search Results


    Suppression of the BDNF/TrkB signaling pathway by K252a can partly reverse the KCC2 downregulation and dysfunction after hypoxia injury. (A) NeuN and KCC2 immunolabeling in the hippocampal CA1 region of MCAO‐R mice, and those pretreated with K252a are depicted in confocal scanning images. Scale bars: 50 μm. (B) Quantitative assessment of membrane KCC2 labeling density in fluorescently labeled cells relative to NeuN (Sham: N = 4, MCAO‐R N = 7, MCAO‐ R + K252a: N = 7). (C) Confocal microscopy images illustrate KCC2 (green) and NeuN (blue‐violet) expression in cultured hippocampal neurons exposed to OGD/R with or without K252a. (Control: N = 23 cells; OGD/R: N = 21 cells; OGD/ R + K252a: N = 32 cells, all from N = 5 cultures). Scale bar: 5 μm. (D) Quantitative assessment of membrane KCC2 in cultured hippocampal neurons. (E) Experimental determination of E GABA recorded by a small‐tip whole‐cell patch clamp is depicted in I‐V plots. (F) Statistical analysis indicates a significant positive shift in E GABA after MCAO‐R, which is partially reversed by K252a (MCAO‐ R + K252a: −55.0 ± 4.2 mV, N = 3, n = 21 vs. MCAO‐R: −52.1 ± 3.8 mV, N = 3, n = 15, p = 0.08; MCAO‐ R + K252a vs. Sham: −57.5 ± 3.6 mV, N = 4, n = 19, p = 0.12). (G) Patch clamp recordings using a low‐chloride electrode solution demonstrate that both the amplitude (H) and frequency (I) of mIPSCs, which are KCC2‐dependent, are significantly reduced by MCAO‐R, with only the amplitude being partially rescued by pretreatment with K252a (MCAO‐R: 17.0 ± 3.4 pA, N = 3, n = 17 vs. MCAO‐ R + K252a:19.3 ± 2.8 pA, N = 3, n = 18, p = 0.13; MCAO‐R + K252a vs. Sham:21.3 ± 3.3 pA, N = 3, n = 15). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the Sham group; ## p < 0.01 and ### p < 0.001 compared to the MCAO‐R group or OGD/R group.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: KCC2 Dysfunction Mediated by Microglial BDNF / TrkB Signaling Exacerbates Early Post‐Stroke Seizure Susceptibility

    doi: 10.1002/cns.70795

    Figure Lengend Snippet: Suppression of the BDNF/TrkB signaling pathway by K252a can partly reverse the KCC2 downregulation and dysfunction after hypoxia injury. (A) NeuN and KCC2 immunolabeling in the hippocampal CA1 region of MCAO‐R mice, and those pretreated with K252a are depicted in confocal scanning images. Scale bars: 50 μm. (B) Quantitative assessment of membrane KCC2 labeling density in fluorescently labeled cells relative to NeuN (Sham: N = 4, MCAO‐R N = 7, MCAO‐ R + K252a: N = 7). (C) Confocal microscopy images illustrate KCC2 (green) and NeuN (blue‐violet) expression in cultured hippocampal neurons exposed to OGD/R with or without K252a. (Control: N = 23 cells; OGD/R: N = 21 cells; OGD/ R + K252a: N = 32 cells, all from N = 5 cultures). Scale bar: 5 μm. (D) Quantitative assessment of membrane KCC2 in cultured hippocampal neurons. (E) Experimental determination of E GABA recorded by a small‐tip whole‐cell patch clamp is depicted in I‐V plots. (F) Statistical analysis indicates a significant positive shift in E GABA after MCAO‐R, which is partially reversed by K252a (MCAO‐ R + K252a: −55.0 ± 4.2 mV, N = 3, n = 21 vs. MCAO‐R: −52.1 ± 3.8 mV, N = 3, n = 15, p = 0.08; MCAO‐ R + K252a vs. Sham: −57.5 ± 3.6 mV, N = 4, n = 19, p = 0.12). (G) Patch clamp recordings using a low‐chloride electrode solution demonstrate that both the amplitude (H) and frequency (I) of mIPSCs, which are KCC2‐dependent, are significantly reduced by MCAO‐R, with only the amplitude being partially rescued by pretreatment with K252a (MCAO‐R: 17.0 ± 3.4 pA, N = 3, n = 17 vs. MCAO‐ R + K252a:19.3 ± 2.8 pA, N = 3, n = 18, p = 0.13; MCAO‐R + K252a vs. Sham:21.3 ± 3.3 pA, N = 3, n = 15). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the Sham group; ## p < 0.01 and ### p < 0.001 compared to the MCAO‐R group or OGD/R group.

