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nkcc1 blocker bumetanide  (Tocris)


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    Tocris nkcc1 blocker bumetanide
    ( A ) Log 2 -normalised expression of Th, Drd1, Drd2, Drd3, Drd4, and Drd5 mRNA in olfactory bulb (OB) DA cells. ( B ) Example trace of an action potential fired by a putative anaxonic DA neuron (left) and its monophasic phase-plane plot profile (right). Note the prolonged repolarisation due to Cs-based internal solution. ( C ) Example traces of an auto-evoked inhibition (AEI) response recorded before (magenta) and after (grey) the application of gabazine. The subtraction is shown in the orange inset trace. ( D ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated by dopamine released from the patched DA cell. ( E ) Example traces of an AEI response before (purple) and after (green) applying D1-like and D2-like receptor blockers (SR 95531 hydrobromide and sulpiride, each at 10 µM). ( F ) AEI charge before (purple) and after (green) applying dopamine receptor antagonists; n=6 cells from N=4 mice; paired t-test, p=0.21, n.s.=non-significant. ( G ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated via gap junctions. ( H ) Example trace of an AEI response in the presence of the gap junction blocker carbenoxolone at 100 µM. ( I ) AEI charge in the presence of carbenoxolone at 100 µM. Each dot shows one cell; lines show mean ± SEM; n=9 cells from N=4 mice. ( J ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated by depolarising GABA released from the patched cell. ( K ) Example trace of an AEI response in the presence of the <t>NKCC1</t> blocker bumetanide at 20 µM. ( L ) AEI charge in the presence of bumetanide at 20 µM. All conventions as in F ; n=5 cells from N=3 mice.
    Nkcc1 Blocker Bumetanide, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 97 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Strikingly different neurotransmitter release strategies in dopaminergic subclasses"

    Article Title: Strikingly different neurotransmitter release strategies in dopaminergic subclasses

    Journal: eLife

    doi: 10.7554/eLife.105271

    ( A ) Log 2 -normalised expression of Th, Drd1, Drd2, Drd3, Drd4, and Drd5 mRNA in olfactory bulb (OB) DA cells. ( B ) Example trace of an action potential fired by a putative anaxonic DA neuron (left) and its monophasic phase-plane plot profile (right). Note the prolonged repolarisation due to Cs-based internal solution. ( C ) Example traces of an auto-evoked inhibition (AEI) response recorded before (magenta) and after (grey) the application of gabazine. The subtraction is shown in the orange inset trace. ( D ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated by dopamine released from the patched DA cell. ( E ) Example traces of an AEI response before (purple) and after (green) applying D1-like and D2-like receptor blockers (SR 95531 hydrobromide and sulpiride, each at 10 µM). ( F ) AEI charge before (purple) and after (green) applying dopamine receptor antagonists; n=6 cells from N=4 mice; paired t-test, p=0.21, n.s.=non-significant. ( G ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated via gap junctions. ( H ) Example trace of an AEI response in the presence of the gap junction blocker carbenoxolone at 100 µM. ( I ) AEI charge in the presence of carbenoxolone at 100 µM. Each dot shows one cell; lines show mean ± SEM; n=9 cells from N=4 mice. ( J ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated by depolarising GABA released from the patched cell. ( K ) Example trace of an AEI response in the presence of the NKCC1 blocker bumetanide at 20 µM. ( L ) AEI charge in the presence of bumetanide at 20 µM. All conventions as in F ; n=5 cells from N=3 mice.
    Figure Legend Snippet: ( A ) Log 2 -normalised expression of Th, Drd1, Drd2, Drd3, Drd4, and Drd5 mRNA in olfactory bulb (OB) DA cells. ( B ) Example trace of an action potential fired by a putative anaxonic DA neuron (left) and its monophasic phase-plane plot profile (right). Note the prolonged repolarisation due to Cs-based internal solution. ( C ) Example traces of an auto-evoked inhibition (AEI) response recorded before (magenta) and after (grey) the application of gabazine. The subtraction is shown in the orange inset trace. ( D ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated by dopamine released from the patched DA cell. ( E ) Example traces of an AEI response before (purple) and after (green) applying D1-like and D2-like receptor blockers (SR 95531 hydrobromide and sulpiride, each at 10 µM). ( F ) AEI charge before (purple) and after (green) applying dopamine receptor antagonists; n=6 cells from N=4 mice; paired t-test, p=0.21, n.s.=non-significant. ( G ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated via gap junctions. ( H ) Example trace of an AEI response in the presence of the gap junction blocker carbenoxolone at 100 µM. ( I ) AEI charge in the presence of carbenoxolone at 100 µM. Each dot shows one cell; lines show mean ± SEM; n=9 cells from N=4 mice. ( J ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated by depolarising GABA released from the patched cell. ( K ) Example trace of an AEI response in the presence of the NKCC1 blocker bumetanide at 20 µM. ( L ) AEI charge in the presence of bumetanide at 20 µM. All conventions as in F ; n=5 cells from N=3 mice.

