ap5  (Alomone Labs)


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    Alomone Labs ap5
    Activity-dependent translocation of αCaMKII to dendritic sites near synapses. (A) Hippocampal neuron (12 DIV) expressing mGFP-αCaMKII and mCherry imaged before, during, and after stimulation with 0Mg 2+ /Gly for 5 min. (B, i) Pseudocolor image from dendrite in A. Kymograph (ii–iii) and time-lapse (iv) analyses of the change in the fluorescent intensity ratio (mGFP-αCaMKII/mCherry) over time across the dendrite (i–ii, black line) and across the spine (iii, yellow box, red line). Stimulation period is indicated (Stim). (iv) n = 4 spines and subdendritic regions from the neuron shown in A. Red and white arrows (or brackets) point, respectively, to synaptic and dendritic sites where CaMKII translocated. Bars: (neuron) 10 µm; (dendrite) 5 µm. (C) Normalized ratio (±SEM) of dendritic segment where mGFP-αCaMKII accumulated over total dendritic length after a 5-min 0Mg 2+ /Gly stimulation (Vehicle), in the presence of 50 µM <t>AP5,</t> 1 μM TTX, 10 μM Cd 2+ , or 10 μM CPA. n = 7–24 neurons per condition. *, P
    Ap5, 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/ap5/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ap5 - by Bioz Stars, 2022-01
    93/100 stars

    Images

    1) Product Images from "Translocation of CaMKII to dendritic microtubules supports the plasticity of local synapses"

    Article Title: Translocation of CaMKII to dendritic microtubules supports the plasticity of local synapses

    Journal: The Journal of Cell Biology

    doi: 10.1083/jcb.201202058

    Activity-dependent translocation of αCaMKII to dendritic sites near synapses. (A) Hippocampal neuron (12 DIV) expressing mGFP-αCaMKII and mCherry imaged before, during, and after stimulation with 0Mg 2+ /Gly for 5 min. (B, i) Pseudocolor image from dendrite in A. Kymograph (ii–iii) and time-lapse (iv) analyses of the change in the fluorescent intensity ratio (mGFP-αCaMKII/mCherry) over time across the dendrite (i–ii, black line) and across the spine (iii, yellow box, red line). Stimulation period is indicated (Stim). (iv) n = 4 spines and subdendritic regions from the neuron shown in A. Red and white arrows (or brackets) point, respectively, to synaptic and dendritic sites where CaMKII translocated. Bars: (neuron) 10 µm; (dendrite) 5 µm. (C) Normalized ratio (±SEM) of dendritic segment where mGFP-αCaMKII accumulated over total dendritic length after a 5-min 0Mg 2+ /Gly stimulation (Vehicle), in the presence of 50 µM AP5, 1 μM TTX, 10 μM Cd 2+ , or 10 μM CPA. n = 7–24 neurons per condition. *, P
    Figure Legend Snippet: Activity-dependent translocation of αCaMKII to dendritic sites near synapses. (A) Hippocampal neuron (12 DIV) expressing mGFP-αCaMKII and mCherry imaged before, during, and after stimulation with 0Mg 2+ /Gly for 5 min. (B, i) Pseudocolor image from dendrite in A. Kymograph (ii–iii) and time-lapse (iv) analyses of the change in the fluorescent intensity ratio (mGFP-αCaMKII/mCherry) over time across the dendrite (i–ii, black line) and across the spine (iii, yellow box, red line). Stimulation period is indicated (Stim). (iv) n = 4 spines and subdendritic regions from the neuron shown in A. Red and white arrows (or brackets) point, respectively, to synaptic and dendritic sites where CaMKII translocated. Bars: (neuron) 10 µm; (dendrite) 5 µm. (C) Normalized ratio (±SEM) of dendritic segment where mGFP-αCaMKII accumulated over total dendritic length after a 5-min 0Mg 2+ /Gly stimulation (Vehicle), in the presence of 50 µM AP5, 1 μM TTX, 10 μM Cd 2+ , or 10 μM CPA. n = 7–24 neurons per condition. *, P