    Article Snippet: FUR was purchased from Sigma‐Aldrich, and minocycline, K252a, and CLP290 were from MedChemExpress.

    Techniques: Immunolabeling, Membrane, Labeling, Confocal Microscopy, Expressing, Cell Culture, Control, Patch Clamp

    Alleviating the severity of MCAO‐R‐induced seizures by blocking the BDNF/TrkB signaling and suppressing microglial activation. (A) Representative traces demonstrate the effective suppression of epileptiform burst firing induced by OGD/R in cultured hippocampal neurons by K252a. (B–D) Bar graphs present quantitative analysis, indicating that blocking the BDNF/TrkB signaling pathway with K252a significantly reduces the percentage of neurons exhibiting epileptiform bursting firing (B), the bursting frequency (C), and the total number of APs during 10 min (D) compared to control neurons (Control: N = 18 cells, OGD/R: N = 24 cells; FUR+OGD/R: N = 11 cells, all from N = 3 cultures). (E, F) Pretreatment with K252a or minocycline significantly decreases the occurrence of Racine IV‐V seizures at 40 mg/kg (E) and 50 mg/kg (F) cumulative PTZ dose. The distribution of seizure scores among mice is represented by the R2, R3, R4, and R5. (G‐H) Line charts reveal that K252a or minocycline reduced the percentage of MCAO‐R mice with Racine IV‐V seizures (G) and the average seizure score (H) at a cumulative PTZ dose of 40 and 50 mg/kg. (I) The cumulative PTZ dose required to induce epileptic behaviors with a Racine IV‐V is increased by blocking the BDNF/TrkB signaling pathway and suppressing microglial activation (Sham: N = 10, MCAO‐R: N = 13, MCAO‐ R + K252a: N = 11, MCAO‐R + Mino: N = 10). (J) Simplified schematic summarizing that MCAO‐R induces microglial activation (↑Iba1) and BDNF release, leading to TrkB activation, KCC2 downregulation, a depolarizing shift in E GABA and increased seizure risk, whereas minocycline and K252a act upstream at microglia and TrkB, respectively, to ameliorate this cascade. * p < 0.05 and ** p < 0.01 compared to the Sham group; # p < 0.05 and ## p < 0.01 compared to the MCAO‐R group.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: KCC2 Dysfunction Mediated by Microglial BDNF / TrkB Signaling Exacerbates Early Post‐Stroke Seizure Susceptibility

    doi: 10.1002/cns.70795

    Figure Lengend Snippet: Alleviating the severity of MCAO‐R‐induced seizures by blocking the BDNF/TrkB signaling and suppressing microglial activation. (A) Representative traces demonstrate the effective suppression of epileptiform burst firing induced by OGD/R in cultured hippocampal neurons by K252a. (B–D) Bar graphs present quantitative analysis, indicating that blocking the BDNF/TrkB signaling pathway with K252a significantly reduces the percentage of neurons exhibiting epileptiform bursting firing (B), the bursting frequency (C), and the total number of APs during 10 min (D) compared to control neurons (Control: N = 18 cells, OGD/R: N = 24 cells; FUR+OGD/R: N = 11 cells, all from N = 3 cultures). (E, F) Pretreatment with K252a or minocycline significantly decreases the occurrence of Racine IV‐V seizures at 40 mg/kg (E) and 50 mg/kg (F) cumulative PTZ dose. The distribution of seizure scores among mice is represented by the R2, R3, R4, and R5. (G‐H) Line charts reveal that K252a or minocycline reduced the percentage of MCAO‐R mice with Racine IV‐V seizures (G) and the average seizure score (H) at a cumulative PTZ dose of 40 and 50 mg/kg. (I) The cumulative PTZ dose required to induce epileptic behaviors with a Racine IV‐V is increased by blocking the BDNF/TrkB signaling pathway and suppressing microglial activation (Sham: N = 10, MCAO‐R: N = 13, MCAO‐ R + K252a: N = 11, MCAO‐R + Mino: N = 10). (J) Simplified schematic summarizing that MCAO‐R induces microglial activation (↑Iba1) and BDNF release, leading to TrkB activation, KCC2 downregulation, a depolarizing shift in E GABA and increased seizure risk, whereas minocycline and K252a act upstream at microglia and TrkB, respectively, to ameliorate this cascade. * p < 0.05 and ** p < 0.01 compared to the Sham group; # p < 0.05 and ## p < 0.01 compared to the MCAO‐R group.

    Article Snippet: FUR was purchased from Sigma‐Aldrich, and minocycline, K252a, and CLP290 were from MedChemExpress.

    Techniques: Blocking Assay, Activation Assay, Cell Culture, Control