Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal

Autores
González Inchauspe, C.; Martini, F.J.; Forsythe, I.D.; Uchitel, O.D.
Año de publicación
2004
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Calcium channels of the P/Q subtype mediate transmitter release at the neuromuscular junction and at many central synapses, such as the calyx of Held. Transgenic mice in which α1A channels are ablated provide a powerful tool with which to test compensatory mechanisms at the synapse and to explore mechanisms of presynaptic regulation associated with expression of P/Q channels. Using the calyx of Held preparation from the knock-out (KO) mice, we show here that N-type channels functionally compensate for the absence of P/Q subunits at the calyx and evoke giant synaptic currents [approximately two-thirds of the magnitude of wild-type (WT) responses]. However, although evoked paired-pulse facilitation is prominent in WT, this facilitation is greatly diminished in the KO. In addition, direct recording of presynaptic calcium currents revealed that the major functional difference was the absence of calcium-dependent facilitation at the calyx in the P/Q KO animals. We conclude that one physiological function of P/Q channels is to provide additional facilitatory drive, so contributing to maintenance of transmission as vesicles are depleted during high throughput synaptic transmission.
Fil:González Inchauspe, C. 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.
Fuente
J. Neurosci. 2004;24(46):10379-10383
Materia
Calcium currents
Calyx of Held
Facilitation
Knock-out mice
P/Q channels
Synaptic transmission
calcium channel N type
calcium channel P type
calcium channel Q type
calcium ion
animal tissue
article
calcium current
channel gating
facilitation
knockout mouse
mouse
nerve cell plasticity
nonhuman
presynaptic membrane
priority journal
synaptosome
transgenic mouse
Animals
Brain Stem
Calcium
Calcium Channels, N-Type
Calcium Channels, P-Type
Calcium Channels, Q-Type
Evoked Potentials
Mice
Mice, Knockout
Neuronal Plasticity
Presynaptic Terminals
Protein Subunits
Synapses
Synaptic Transmission
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/2.5/ar
Repositorio
Biblioteca Digital (UBA-FCEN)
Institución
Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
OAI Identificador
paperaa:paper_02706474_v24_n46_p10379_GonzalezInchauspe

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oai_identifier_str paperaa:paper_02706474_v24_n46_p10379_GonzalezInchauspe
network_acronym_str BDUBAFCEN
repository_id_str 1896
network_name_str Biblioteca Digital (UBA-FCEN)
spelling Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminalGonzález Inchauspe, C.Martini, F.J.Forsythe, I.D.Uchitel, O.D.Calcium currentsCalyx of HeldFacilitationKnock-out miceP/Q channelsSynaptic transmissioncalcium channel N typecalcium channel P typecalcium channel Q typecalcium ionanimal tissuearticlecalcium currentchannel gatingfacilitationknockout mousemousenerve cell plasticitynonhumanpresynaptic membranepriority journalsynaptosometransgenic mouseAnimalsBrain StemCalciumCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-TypeEvoked PotentialsMiceMice, KnockoutNeuronal PlasticityPresynaptic TerminalsProtein SubunitsSynapsesSynaptic TransmissionCalcium channels of the P/Q subtype mediate transmitter release at the neuromuscular junction and at many central synapses, such as the calyx of Held. Transgenic mice in which α1A channels are ablated provide a powerful tool with which to test compensatory mechanisms at the synapse and to explore mechanisms of presynaptic regulation associated with expression of P/Q channels. Using the calyx of Held preparation from the knock-out (KO) mice, we show here that N-type channels functionally compensate for the absence of P/Q subunits at the calyx and evoke giant synaptic currents [approximately two-thirds of the magnitude of wild-type (WT) responses]. However, although evoked paired-pulse facilitation is prominent in WT, this facilitation is greatly diminished in the KO. In addition, direct recording of presynaptic calcium currents revealed that the major functional difference was the absence of calcium-dependent facilitation at the calyx in the P/Q KO animals. We conclude that one physiological function of P/Q channels is to provide additional facilitatory drive, so contributing to maintenance of transmission as vesicles are depleted during high throughput synaptic transmission.Fil:González Inchauspe, C. 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.2004info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://hdl.handle.net/20.500.12110/paper_02706474_v24_n46_p10379_GonzalezInchauspeJ. Neurosci. 2004;24(46):10379-10383reponame:Biblioteca Digital (UBA-FCEN)instname:Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturalesinstacron:UBA-FCENenginfo:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/2.5/ar2025-09-29T13:42:57Zpaperaa:paper_02706474_v24_n46_p10379_GonzalezInchauspeInstitucionalhttps://digital.bl.fcen.uba.ar/Universidad públicaNo correspondehttps://digital.bl.fcen.uba.ar/cgi-bin/oaiserver.cgiana@bl.fcen.uba.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:18962025-09-29 13:42:59.081Biblioteca Digital (UBA-FCEN) - Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturalesfalse
dc.title.none.fl_str_mv Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal
title Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal
spellingShingle Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal
González Inchauspe, C.
