ns19504  (Alomone Labs)


Bioz Verified Symbol Alomone Labs is a verified supplier
Bioz Manufacturer Symbol Alomone Labs manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 93

    Structured Review

    Alomone Labs ns19504
    BK channel activator <t>NS19504</t> promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p
    Ns19504, 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/ns19504/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ns19504 - by Bioz Stars, 2022-07
    93/100 stars

    Images

    1) Product Images from "BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke"

    Article Title: BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2021.683769

    BK channel activator NS19504 promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p
    Figure Legend Snippet: BK channel activator NS19504 promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p

    Techniques Used: Cell Culture

    Activation of BK channels ameliorated stroke outcomes. (A) Experiment design of the animal experiment. Three days before tMCAO, mice were subjected behavior training. After a 90-min tMCAO surgery, mice were divided randomly into four groups (sham, DMSO, NS19504, and Paxilline). At 1, 3, 7, and 14 days, behavior tests were performed, and protein and RNA samples were collected. (B) Weight changes of mice in three groups at 1, 2, 3, 7, and 14 days after tMCAO. (C) Modified Neurological Severity Score of three groups at 1, 3, 7, and 14 days after tMCAO. (D) Average score per second of three groups of hinging wire at 3 days after tMCAO. (E) Survivorship curve during 14 days of three groups after tMCAO. Data are mean + SE, n = 21–23 per group at 1 day, n = 17–23 per group at 3 days, n = 8–13 per group at 7 days, n = 3–9 per group at 14 days. *NS19504 vs. Paxilline group, ** p
    Figure Legend Snippet: Activation of BK channels ameliorated stroke outcomes. (A) Experiment design of the animal experiment. Three days before tMCAO, mice were subjected behavior training. After a 90-min tMCAO surgery, mice were divided randomly into four groups (sham, DMSO, NS19504, and Paxilline). At 1, 3, 7, and 14 days, behavior tests were performed, and protein and RNA samples were collected. (B) Weight changes of mice in three groups at 1, 2, 3, 7, and 14 days after tMCAO. (C) Modified Neurological Severity Score of three groups at 1, 3, 7, and 14 days after tMCAO. (D) Average score per second of three groups of hinging wire at 3 days after tMCAO. (E) Survivorship curve during 14 days of three groups after tMCAO. Data are mean + SE, n = 21–23 per group at 1 day, n = 17–23 per group at 3 days, n = 8–13 per group at 7 days, n = 3–9 per group at 14 days. *NS19504 vs. Paxilline group, ** p

    Techniques Used: Activation Assay, Mouse Assay, Modification

    Activation of BK channels promoted the phagocytic function of microglia after tMCAO and decreased neuronal apoptosis . (A) Representative photomicrograms of IBA1 + microglia (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (B) Bar graph shows quantitative analysis of the number of IBA1 + TUNEL + cells per field. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p
    Figure Legend Snippet: Activation of BK channels promoted the phagocytic function of microglia after tMCAO and decreased neuronal apoptosis . (A) Representative photomicrograms of IBA1 + microglia (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (B) Bar graph shows quantitative analysis of the number of IBA1 + TUNEL + cells per field. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p

    Techniques Used: Activation Assay, TUNEL Assay, Slice Preparation

    Inflammatory factors and phosphorylated-ERK expressions under different treatments at 3 days after tMCAO . (A) Bar graph represents the relative mRNA levels of inflammatory factors including TNF-α, TGF-β, IL-10, IL-6, IL-1β, and IL-1α. Data are mean + SE, n = 3 per group. (B) Representative image of Western blot of phosphorylated-ERK1/2 (p-ERK), total-ERK1/2 (t-ERK), and β-actin at 3 days after tMCAO. (C) Bar graph showing the relative protein levels of p -ERK vs. t-ERK at 3 day after tMCAO. Data are mean + SE, n = 9 per group. *NS19504 vs. Paxilline group, * p
    Figure Legend Snippet: Inflammatory factors and phosphorylated-ERK expressions under different treatments at 3 days after tMCAO . (A) Bar graph represents the relative mRNA levels of inflammatory factors including TNF-α, TGF-β, IL-10, IL-6, IL-1β, and IL-1α. Data are mean + SE, n = 3 per group. (B) Representative image of Western blot of phosphorylated-ERK1/2 (p-ERK), total-ERK1/2 (t-ERK), and β-actin at 3 days after tMCAO. (C) Bar graph showing the relative protein levels of p -ERK vs. t-ERK at 3 day after tMCAO. Data are mean + SE, n = 9 per group. *NS19504 vs. Paxilline group, * p