    Techniques Used: Activity Assay, Translocation Assay, Expressing

    2) Product Images from "HIV and opiates dysregulate K+-Cl− cotransporter 2 (KCC2) to cause GABAergic dysfunction in primary human neurons and Tat-transgenic mice"

    Article Title: HIV and opiates dysregulate K+-Cl− cotransporter 2 (KCC2) to cause GABAergic dysfunction in primary human neurons and Tat-transgenic mice

    Journal: Neurobiology of disease

    doi: 10.1016/j.nbd.2020.104878

    hNeurons lose KCC2 immunoreactivity after exposure to HIV-Tat ± morphine. ( A ) Representative images of hNeuron cultures immunolabeled for MAP2 and KCC2. Loss of KCC2 immunoreactivity can be noted in cells treated with both 50 nM Tat 1-86 and 50 nM Tat 1-86 + morphine. Rescue is seen in 50 nM Tat 1-86 + AP5 (scale bar = 50 μm). ( B, C ) The percentage of cells immunoreactive for KCC2. Both 6 h ( B ) and 24 h ( C ) exposure to 50 - 100 nM Tat 1-86 ± morphine results in significant decrease in KCC2 immunoreactivity compared to their respective controls ( † p
    Figure Legend Snippet: hNeurons lose KCC2 immunoreactivity after exposure to HIV-Tat ± morphine. ( A ) Representative images of hNeuron cultures immunolabeled for MAP2 and KCC2. Loss of KCC2 immunoreactivity can be noted in cells treated with both 50 nM Tat 1-86 and 50 nM Tat 1-86 + morphine. Rescue is seen in 50 nM Tat 1-86 + AP5 (scale bar = 50 μm). ( B, C ) The percentage of cells immunoreactive for KCC2. Both 6 h ( B ) and 24 h ( C ) exposure to 50 - 100 nM Tat 1-86 ± morphine results in significant decrease in KCC2 immunoreactivity compared to their respective controls ( † p

    Techniques Used: Immunolabeling

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    • tta a2  (Alomone Labs)
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    Alomone Labs tta a2
    Effect of T-type Ca 2+ channel blockers and genetic deletion of Ca v 3.2 on CPA-induced bladder pain-like nociceptive behavior ( A , D , G , J ), referred hyperalgesia ( B , E , H , K ) and bladder swelling ( C , F , I , L ) in mice. ( A – F ) In ddY mice, 6-prenylnaringenin (6-PNG), a hop-derived T-type Ca 2+ channel blocker, or KTt-45, a derivative of 6-PNG, at 10 and 30 mg/kg was administered i.p. 3 h 15 min after i.p. CPA at 400 mg/kg. ( G – I ) In C57BL/6 mice, <t>TTA-A2</t> at 1 mg/kg was administered i.p. 3 h after the CPA treatment. ( J – L ) CPA at 400 mg/kg was administered i.p. to wild-type (WT) and Ca v 3.2-knockout mice (KO) of a C57BL/6J background. Nociceptive behaviors were counted for 30 min starting 3.5 h after CPA treatment, followed immediately by evaluation of referred hyperalgesia/allodynia and then measurement of wet tissue weight of the excised bladder. V, vehicle. Data show the mean with S.E.M. for 6–8 (A–C), 5 (D–F), 5–6 (G–I) or 6 (J–L) mice. * p
    Tta A2, 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/tta a2/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tta a2 - by Bioz Stars, 2022-01
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    Effect of T-type Ca 2+ channel blockers and genetic deletion of Ca v 3.2 on CPA-induced bladder pain-like nociceptive behavior ( A , D , G , J ), referred hyperalgesia ( B , E , H , K ) and bladder swelling ( C , F , I , L ) in mice. ( A – F ) In ddY mice, 6-prenylnaringenin (6-PNG), a hop-derived T-type Ca 2+ channel blocker, or KTt-45, a derivative of 6-PNG, at 10 and 30 mg/kg was administered i.p. 3 h 15 min after i.p. CPA at 400 mg/kg. ( G – I ) In C57BL/6 mice, TTA-A2 at 1 mg/kg was administered i.p. 3 h after the CPA treatment. ( J – L ) CPA at 400 mg/kg was administered i.p. to wild-type (WT) and Ca v 3.2-knockout mice (KO) of a C57BL/6J background. Nociceptive behaviors were counted for 30 min starting 3.5 h after CPA treatment, followed immediately by evaluation of referred hyperalgesia/allodynia and then measurement of wet tissue weight of the excised bladder. V, vehicle. Data show the mean with S.E.M. for 6–8 (A–C), 5 (D–F), 5–6 (G–I) or 6 (J–L) mice. * p