    Techniques Used: Expressing, Inhibition



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    ( A ) Log 2 -normalised expression of Th, Drd1, Drd2, Drd3, Drd4, and Drd5 mRNA in olfactory bulb (OB) DA cells. ( B ) Example trace of an action potential fired by a putative anaxonic DA neuron (left) and its monophasic phase-plane plot profile (right). Note the prolonged repolarisation due to Cs-based internal solution. ( C ) Example traces of an auto-evoked inhibition (AEI) response recorded before (magenta) and after (grey) the application of gabazine. The subtraction is shown in the orange inset trace. ( D ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated by dopamine released from the patched DA cell. ( E ) Example traces of an AEI response before (purple) and after (green) applying D1-like and D2-like receptor blockers (SR 95531 hydrobromide and sulpiride, each at 10 µM). ( F ) AEI charge before (purple) and after (green) applying dopamine receptor antagonists; n=6 cells from N=4 mice; paired t-test, p=0.21, n.s.=non-significant. ( G ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated via gap junctions. ( H ) Example trace of an AEI response in the presence of the gap junction blocker carbenoxolone at 100 µM. ( I ) AEI charge in the presence of carbenoxolone at 100 µM. Each dot shows one cell; lines show mean ± SEM; n=9 cells from N=4 mice. ( J ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated by depolarising GABA released from the patched cell. ( K ) Example trace of an AEI response in the presence of the <t>NKCC1</t> blocker bumetanide at 20 µM. ( L ) AEI charge in the presence of bumetanide at 20 µM. All conventions as in F ; n=5 cells from N=3 mice.
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    Effects of KCC and NKCC inhibition on GABAA-mediated inhibition of median preoptic nucleus (MnPO) neurons. A: representative examples of responses to muscimol (100 µM) in MnPO neurons from chronic intermittent hypoxia (CIH)-treated rats injected with scrambled (Scr) and angiotensin type 1 (AT1a) KD incubated with KCC2 inhibitor VU 0240551 (10 µM). B: KCC2 blockade recovers muscimol (100 µM) inhibition in CIH/Scr/VU and blocks muscimol excitation in CIH/AT1a/VU (CIH/Scr/VU n = 7, CIH/AT1a/VU n = 9). C: representative examples of responses to muscimol (100 µM) in MnPO neurons from CIH-treated rats injected with Scr and AT1a KD incubated with <t>NKCC1</t> inhibitor bumetanide (10 µM). D: NKCC1 blockade recovers muscimol (100 µM) inhibition in CIH/Scr/Bumet and blocks muscimol excitation in CIH/AT1a/Bumet (CIH/Scr/Bumet n = 9, CIH/AT1a/Bumet n = 6). E: muscimol inhibition is attenuated in normoxic AT1a KD MnPO neurons [normoxic/scrambled (Norm/Scr) n = 10, Norm/AT1a n = 10]. F: GABAA activation produces blunted inhibition in CIH/Scr and excitation in CIH/AT1a MnPO neurons (CIH/Scr n = 13, CIH/AT1a n = 15). Each n represents the numbers of neurons. G: summary of area under the curve (AUC) data. **P < 0.01 vs. CIH/Scr. Analyses used Holm-Sidak post hoc test.
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    Image Search Results