    Techniques Used: Western Blot

    2) Product Images from "BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke"

    Article Title: BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2021.683769

    BK channel activator NS19504 promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p
    Figure Legend Snippet: BK channel activator NS19504 promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p

    Techniques Used: Cell Culture

    Activation of BK channels ameliorated stroke outcomes. (A) Experiment design of the animal experiment. Three days before tMCAO, mice were subjected behavior training. After a 90-min tMCAO surgery, mice were divided randomly into four groups (sham, DMSO, NS19504, and Paxilline). At 1, 3, 7, and 14 days, behavior tests were performed, and protein and RNA samples were collected. (B) Weight changes of mice in three groups at 1, 2, 3, 7, and 14 days after tMCAO. (C) Modified Neurological Severity Score of three groups at 1, 3, 7, and 14 days after tMCAO. (D) Average score per second of three groups of hinging wire at 3 days after tMCAO. (E) Survivorship curve during 14 days of three groups after tMCAO. Data are mean + SE, n = 21–23 per group at 1 day, n = 17–23 per group at 3 days, n = 8–13 per group at 7 days, n = 3–9 per group at 14 days. *NS19504 vs. Paxilline group, ** p
    Figure Legend Snippet: Activation of BK channels ameliorated stroke outcomes. (A) Experiment design of the animal experiment. Three days before tMCAO, mice were subjected behavior training. After a 90-min tMCAO surgery, mice were divided randomly into four groups (sham, DMSO, NS19504, and Paxilline). At 1, 3, 7, and 14 days, behavior tests were performed, and protein and RNA samples were collected. (B) Weight changes of mice in three groups at 1, 2, 3, 7, and 14 days after tMCAO. (C) Modified Neurological Severity Score of three groups at 1, 3, 7, and 14 days after tMCAO. (D) Average score per second of three groups of hinging wire at 3 days after tMCAO. (E) Survivorship curve during 14 days of three groups after tMCAO. Data are mean + SE, n = 21–23 per group at 1 day, n = 17–23 per group at 3 days, n = 8–13 per group at 7 days, n = 3–9 per group at 14 days. *NS19504 vs. Paxilline group, ** p

    Techniques Used: Activation Assay, Mouse Assay, Modification

    Activation of BK channels promoted the phagocytic function of microglia after tMCAO and decreased neuronal apoptosis . (A) Representative photomicrograms of IBA1 + microglia (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (B) Bar graph shows quantitative analysis of the number of IBA1 + TUNEL + cells per field. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p
    Figure Legend Snippet: Activation of BK channels promoted the phagocytic function of microglia after tMCAO and decreased neuronal apoptosis . (A) Representative photomicrograms of IBA1 + microglia (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (B) Bar graph shows quantitative analysis of the number of IBA1 + TUNEL + cells per field. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p

    Techniques Used: Activation Assay, TUNEL Assay, Slice Preparation

    Inflammatory factors and phosphorylated-ERK expressions under different treatments at 3 days after tMCAO . (A) Bar graph represents the relative mRNA levels of inflammatory factors including TNF-α, TGF-β, IL-10, IL-6, IL-1β, and IL-1α. Data are mean + SE, n = 3 per group. (B) Representative image of Western blot of phosphorylated-ERK1/2 (p-ERK), total-ERK1/2 (t-ERK), and β-actin at 3 days after tMCAO. (C) Bar graph showing the relative protein levels of p -ERK vs. t-ERK at 3 day after tMCAO. Data are mean + SE, n = 9 per group. *NS19504 vs. Paxilline group, * p
    Figure Legend Snippet: Inflammatory factors and phosphorylated-ERK expressions under different treatments at 3 days after tMCAO . (A) Bar graph represents the relative mRNA levels of inflammatory factors including TNF-α, TGF-β, IL-10, IL-6, IL-1β, and IL-1α. Data are mean + SE, n = 3 per group. (B) Representative image of Western blot of phosphorylated-ERK1/2 (p-ERK), total-ERK1/2 (t-ERK), and β-actin at 3 days after tMCAO. (C) Bar graph showing the relative protein levels of p -ERK vs. t-ERK at 3 day after tMCAO. Data are mean + SE, n = 9 per group. *NS19504 vs. Paxilline group, * p