    Journal: Cells

    Article Title: Cystitis-Related Bladder Pain Involves ATP-Dependent HMGB1 Release from Macrophages and Its Downstream H2S/Cav3.2 Signaling in Mice

    doi: 10.3390/cells9081748

    Figure Lengend Snippet: Effect of T-type Ca 2+ channel blockers and genetic deletion of Ca v 3.2 on CPA-induced bladder pain-like nociceptive behavior ( A , D , G , J ), referred hyperalgesia ( B , E , H , K ) and bladder swelling ( C , F , I , L ) in mice. ( A – F ) In ddY mice, 6-prenylnaringenin (6-PNG), a hop-derived T-type Ca 2+ channel blocker, or KTt-45, a derivative of 6-PNG, at 10 and 30 mg/kg was administered i.p. 3 h 15 min after i.p. CPA at 400 mg/kg. ( G – I ) In C57BL/6 mice, TTA-A2 at 1 mg/kg was administered i.p. 3 h after the CPA treatment. ( J – L ) CPA at 400 mg/kg was administered i.p. to wild-type (WT) and Ca v 3.2-knockout mice (KO) of a C57BL/6J background. Nociceptive behaviors were counted for 30 min starting 3.5 h after CPA treatment, followed immediately by evaluation of referred hyperalgesia/allodynia and then measurement of wet tissue weight of the excised bladder. V, vehicle. Data show the mean with S.E.M. for 6–8 (A–C), 5 (D–F), 5–6 (G–I) or 6 (J–L) mice. * p

    Article Snippet: TTA-A2 was obtained from Alomone Labs. (Jerusalem, Israel), and A438079, 5-BDBD and AZ 10606120 were from Tocris Bioscience (Bristol, UK). (2R/S)-6-Prenylnaringenin (6-PNG) and KTt-45 [6-(3-ethylpent-2-enyl)-5,7-dihydroxy-2-(2-hydroxyphenyl)chroman-4-one] were synthesized in-house, as reported previously [ ].

    Techniques: Mouse Assay, Derivative Assay, Knock-Out

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Journal: PLoS ONE

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    doi: 10.1371/journal.pone.0206986

    Figure Lengend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Article Snippet: While T-type calcium channel inhibitor NNC 55–0396 (1 μM) significantly inhibited SAK3-promoted hippocampal DA and 5-HT releases, the same dose of TTA-A2 (1 μM) failed to inhibit SAK3 effect completely.

    Techniques:

    SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Journal: PLoS ONE

    Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

    doi: 10.1371/journal.pone.0206986

    Figure Lengend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

    Article Snippet: T-type calcium channel inhibitor, NNC 55–0396 (1 μM: Sigma-Aldrich, St-Louis, MO) [ ], TTA-A2 (1 μM: Alomone Labs, Jerusalem, Israel), α7 nAChR antagonist MLA (1 nM: Sigma-Aldrich), and α4β2 nAChR antagonist DhβE (100 μM: Tocris, Bristol, UK) were dissolved in Ringer’s solution.

    Techniques: