Reduced facilitation and vesicular uptake in crustacean and mammalian neuromuscular junction by T-588, a neuroprotective compound
Bath application of compound T-588, a neuroprotective agent, reduced paired-pulse and repetitive-pulse facilitation at mammalian and crustacean neuromuscular junctions. In addition, it reduced voltage-gated sodium and potassium currents in a use-dependent fashion, but had only a small effect on the...
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Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_00278424_v96_n25_p14588_Hirata |
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paperaa:paper_00278424_v96_n25_p14588_Hirata2023-06-12T16:45:22Z Reduced facilitation and vesicular uptake in crustacean and mammalian neuromuscular junction by T-588, a neuroprotective compound Proc. Natl. Acad. Sci. U. S. A. 1999;96(25):14588-14593 Hirata, K. Nakagawa, M. Urbano, F.J. Rosato-Siri, M.D. Moreira, J.E. Uchitel, O.D. Sugimori, M. Llinás, R. FM 1-43 Two-photon microscopy Ultrastructure Voltage clamp 1 (benzo[b]thien 5 yl) 2 (2 diethylaminoethoxy)ethanol acetylcholine release animal cell article calcium conductance cell death cell ultrastructure drug effect facilitation mouse nerve cell neuromuscular synapse neuroprotection nonhuman potassium current priority journal sodium current synaptic transmission Action Potentials Animals Astacoidea Calcium Diethylamines Endocytosis Glutamic Acid Male Mice Neuromuscular Junction Neuroprotective Agents Potassium Channels Sodium Channels Synaptic Transmission Synaptic Vesicles Thiophenes Animalia Astacoidea Crustacea Mammalia Bath application of compound T-588, a neuroprotective agent, reduced paired-pulse and repetitive-pulse facilitation at mammalian and crustacean neuromuscular junctions. In addition, it reduced voltage-gated sodium and potassium currents in a use-dependent fashion, but had only a small effect on the presynaptic Ca 2+ conductance. By contrast, it blocked FM 1-43 vesicular uptake but not its release, in both species. Postsynaptically, T-588 reduced acetylcholine currents at the mammalian junction in a voltage-independent manner, but had no effect on the crayfish glutamate junction. All of these effects were rapidly reversible and were observed at concentrations close to the compound's acute protective level. We propose that this set of mechanisms, which reduces high-frequency synaptic transmission, is an important contributory factor in the neuroprotective action of T-588. Fil:Rosato-Siri, M.D. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Uchitel, O.D. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 1999 info:eu-repo/semantics/article info:ar-repo/semantics/artículo info:eu-repo/semantics/publishedVersion application/pdf eng info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_00278424_v96_n25_p14588_Hirata |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-134 |
collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
language |
Inglés |
orig_language_str_mv |
eng |
topic |
FM 1-43 Two-photon microscopy Ultrastructure Voltage clamp 1 (benzo[b]thien 5 yl) 2 (2 diethylaminoethoxy)ethanol acetylcholine release animal cell article calcium conductance cell death cell ultrastructure drug effect facilitation mouse nerve cell neuromuscular synapse neuroprotection nonhuman potassium current priority journal sodium current synaptic transmission Action Potentials Animals Astacoidea Calcium Diethylamines Endocytosis Glutamic Acid Male Mice Neuromuscular Junction Neuroprotective Agents Potassium Channels Sodium Channels Synaptic Transmission Synaptic Vesicles Thiophenes Animalia Astacoidea Crustacea Mammalia |
spellingShingle |
FM 1-43 Two-photon microscopy Ultrastructure Voltage clamp 1 (benzo[b]thien 5 yl) 2 (2 diethylaminoethoxy)ethanol acetylcholine release animal cell article calcium conductance cell death cell ultrastructure drug effect facilitation mouse nerve cell neuromuscular synapse neuroprotection nonhuman potassium current priority journal sodium current synaptic transmission Action Potentials Animals Astacoidea Calcium Diethylamines Endocytosis Glutamic Acid Male Mice Neuromuscular Junction Neuroprotective Agents Potassium Channels Sodium Channels Synaptic Transmission Synaptic Vesicles Thiophenes Animalia Astacoidea Crustacea Mammalia Hirata, K. Nakagawa, M. Urbano, F.J. Rosato-Siri, M.D. Moreira, J.E. Uchitel, O.D. Sugimori, M. Llinás, R. Reduced facilitation and vesicular uptake in crustacean and mammalian neuromuscular junction by T-588, a neuroprotective compound |
topic_facet |
FM 1-43 Two-photon microscopy Ultrastructure Voltage clamp 1 (benzo[b]thien 5 yl) 2 (2 diethylaminoethoxy)ethanol acetylcholine release animal cell article calcium conductance cell death cell ultrastructure drug effect facilitation mouse nerve cell neuromuscular synapse neuroprotection nonhuman potassium current priority journal sodium current synaptic transmission Action Potentials Animals Astacoidea Calcium Diethylamines Endocytosis Glutamic Acid Male Mice Neuromuscular Junction Neuroprotective Agents Potassium Channels Sodium Channels Synaptic Transmission Synaptic Vesicles Thiophenes Animalia Astacoidea Crustacea Mammalia |
description |
Bath application of compound T-588, a neuroprotective agent, reduced paired-pulse and repetitive-pulse facilitation at mammalian and crustacean neuromuscular junctions. In addition, it reduced voltage-gated sodium and potassium currents in a use-dependent fashion, but had only a small effect on the presynaptic Ca 2+ conductance. By contrast, it blocked FM 1-43 vesicular uptake but not its release, in both species. Postsynaptically, T-588 reduced acetylcholine currents at the mammalian junction in a voltage-independent manner, but had no effect on the crayfish glutamate junction. All of these effects were rapidly reversible and were observed at concentrations close to the compound's acute protective level. We propose that this set of mechanisms, which reduces high-frequency synaptic transmission, is an important contributory factor in the neuroprotective action of T-588. |
format |
Artículo Artículo publishedVersion |
author |
Hirata, K. Nakagawa, M. Urbano, F.J. Rosato-Siri, M.D. Moreira, J.E. Uchitel, O.D. Sugimori, M. Llinás, R. |
author_facet |
Hirata, K. Nakagawa, M. Urbano, F.J. Rosato-Siri, M.D. Moreira, J.E. Uchitel, O.D. Sugimori, M. Llinás, R. |
author_sort |
Hirata, K. |
title |
Reduced facilitation and vesicular uptake in crustacean and mammalian neuromuscular junction by T-588, a neuroprotective compound |
title_short |
Reduced facilitation and vesicular uptake in crustacean and mammalian neuromuscular junction by T-588, a neuroprotective compound |
title_full |
Reduced facilitation and vesicular uptake in crustacean and mammalian neuromuscular junction by T-588, a neuroprotective compound |
title_fullStr |
Reduced facilitation and vesicular uptake in crustacean and mammalian neuromuscular junction by T-588, a neuroprotective compound |
title_full_unstemmed |
Reduced facilitation and vesicular uptake in crustacean and mammalian neuromuscular junction by T-588, a neuroprotective compound |
title_sort |
reduced facilitation and vesicular uptake in crustacean and mammalian neuromuscular junction by t-588, a neuroprotective compound |
publishDate |
1999 |
url |
http://hdl.handle.net/20.500.12110/paper_00278424_v96_n25_p14588_Hirata |
work_keys_str_mv |
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