    Techniques Used: Western Blot

    3) Product Images from "BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke"

    Article Title: BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2021.683769

    BK channel activator NS19504 promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p
    Figure Legend Snippet: BK channel activator NS19504 promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p

    Techniques Used: Cell Culture

    Activation of BK channels ameliorated stroke outcomes. (A) Experiment design of the animal experiment. Three days before tMCAO, mice were subjected behavior training. After a 90-min tMCAO surgery, mice were divided randomly into four groups (sham, DMSO, NS19504, and Paxilline). At 1, 3, 7, and 14 days, behavior tests were performed, and protein and RNA samples were collected. (B) Weight changes of mice in three groups at 1, 2, 3, 7, and 14 days after tMCAO. (C) Modified Neurological Severity Score of three groups at 1, 3, 7, and 14 days after tMCAO. (D) Average score per second of three groups of hinging wire at 3 days after tMCAO. (E) Survivorship curve during 14 days of three groups after tMCAO. Data are mean + SE, n = 21–23 per group at 1 day, n = 17–23 per group at 3 days, n = 8–13 per group at 7 days, n = 3–9 per group at 14 days. *NS19504 vs. Paxilline group, ** p
    Figure Legend Snippet: Activation of BK channels ameliorated stroke outcomes. (A) Experiment design of the animal experiment. Three days before tMCAO, mice were subjected behavior training. After a 90-min tMCAO surgery, mice were divided randomly into four groups (sham, DMSO, NS19504, and Paxilline). At 1, 3, 7, and 14 days, behavior tests were performed, and protein and RNA samples were collected. (B) Weight changes of mice in three groups at 1, 2, 3, 7, and 14 days after tMCAO. (C) Modified Neurological Severity Score of three groups at 1, 3, 7, and 14 days after tMCAO. (D) Average score per second of three groups of hinging wire at 3 days after tMCAO. (E) Survivorship curve during 14 days of three groups after tMCAO. Data are mean + SE, n = 21–23 per group at 1 day, n = 17–23 per group at 3 days, n = 8–13 per group at 7 days, n = 3–9 per group at 14 days. *NS19504 vs. Paxilline group, ** p

    Techniques Used: Activation Assay, Mouse Assay, Modification

    Activation of BK channels promoted the phagocytic function of microglia after tMCAO and decreased neuronal apoptosis . (A) Representative photomicrograms of IBA1 + microglia (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (B) Bar graph shows quantitative analysis of the number of IBA1 + TUNEL + cells per field. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p
    Figure Legend Snippet: Activation of BK channels promoted the phagocytic function of microglia after tMCAO and decreased neuronal apoptosis . (A) Representative photomicrograms of IBA1 + microglia (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (B) Bar graph shows quantitative analysis of the number of IBA1 + TUNEL + cells per field. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p

    Techniques Used: Activation Assay, TUNEL Assay, Slice Preparation

    Inflammatory factors and phosphorylated-ERK expressions under different treatments at 3 days after tMCAO . (A) Bar graph represents the relative mRNA levels of inflammatory factors including TNF-α, TGF-β, IL-10, IL-6, IL-1β, and IL-1α. Data are mean + SE, n = 3 per group. (B) Representative image of Western blot of phosphorylated-ERK1/2 (p-ERK), total-ERK1/2 (t-ERK), and β-actin at 3 days after tMCAO. (C) Bar graph showing the relative protein levels of p -ERK vs. t-ERK at 3 day after tMCAO. Data are mean + SE, n = 9 per group. *NS19504 vs. Paxilline group, * p
    Figure Legend Snippet: Inflammatory factors and phosphorylated-ERK expressions under different treatments at 3 days after tMCAO . (A) Bar graph represents the relative mRNA levels of inflammatory factors including TNF-α, TGF-β, IL-10, IL-6, IL-1β, and IL-1α. Data are mean + SE, n = 3 per group. (B) Representative image of Western blot of phosphorylated-ERK1/2 (p-ERK), total-ERK1/2 (t-ERK), and β-actin at 3 days after tMCAO. (C) Bar graph showing the relative protein levels of p -ERK vs. t-ERK at 3 day after tMCAO. Data are mean + SE, n = 9 per group. *NS19504 vs. Paxilline group, * p

