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
- Institución
- Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
- OAI Identificador
- paperaa:paper_02706474_v24_n46_p10379_GonzalezInchauspe
Ver los metadatos del registro completo
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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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score |
13.070432 |