Altered properties of quantal neurotransmitter release at endplates of mice lacking P/Q-type Ca2+ channels
Transmission at the mouse neuromuscular junction normally relies on P/Q-type channels, but became jointly dependent on both N-and R-type Ca2+ channels when the P/Q-type channel α1A subunit was deleted. R-type channels lay close to Ca2+ sensors for exocytosis and IK(Ca) channel activation, like the P...
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Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_00278424_v100_n6_p3491_Urbano https://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=artiaex&d=paper_00278424_v100_n6_p3491_Urbano_oai |
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I28-R145-paper_00278424_v100_n6_p3491_Urbano_oai2024-08-16 Urbano, F.J. Piedras-Rentería, E.S. Jun, K. Shin, H.-S. Uchitel, O.D. Tsien, R.W. 2003 Transmission at the mouse neuromuscular junction normally relies on P/Q-type channels, but became jointly dependent on both N-and R-type Ca2+ channels when the P/Q-type channel α1A subunit was deleted. R-type channels lay close to Ca2+ sensors for exocytosis and IK(Ca) channel activation, like the P/Q-type channels they replaced. In contrast, N-type channels were less well localized, but abundant enough to influence secretion strongly, particularly when action potentials were prolonged. Our data suggested that active zone structures may select among multiple Ca2+ channels in the hierarchy P/Q>R>N. The α1A-/- neuromuscular junction displayed several other differences from wild-type: lowered quantal content but greater ability to withstand reductions in the Ca2+/Mg2+ ratio, and little or no paired-pulse facilitation, the latter findings possibly reflecting compensatory mechanisms at individual release sites. Changes in presynaptic function were also associated with a significant reduction in the size of postsynaptic acetylcholine receptor clusters. Fil:Uchitel, O.D. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. application/pdf http://hdl.handle.net/20.500.12110/paper_00278424_v100_n6_p3491_Urbano info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar Proc. Natl. Acad. Sci. U. S. A. 2003;100(6):3491-3496 α1A knockout Ca2+-activated potassium channel Neuromuscular junction Paired-pulse facilitation SNX-482 calcium channel calcium ion cholinergic receptor magnesium ion action potential animal cell article channel gating exocytosis mouse nerve ending neuromuscular synapse neurotransmission neurotransmitter release nonhuman priority journal 4-Aminopyridine Animals Calcium Channels, N-Type Calcium Channels, P-Type Calcium Channels, Q-Type Calcium Channels, R-Type Mice Mice, Knockout Models, Neurological Motor Endplate Neuronal Plasticity Neurotransmitter Agents Synaptic Transmission Animalia Altered properties of quantal neurotransmitter release at endplates of mice lacking P/Q-type Ca2+ channels info:eu-repo/semantics/article info:ar-repo/semantics/artículo info:eu-repo/semantics/publishedVersion https://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=artiaex&d=paper_00278424_v100_n6_p3491_Urbano_oai |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-145 |
collection |
Repositorio Digital de la Universidad de Buenos Aires (UBA) |
topic |
α1A knockout Ca2+-activated potassium channel Neuromuscular junction Paired-pulse facilitation SNX-482 calcium channel calcium ion cholinergic receptor magnesium ion action potential animal cell article channel gating exocytosis mouse nerve ending neuromuscular synapse neurotransmission neurotransmitter release nonhuman priority journal 4-Aminopyridine Animals Calcium Channels, N-Type Calcium Channels, P-Type Calcium Channels, Q-Type Calcium Channels, R-Type Mice Mice, Knockout Models, Neurological Motor Endplate Neuronal Plasticity Neurotransmitter Agents Synaptic Transmission Animalia |
spellingShingle |
α1A knockout Ca2+-activated potassium channel Neuromuscular junction Paired-pulse facilitation SNX-482 calcium channel calcium ion cholinergic receptor magnesium ion action potential animal cell article channel gating exocytosis mouse nerve ending neuromuscular synapse neurotransmission neurotransmitter release nonhuman priority journal 4-Aminopyridine Animals Calcium Channels, N-Type Calcium Channels, P-Type Calcium Channels, Q-Type Calcium Channels, R-Type Mice Mice, Knockout Models, Neurological Motor Endplate Neuronal Plasticity Neurotransmitter Agents Synaptic Transmission Animalia Urbano, F.J. Piedras-Rentería, E.S. Jun, K. Shin, H.-S. Uchitel, O.D. Tsien, R.W. Altered properties of quantal neurotransmitter release at endplates of mice lacking P/Q-type Ca2+ channels |
topic_facet |
α1A knockout Ca2+-activated potassium channel Neuromuscular junction Paired-pulse facilitation SNX-482 calcium channel calcium ion cholinergic receptor magnesium ion action potential animal cell article channel gating exocytosis mouse nerve ending neuromuscular synapse neurotransmission neurotransmitter release nonhuman priority journal 4-Aminopyridine Animals Calcium Channels, N-Type Calcium Channels, P-Type Calcium Channels, Q-Type Calcium Channels, R-Type Mice Mice, Knockout Models, Neurological Motor Endplate Neuronal Plasticity Neurotransmitter Agents Synaptic Transmission Animalia |
description |
Transmission at the mouse neuromuscular junction normally relies on P/Q-type channels, but became jointly dependent on both N-and R-type Ca2+ channels when the P/Q-type channel α1A subunit was deleted. R-type channels lay close to Ca2+ sensors for exocytosis and IK(Ca) channel activation, like the P/Q-type channels they replaced. In contrast, N-type channels were less well localized, but abundant enough to influence secretion strongly, particularly when action potentials were prolonged. Our data suggested that active zone structures may select among multiple Ca2+ channels in the hierarchy P/Q>R>N. The α1A-/- neuromuscular junction displayed several other differences from wild-type: lowered quantal content but greater ability to withstand reductions in the Ca2+/Mg2+ ratio, and little or no paired-pulse facilitation, the latter findings possibly reflecting compensatory mechanisms at individual release sites. Changes in presynaptic function were also associated with a significant reduction in the size of postsynaptic acetylcholine receptor clusters. |
format |
Artículo Artículo publishedVersion |
author |
Urbano, F.J. Piedras-Rentería, E.S. Jun, K. Shin, H.-S. Uchitel, O.D. Tsien, R.W. |
author_facet |
Urbano, F.J. Piedras-Rentería, E.S. Jun, K. Shin, H.-S. Uchitel, O.D. Tsien, R.W. |
author_sort |
Urbano, F.J. |
title |
Altered properties of quantal neurotransmitter release at endplates of mice lacking P/Q-type Ca2+ channels |
title_short |
Altered properties of quantal neurotransmitter release at endplates of mice lacking P/Q-type Ca2+ channels |
title_full |
Altered properties of quantal neurotransmitter release at endplates of mice lacking P/Q-type Ca2+ channels |
title_fullStr |
Altered properties of quantal neurotransmitter release at endplates of mice lacking P/Q-type Ca2+ channels |
title_full_unstemmed |
Altered properties of quantal neurotransmitter release at endplates of mice lacking P/Q-type Ca2+ channels |
title_sort |
altered properties of quantal neurotransmitter release at endplates of mice lacking p/q-type ca2+ channels |
publishDate |
2003 |
url |
http://hdl.handle.net/20.500.12110/paper_00278424_v100_n6_p3491_Urbano https://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=artiaex&d=paper_00278424_v100_n6_p3491_Urbano_oai |
work_keys_str_mv |
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_version_ |
1809356797813719040 |