    Techniques Used: Western Blot

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 93
    Alomone Labs ns19504
    BK channel activator <t>NS19504</t> promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p
    Ns19504, 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/ns19504/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ns19504 - by Bioz Stars, 2022-07
    93/100 stars
      Buy from Supplier

    91
    Alomone Labs phenytoin
    <t>Phenytoin</t> reduces I NaP in PVBCs. (A) A representative reconstruction of an anatomically and neurochemically identified PVBC. The cell was filled with biocytin during whole-cell patch-clamp recordings and was imaged using a Zeiss confocal microscope. Axon arbors were restricted to the pyramidal cell layer of the CA1 region, whereas the dendrites covered most CA1 layers. The recorded PV+ cell showed tdTomato (TOM, thus PV+, right column). Ori., stratum oriens; Pyr., stratum pyramidale; Rad., stratum radiatum. (B) Under control conditions in the presence of synaptic blockers, a neurochemically identified PVBC manifested current responses to voltage ramps (−80 mV to −20 mV, 50 mVs −1 ) before (black trace) and during (red trace) bath application of TTX (1 μM). The subtracted current was referred to as I NaP (green trace). (C, D) In slices pretreated with phenytoin, similar voltage ramps produced negligible I NaP (C) or reduced I NaP (D) in neurochemically identified PVBCs. (E) Summary data of I NaP peak current values. Numbers in bar graph indicate number of PVBCs. (F, G) The TTX-subtracted current responses ( I NaP ) shown in B and C were converted to conductance in F and G, respectively. Note that there was negligible conductance in the PVBC, which was recorded from a hippocampal slice pretreated with phenytoin. * p
    Phenytoin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phenytoin/product/Alomone Labs
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    phenytoin - by Bioz Stars, 2022-07
    91/100 stars
      Buy from Supplier

    Image Search Results


    BK channel activator NS19504 promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke

    doi: 10.3389/fncel.2021.683769

    Figure Lengend Snippet: BK channel activator NS19504 promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p

    Article Snippet: The injection concentrations of Paxilline and NS19504 were 500 μM and 5 mM, respectively, having the same concentration of DMSO [10% ( )].

    Techniques: Cell Culture

    Activation of BK channels ameliorated stroke outcomes. (A) Experiment design of the animal experiment. Three days before tMCAO, mice were subjected behavior training. After a 90-min tMCAO surgery, mice were divided randomly into four groups (sham, DMSO, NS19504, and Paxilline). At 1, 3, 7, and 14 days, behavior tests were performed, and protein and RNA samples were collected. (B) Weight changes of mice in three groups at 1, 2, 3, 7, and 14 days after tMCAO. (C) Modified Neurological Severity Score of three groups at 1, 3, 7, and 14 days after tMCAO. (D) Average score per second of three groups of hinging wire at 3 days after tMCAO. (E) Survivorship curve during 14 days of three groups after tMCAO. Data are mean + SE, n = 21–23 per group at 1 day, n = 17–23 per group at 3 days, n = 8–13 per group at 7 days, n = 3–9 per group at 14 days. *NS19504 vs. Paxilline group, ** p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke

    doi: 10.3389/fncel.2021.683769

    Figure Lengend Snippet: Activation of BK channels ameliorated stroke outcomes. (A) Experiment design of the animal experiment. Three days before tMCAO, mice were subjected behavior training. After a 90-min tMCAO surgery, mice were divided randomly into four groups (sham, DMSO, NS19504, and Paxilline). At 1, 3, 7, and 14 days, behavior tests were performed, and protein and RNA samples were collected. (B) Weight changes of mice in three groups at 1, 2, 3, 7, and 14 days after tMCAO. (C) Modified Neurological Severity Score of three groups at 1, 3, 7, and 14 days after tMCAO. (D) Average score per second of three groups of hinging wire at 3 days after tMCAO. (E) Survivorship curve during 14 days of three groups after tMCAO. Data are mean + SE, n = 21–23 per group at 1 day, n = 17–23 per group at 3 days, n = 8–13 per group at 7 days, n = 3–9 per group at 14 days. *NS19504 vs. Paxilline group, ** p

    Article Snippet: The injection concentrations of Paxilline and NS19504 were 500 μM and 5 mM, respectively, having the same concentration of DMSO [10% ( )].