    ( A ) Log 2 -normalised expression of Th, Drd1, Drd2, Drd3, Drd4, and Drd5 mRNA in olfactory bulb (OB) DA cells. ( B ) Example trace of an action potential fired by a putative anaxonic DA neuron (left) and its monophasic phase-plane plot profile (right). Note the prolonged repolarisation due to Cs-based internal solution. ( C ) Example traces of an auto-evoked inhibition (AEI) response recorded before (magenta) and after (grey) the application of gabazine. The subtraction is shown in the orange inset trace. ( D ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated by dopamine released from the patched DA cell. ( E ) Example traces of an AEI response before (purple) and after (green) applying D1-like and D2-like receptor blockers (SR 95531 hydrobromide and sulpiride, each at 10 µM). ( F ) AEI charge before (purple) and after (green) applying dopamine receptor antagonists; n=6 cells from N=4 mice; paired t-test, p=0.21, n.s.=non-significant. ( G ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated via gap junctions. ( H ) Example trace of an AEI response in the presence of the gap junction blocker carbenoxolone at 100 µM. ( I ) AEI charge in the presence of carbenoxolone at 100 µM. Each dot shows one cell; lines show mean ± SEM; n=9 cells from N=4 mice. ( J ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated by depolarising GABA released from the patched cell. ( K ) Example trace of an AEI response in the presence of the NKCC1 blocker bumetanide at 20 µM. ( L ) AEI charge in the presence of bumetanide at 20 µM. All conventions as in F ; n=5 cells from N=3 mice.

    Journal: eLife

    Article Title: Strikingly different neurotransmitter release strategies in dopaminergic subclasses

    doi: 10.7554/eLife.105271

    Figure Lengend Snippet: ( A ) Log 2 -normalised expression of Th, Drd1, Drd2, Drd3, Drd4, and Drd5 mRNA in olfactory bulb (OB) DA cells. ( B ) Example trace of an action potential fired by a putative anaxonic DA neuron (left) and its monophasic phase-plane plot profile (right). Note the prolonged repolarisation due to Cs-based internal solution. ( C ) Example traces of an auto-evoked inhibition (AEI) response recorded before (magenta) and after (grey) the application of gabazine. The subtraction is shown in the orange inset trace. ( D ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated by dopamine released from the patched DA cell. ( E ) Example traces of an AEI response before (purple) and after (green) applying D1-like and D2-like receptor blockers (SR 95531 hydrobromide and sulpiride, each at 10 µM). ( F ) AEI charge before (purple) and after (green) applying dopamine receptor antagonists; n=6 cells from N=4 mice; paired t-test, p=0.21, n.s.=non-significant. ( G ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated via gap junctions. ( H ) Example trace of an AEI response in the presence of the gap junction blocker carbenoxolone at 100 µM. ( I ) AEI charge in the presence of carbenoxolone at 100 µM. Each dot shows one cell; lines show mean ± SEM; n=9 cells from N=4 mice. ( J ) Schematic showing the potential involvement in the AEI response of neighbouring GABAergic neurons activated by depolarising GABA released from the patched cell. ( K ) Example trace of an AEI response in the presence of the NKCC1 blocker bumetanide at 20 µM. ( L ) AEI charge in the presence of bumetanide at 20 µM. All conventions as in F ; n=5 cells from N=3 mice.

    Article Snippet: The gap junction blocker carbenoxolone disodium at 100 μM (3096, Tocris) and the NKCC1 blocker bumetanide at 20 μM (3108, Tocris) were applied in the bath from the beginning and kept in the ACSF for at least 20–40 min. We adopted this strategy due to two key considerations: (1) carbenoxolone-induced instability in the membrane properties of the neurons during the initial minutes of application, and (2) sufficient time was required for chloride transporters to reach a steady intracellular chloride concentration ([Cl - ]) in response to bumetanide.

    Techniques: Expressing, Inhibition

    Effects of KCC and NKCC inhibition on GABAA-mediated inhibition of median preoptic nucleus (MnPO) neurons. A: representative examples of responses to muscimol (100 µM) in MnPO neurons from chronic intermittent hypoxia (CIH)-treated rats injected with scrambled (Scr) and angiotensin type 1 (AT1a) KD incubated with KCC2 inhibitor VU 0240551 (10 µM). B: KCC2 blockade recovers muscimol (100 µM) inhibition in CIH/Scr/VU and blocks muscimol excitation in CIH/AT1a/VU (CIH/Scr/VU n = 7, CIH/AT1a/VU n = 9). C: representative examples of responses to muscimol (100 µM) in MnPO neurons from CIH-treated rats injected with Scr and AT1a KD incubated with NKCC1 inhibitor bumetanide (10 µM). D: NKCC1 blockade recovers muscimol (100 µM) inhibition in CIH/Scr/Bumet and blocks muscimol excitation in CIH/AT1a/Bumet (CIH/Scr/Bumet n = 9, CIH/AT1a/Bumet n = 6). E: muscimol inhibition is attenuated in normoxic AT1a KD MnPO neurons [normoxic/scrambled (Norm/Scr) n = 10, Norm/AT1a n = 10]. F: GABAA activation produces blunted inhibition in CIH/Scr and excitation in CIH/AT1a MnPO neurons (CIH/Scr n = 13, CIH/AT1a n = 15). Each n represents the numbers of neurons. G: summary of area under the curve (AUC) data. **P < 0.01 vs. CIH/Scr. Analyses used Holm-Sidak post hoc test.

