nkcc1 blocker bumetanide Search Results


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 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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 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