    Techniques: Activation Assay, Mouse Assay, Modification

    Activation of BK channels promoted the phagocytic function of microglia after tMCAO and decreased neuronal apoptosis . (A) Representative photomicrograms of IBA1 + microglia (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (B) Bar graph shows quantitative analysis of the number of IBA1 + TUNEL + cells per field. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke

    doi: 10.3389/fncel.2021.683769

    Figure Lengend Snippet: Activation of BK channels promoted the phagocytic function of microglia after tMCAO and decreased neuronal apoptosis . (A) Representative photomicrograms of IBA1 + microglia (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (B) Bar graph shows quantitative analysis of the number of IBA1 + TUNEL + cells per field. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p

    Article Snippet: The injection concentrations of Paxilline and NS19504 were 500 μM and 5 mM, respectively, having the same concentration of DMSO [10% ( )].

    Techniques: Activation Assay, TUNEL Assay, Slice Preparation

    Inflammatory factors and phosphorylated-ERK expressions under different treatments at 3 days after tMCAO . (A) Bar graph represents the relative mRNA levels of inflammatory factors including TNF-α, TGF-β, IL-10, IL-6, IL-1β, and IL-1α. Data are mean + SE, n = 3 per group. (B) Representative image of Western blot of phosphorylated-ERK1/2 (p-ERK), total-ERK1/2 (t-ERK), and β-actin at 3 days after tMCAO. (C) Bar graph showing the relative protein levels of p -ERK vs. t-ERK at 3 day after tMCAO. Data are mean + SE, n = 9 per group. *NS19504 vs. Paxilline group, * p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke

    doi: 10.3389/fncel.2021.683769

    Figure Lengend Snippet: Inflammatory factors and phosphorylated-ERK expressions under different treatments at 3 days after tMCAO . (A) Bar graph represents the relative mRNA levels of inflammatory factors including TNF-α, TGF-β, IL-10, IL-6, IL-1β, and IL-1α. Data are mean + SE, n = 3 per group. (B) Representative image of Western blot of phosphorylated-ERK1/2 (p-ERK), total-ERK1/2 (t-ERK), and β-actin at 3 days after tMCAO. (C) Bar graph showing the relative protein levels of p -ERK vs. t-ERK at 3 day after tMCAO. Data are mean + SE, n = 9 per group. *NS19504 vs. Paxilline group, * p

    Article Snippet: The injection concentrations of Paxilline and NS19504 were 500 μM and 5 mM, respectively, having the same concentration of DMSO [10% ( )].

    Techniques: Western Blot

    Phenytoin reduces I NaP in PVBCs. (A) A representative reconstruction of an anatomically and neurochemically identified PVBC. The cell was filled with biocytin during whole-cell patch-clamp recordings and was imaged using a Zeiss confocal microscope. Axon arbors were restricted to the pyramidal cell layer of the CA1 region, whereas the dendrites covered most CA1 layers. The recorded PV+ cell showed tdTomato (TOM, thus PV+, right column). Ori., stratum oriens; Pyr., stratum pyramidale; Rad., stratum radiatum. (B) Under control conditions in the presence of synaptic blockers, a neurochemically identified PVBC manifested current responses to voltage ramps (−80 mV to −20 mV, 50 mVs −1 ) before (black trace) and during (red trace) bath application of TTX (1 μM). The subtracted current was referred to as I NaP (green trace). (C, D) In slices pretreated with phenytoin, similar voltage ramps produced negligible I NaP (C) or reduced I NaP (D) in neurochemically identified PVBCs. (E) Summary data of I NaP peak current values. Numbers in bar graph indicate number of PVBCs. (F, G) The TTX-subtracted current responses ( I NaP ) shown in B and C were converted to conductance in F and G, respectively. Note that there was negligible conductance in the PVBC, which was recorded from a hippocampal slice pretreated with phenytoin. * p