Calcium currents
Calyx of Held
Facilitation
Knock-out mice
P/Q channels
Synaptic transmission
calcium channel N type
calcium channel P type
calcium channel Q type
calcium ion
animal tissue
article
calcium current
channel gating
facilitation
knockout mouse
mouse
nerve cell plasticity
nonhuman
presynaptic membrane
priority journal
synaptosome
transgenic mouse
Animals
Brain Stem
Calcium
Calcium Channels, N-Type
Calcium Channels, P-Type
Calcium Channels, Q-Type
Evoked Potentials
Mice
Mice, Knockout
Neuronal Plasticity
Presynaptic Terminals
Protein Subunits
Synapses
Synaptic Transmission
title_short Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal
title_full Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal
title_fullStr Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal
title_full_unstemmed Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal
title_sort Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal
dc.creator.none.fl_str_mv González Inchauspe, C.
Martini, F.J.
Forsythe, I.D.
Uchitel, O.D.
author González Inchauspe, C.
author_facet González Inchauspe, C.
Martini, F.J.
Forsythe, I.D.
Uchitel, O.D.
author_role author
author2 Martini, F.J.
Forsythe, I.D.
Uchitel, O.D.
author2_role author
author
author
dc.subject.none.fl_str_mv Calcium currents
Calyx of Held
Facilitation
Knock-out mice
P/Q channels
Synaptic transmission
calcium channel N type
calcium channel P type
calcium channel Q type
calcium ion
animal tissue
article
calcium current
channel gating
facilitation
knockout mouse
mouse
nerve cell plasticity
nonhuman
presynaptic membrane
priority journal
synaptosome
transgenic mouse
Animals
Brain Stem
Calcium
Calcium Channels, N-Type
Calcium Channels, P-Type
Calcium Channels, Q-Type
Evoked Potentials
Mice
Mice, Knockout
Neuronal Plasticity
Presynaptic Terminals
Protein Subunits
Synapses
Synaptic Transmission
topic Calcium currents
Calyx of Held
Facilitation
Knock-out mice
P/Q channels
Synaptic transmission
calcium channel N type
calcium channel P type
calcium channel Q type
calcium ion
animal tissue
article
calcium current
channel gating
facilitation
knockout mouse
mouse
nerve cell plasticity
nonhuman
presynaptic membrane
priority journal
synaptosome
transgenic mouse
Animals
Brain Stem
Calcium
Calcium Channels, N-Type
Calcium Channels, P-Type
Calcium Channels, Q-Type
Evoked Potentials
Mice
Mice, Knockout
Neuronal Plasticity
Presynaptic Terminals
Protein Subunits
Synapses
Synaptic Transmission
dc.description.none.fl_txt_mv Calcium channels of the P/Q subtype mediate transmitter release at the neuromuscular junction and at many central synapses, such as the calyx of Held. Transgenic mice in which α1A channels are ablated provide a powerful tool with which to test compensatory mechanisms at the synapse and to explore mechanisms of presynaptic regulation associated with expression of P/Q channels. Using the calyx of Held preparation from the knock-out (KO) mice, we show here that N-type channels functionally compensate for the absence of P/Q subunits at the calyx and evoke giant synaptic currents [approximately two-thirds of the magnitude of wild-type (WT) responses]. However, although evoked paired-pulse facilitation is prominent in WT, this facilitation is greatly diminished in the KO. In addition, direct recording of presynaptic calcium currents revealed that the major functional difference was the absence of calcium-dependent facilitation at the calyx in the P/Q KO animals. We conclude that one physiological function of P/Q channels is to provide additional facilitatory drive, so contributing to maintenance of transmission as vesicles are depleted during high throughput synaptic transmission.
Fil:González Inchauspe, C. 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.
description Calcium channels of the P/Q subtype mediate transmitter release at the neuromuscular junction and at many central synapses, such as the calyx of Held. Transgenic mice in which α1A channels are ablated provide a powerful tool with which to test compensatory mechanisms at the synapse and to explore mechanisms of presynaptic regulation associated with expression of P/Q channels. Using the calyx of Held preparation from the knock-out (KO) mice, we show here that N-type channels functionally compensate for the absence of P/Q subunits at the calyx and evoke giant synaptic currents [approximately two-thirds of the magnitude of wild-type (WT) responses]. However, although evoked paired-pulse facilitation is prominent in WT, this facilitation is greatly diminished in the KO. In addition, direct recording of presynaptic calcium currents revealed that the major functional difference was the absence of calcium-dependent facilitation at the calyx in the P/Q KO animals. We conclude that one physiological function of P/Q channels is to provide additional facilitatory drive, so contributing to maintenance of transmission as vesicles are depleted during high throughput synaptic transmission.
publishDate 2004
dc.date.none.fl_str_mv 2004
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/20.500.12110/paper_02706474_v24_n46_p10379_GonzalezInchauspe
url http://hdl.handle.net/20.500.12110/paper_02706474_v24_n46_p10379_GonzalezInchauspe
dc.language.none.fl_str_mv eng
language eng
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/2.5/ar
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/2.5/ar
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv J. Neurosci. 2004;24(46):10379-10383
reponame:Biblioteca Digital (UBA-FCEN)
instname:Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
instacron:UBA-FCEN
reponame_str Biblioteca Digital (UBA-FCEN)
collection Biblioteca Digital (UBA-FCEN)
instname_str Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
instacron_str UBA-FCEN
institution UBA-FCEN
repository.name.fl_str_mv Biblioteca Digital (UBA-FCEN) - Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
repository.mail.fl_str_mv ana@bl.fcen.uba.ar
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