    Journal: American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

    Article Title: AT1a-dependent GABA A inhibition in the MnPO following chronic intermittent hypoxia

    doi: 10.1152/ajpregu.00030.2021

    Figure Lengend Snippet: Effects of KCC and NKCC inhibition on GABAA-mediated inhibition of median preoptic nucleus (MnPO) neurons. A: representative examples of responses to muscimol (100 µM) in MnPO neurons from chronic intermittent hypoxia (CIH)-treated rats injected with scrambled (Scr) and angiotensin type 1 (AT1a) KD incubated with KCC2 inhibitor VU 0240551 (10 µM). B: KCC2 blockade recovers muscimol (100 µM) inhibition in CIH/Scr/VU and blocks muscimol excitation in CIH/AT1a/VU (CIH/Scr/VU n = 7, CIH/AT1a/VU n = 9). C: representative examples of responses to muscimol (100 µM) in MnPO neurons from CIH-treated rats injected with Scr and AT1a KD incubated with NKCC1 inhibitor bumetanide (10 µM). D: NKCC1 blockade recovers muscimol (100 µM) inhibition in CIH/Scr/Bumet and blocks muscimol excitation in CIH/AT1a/Bumet (CIH/Scr/Bumet n = 9, CIH/AT1a/Bumet n = 6). E: muscimol inhibition is attenuated in normoxic AT1a KD MnPO neurons [normoxic/scrambled (Norm/Scr) n = 10, Norm/AT1a n = 10]. F: GABAA activation produces blunted inhibition in CIH/Scr and excitation in CIH/AT1a MnPO neurons (CIH/Scr n = 13, CIH/AT1a n = 15). Each n represents the numbers of neurons. G: summary of area under the curve (AUC) data. **P < 0.01 vs. CIH/Scr. Analyses used Holm-Sidak post hoc test.

    Article Snippet: In some cases, focal application of muscimol (100 μM) occurred in the presence of a bath-applied KCC2 blocker (VU0240551, Tocris, 10 μM) or a Na-K-2Cl cotransporter isoform 1 (NKCC1) blocker (bumetanide, Tocris, 10 μM).

    Techniques: Inhibition, Injection, Incubation, Activation Assay

    During normoxia, basal angiotensin II receptor type 1 (AT1R) activation mediates KCC2 function, which maintains a low intracellular concentration of Cl− and contributes to the inhibitory action of GABAA receptor activation. During chronic intermittent hypoxia (CIH), increases in AT1R activation results in a functional shift in the activity of NKCC1 and KCC2 that favors NKCC1. This functional change results in a depolarizing shift in the Cl− gradient that makes GABAA receptor activation less inhibitory, or in some cases, excitatory.

    Journal: American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

    Article Title: AT1a-dependent GABA A inhibition in the MnPO following chronic intermittent hypoxia

    doi: 10.1152/ajpregu.00030.2021

    Figure Lengend Snippet: During normoxia, basal angiotensin II receptor type 1 (AT1R) activation mediates KCC2 function, which maintains a low intracellular concentration of Cl− and contributes to the inhibitory action of GABAA receptor activation. During chronic intermittent hypoxia (CIH), increases in AT1R activation results in a functional shift in the activity of NKCC1 and KCC2 that favors NKCC1. This functional change results in a depolarizing shift in the Cl− gradient that makes GABAA receptor activation less inhibitory, or in some cases, excitatory.

    Article Snippet: In some cases, focal application of muscimol (100 μM) occurred in the presence of a bath-applied KCC2 blocker (VU0240551, Tocris, 10 μM) or a Na-K-2Cl cotransporter isoform 1 (NKCC1) blocker (bumetanide, Tocris, 10 μM).

    Techniques: Activation Assay, Concentration Assay, Functional Assay, Activity Assay