    Journal: Neuropharmacology

    Article Title: The critical role of persistent sodium current in hippocampal gamma oscillations

    doi: 10.1016/j.neuropharm.2019.107787

    Figure Lengend Snippet: Phenytoin reduces I NaP in PVBCs. (A) A representative reconstruction of an anatomically and neurochemically identified PVBC. The cell was filled with biocytin during whole-cell patch-clamp recordings and was imaged using a Zeiss confocal microscope. Axon arbors were restricted to the pyramidal cell layer of the CA1 region, whereas the dendrites covered most CA1 layers. The recorded PV+ cell showed tdTomato (TOM, thus PV+, right column). Ori., stratum oriens; Pyr., stratum pyramidale; Rad., stratum radiatum. (B) Under control conditions in the presence of synaptic blockers, a neurochemically identified PVBC manifested current responses to voltage ramps (−80 mV to −20 mV, 50 mVs −1 ) before (black trace) and during (red trace) bath application of TTX (1 μM). The subtracted current was referred to as I NaP (green trace). (C, D) In slices pretreated with phenytoin, similar voltage ramps produced negligible I NaP (C) or reduced I NaP (D) in neurochemically identified PVBCs. (E) Summary data of I NaP peak current values. Numbers in bar graph indicate number of PVBCs. (F, G) The TTX-subtracted current responses ( I NaP ) shown in B and C were converted to conductance in F and G, respectively. Note that there was negligible conductance in the PVBC, which was recorded from a hippocampal slice pretreated with phenytoin. * p

    Article Snippet: APV, NBQX, and phenytoin were obtained from Alomone Labs (Jerusalem, Israel)., SR95531, and tetrodotoxin were purchased from Tocris Bioscience (Ellisville, MO, USA).

    Techniques: Patch Clamp, Microscopy, Produced

    Phenytoin reduces I NaP in CA1 pyramidal cells. (A) section for the details). Dendrites of the recorded pyramidal cell covered most CA1 layers. The soma was located in the pyramidal cell layer. Ori., stratum oriens; Pyr., stratum pyramidale; Rad., stratum radiatum; L.M., stratum lacunosum-moleculare. (B) Under control conditions in the presence of synaptic blockers, voltage ramps (−80 mV to −20 mV, 50 mVs −1 ) were used to evoke I NaP in a pyramidal cell. (C) In a hippocampal slice pretreated with phenytoin, similar voltage ramps produced a decrease in I NaP of a pyramidal cell. (D) Summary data of I NaP peak current values. Numbers in the bars indicate number for pyramidal cells. (E, F) The TTX-subtracted current responses ( I NaP ) shown in B and C were converted to conductance in E and F, respectively. Note that there was lower amplitude conductance in the pyramidal cell, which was recorded from a hippocampal slice pretreated with phenytoin, compared to that in the pyramidal cell, which was recorded from a hippocampal slice pretreated with DMSO control ACSF. * p

    Journal: Neuropharmacology

    Article Title: The critical role of persistent sodium current in hippocampal gamma oscillations

    doi: 10.1016/j.neuropharm.2019.107787

    Figure Lengend Snippet: Phenytoin reduces I NaP in CA1 pyramidal cells. (A) section for the details). Dendrites of the recorded pyramidal cell covered most CA1 layers. The soma was located in the pyramidal cell layer. Ori., stratum oriens; Pyr., stratum pyramidale; Rad., stratum radiatum; L.M., stratum lacunosum-moleculare. (B) Under control conditions in the presence of synaptic blockers, voltage ramps (−80 mV to −20 mV, 50 mVs −1 ) were used to evoke I NaP in a pyramidal cell. (C) In a hippocampal slice pretreated with phenytoin, similar voltage ramps produced a decrease in I NaP of a pyramidal cell. (D) Summary data of I NaP peak current values. Numbers in the bars indicate number for pyramidal cells. (E, F) The TTX-subtracted current responses ( I NaP ) shown in B and C were converted to conductance in E and F, respectively. Note that there was lower amplitude conductance in the pyramidal cell, which was recorded from a hippocampal slice pretreated with phenytoin, compared to that in the pyramidal cell, which was recorded from a hippocampal slice pretreated with DMSO control ACSF. * p

    Article Snippet: APV, NBQX, and phenytoin were obtained from Alomone Labs (Jerusalem, Israel)., SR95531, and tetrodotoxin were purchased from Tocris Bioscience (Ellisville, MO, USA).

