Drugs used included GABA, hexamethonium bromide (both from Sigma Aldrich, Castle Hill, New South Wales, Australia), Bicuculline, [S-(R*,R*)]-[3-[[1-(3,4-Dichlorophenyl)ethyl]amino]-2-hydroxypropyl](cyclohexylmethyl) phosphinic acid (CGP 54626) and (1,2,5,6-Tetrahydropyridin-4-yl)methylphosphinic acid (TPMPA) (all from Tocris Bioscience, Avonmouth Bristol UK). All drugs were diluted in distilled water to make stock solutions and then again in physiological saline to their working concentration on the day of experimentation.
1 2 5 6 tetrahydropyridin 4 yl methylphosphinic acid tpmpa
Manufactured by Bio-Techne
Sourced in United Kingdom
(1,2,5,6-Tetrahydropyridin-4-yl)methylphosphinic acid (TPMPA) is a chemical compound used in research applications. It functions as a GABAA receptor antagonist. This compound is utilized in laboratory studies to investigate the role of GABAA receptors in various biological processes.
Automatically generated - may contain errors
Lab products found in correlation
Gabazine, by Bio-Techne (2 mentions)
L 2 amino 4 phosphonobutyric acid l ap4, by Bio-Techne (2 mentions)
0.5 strychnine, by Merck Group (2 mentions)
Hexamethonium bromide, by Merck Group (1 mentions)
Bicuculline, by Bio-Techne (1 mentions)
S r r 3 1 3 4 dichlorophenyl ethyl amino 2 hydroxypropyl cyclohexylmethyl phosphinic acid cgp 54626, by Bio-Techne (1 mentions)
Picrotoxin, by Bio-Techne (1 mentions)
Dl ap5, by Bio-Techne (1 mentions)
Dl ap4, by Bio-Techne (1 mentions)
6 7 dinitroquinoxaline 2 3 dione dnqx, by Bio-Techne (1 mentions)
4 protocols using 1 2 5 6 tetrahydropyridin 4 yl methylphosphinic acid tpmpa
1
Pharmacological Modulation of Neuronal Pathways
2
Synaptic Blockade in Retina Explant
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Blocking of various synapses was achieved by bath applying various pharmacological substances dissolved in aCSF, which superfused the explanted retina as described. Gap junctions were blocked with 50 µM MFA (Sigma Aldrich) that was applied for 30 min before the data were recorded. Glutamatergic signaling was blocked using a combination of three compounds: 100 µM 6,7-dinitroquinoxaline-2,3-dione (DNQX; Tocris Bioscience, Bristol, UK) was used to block the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamatergic synapses, 100 µM DL-AP5 (Tocris Bioscience) was used to block the N-methyl-D-aspartate (NMDA) glutamatergic synapses, and 150 µM DL-AP4 (Tocris Bioscience) was used to block the metabotropic (mGluR6) synapses. As an mGluR6 agonist, DL-AP4 did not allow the investigation of synapses downstream of the transfected ON bipolar cells. Gamma-aminobutyric acid (GABA)a and GABAc receptors were antagonized with 20 µM picrotoxin and 50 µM 1,2,5,6-tetrahydropyridin-4-yl)methylphosphinic acid (TPMPA), respectively (Tocris Bioscience).
3
Pharmacological Modulation of Cholinergic Circuits
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All drugs were bath applied for at least ten minutes before recordings. The following drug concentrations were used (in μM): 10 Gabazine (Tocris Bioscience, Bristol, UK)50 (link), 75 TPMPA (1,2,5,6-Tetrahydropyridin-4-yl)methylphosphinic acid, Tocris Bioscience)50 (link), 50 L-AP4 (L-(+)-2-Amino-4-phosphonobutyric acid, Tocris Bioscience) and 0.5 strychnine (Sigma-Aldrich)51 (link). Drug solutions were carboxygenated and warmed to ~37°C before application. Pharmacological experiments were exclusively performed in the On and Off ChAT-immunoreactive bands, which are labelled in red fluorescence in ChAT:Cre c Ai9tdTomato crossbred animals.
4
Pharmacological Modulation of Cholinergic Circuits
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