    Techniques: Produced

    Phenytoin reduces excitability of CA1 pyramidal cells. (A) Examples of APs from pyramidal cells (1 s-long pulses, +150 pA, 200 pA, or +500 pA from −65 mV). The voltage traces displayed in the left column were from a pyramidal cell in a hippocampal slice pretreated with DMSO control ACSF, whereas the voltage traces shown in the right column were from a pyramidal cell in a hippocampal slice pretreated with phenytoin. (B) Summary of the firing frequency of the recorded pyramidal cells. (C) Summary of the rheobase of the recorded pyramidal cells. Numbers in the bars represents number for pyramidal cells. * p

    Journal: Neuropharmacology

    Article Title: The critical role of persistent sodium current in hippocampal gamma oscillations

    doi: 10.1016/j.neuropharm.2019.107787

    Figure Lengend Snippet: Phenytoin reduces excitability of CA1 pyramidal cells. (A) Examples of APs from pyramidal cells (1 s-long pulses, +150 pA, 200 pA, or +500 pA from −65 mV). The voltage traces displayed in the left column were from a pyramidal cell in a hippocampal slice pretreated with DMSO control ACSF, whereas the voltage traces shown in the right column were from a pyramidal cell in a hippocampal slice pretreated with phenytoin. (B) Summary of the firing frequency of the recorded pyramidal cells. (C) Summary of the rheobase of the recorded pyramidal cells. Numbers in the bars represents number for pyramidal cells. * p

    Article Snippet: APV, NBQX, and phenytoin were obtained from Alomone Labs (Jerusalem, Israel)., SR95531, and tetrodotoxin were purchased from Tocris Bioscience (Ellisville, MO, USA).

    Techniques:

    Antioscillatory effects of phenytoin on hippocampal gamma oscillations. (A, B, C, D) CA1 gamma oscillations evoked by light ramps before and during bath application of phenytoin (A, 40 μM; C, 100 μM). Light ramps were delivered to the CA1 region every 2 min for 40 min of LFP recording sessions. The power spectra in B and D were constructed from the 1.4 s-long LFP traces shown in A and C, respectively. (E) Normalized gamma power before and during bath application of phenytoin (10 min control period followed by 30 min drug period). Note that gamma oscillations were stable in DMSO control ACSF over 40 min, but oscillations were reduced by therapeutic concentrations of phenytoin ( i.e. , 40 μM and 100 μM). (F) Gamma power during drug application (30-40 min shown in E) and DMSO control period (30-40 min) normalized to gamma power prior to drug exposure (0-10 min). Numbers in the bars indicate numbers of hippocampal slices used for phenytoin or DMSO control experiments. (G) Normalized peak frequencies of gamma oscillations. Note that the peak frequencies were stable in DMSO control ACSF over 40 min, but they were reduced by phenytoin along with a decrease in gamma power. (H) Peak frequencies during drug application (30-40 min shown in G) and DMSO control period (30-40 min) normalized to peak frequencies prior to drug exposure (0-10 min). n.s., not significant; * p

    Journal: Neuropharmacology

    Article Title: The critical role of persistent sodium current in hippocampal gamma oscillations

    doi: 10.1016/j.neuropharm.2019.107787

    Figure Lengend Snippet: Antioscillatory effects of phenytoin on hippocampal gamma oscillations. (A, B, C, D) CA1 gamma oscillations evoked by light ramps before and during bath application of phenytoin (A, 40 μM; C, 100 μM). Light ramps were delivered to the CA1 region every 2 min for 40 min of LFP recording sessions. The power spectra in B and D were constructed from the 1.4 s-long LFP traces shown in A and C, respectively. (E) Normalized gamma power before and during bath application of phenytoin (10 min control period followed by 30 min drug period). Note that gamma oscillations were stable in DMSO control ACSF over 40 min, but oscillations were reduced by therapeutic concentrations of phenytoin ( i.e. , 40 μM and 100 μM). (F) Gamma power during drug application (30-40 min shown in E) and DMSO control period (30-40 min) normalized to gamma power prior to drug exposure (0-10 min). Numbers in the bars indicate numbers of hippocampal slices used for phenytoin or DMSO control experiments. (G) Normalized peak frequencies of gamma oscillations. Note that the peak frequencies were stable in DMSO control ACSF over 40 min, but they were reduced by phenytoin along with a decrease in gamma power. (H) Peak frequencies during drug application (30-40 min shown in G) and DMSO control period (30-40 min) normalized to peak frequencies prior to drug exposure (0-10 min). n.s., not significant; * p

    Article Snippet: APV, NBQX, and phenytoin were obtained from Alomone Labs (Jerusalem, Israel)., SR95531, and tetrodotoxin were purchased from Tocris Bioscience (Ellisville, MO, USA).

    Techniques: Construct