Differential expression of α1 and β subunits of voltage dependent Ca2+ channel at the neuromuscular junction of normal and P/Q Ca2+ channel knockout mouse

Voltage-dependent calcium channels (VDCC) have a key role in neuronal function transforming the voltage signals into intracellular calcium signals. They are composed of the pore-forming α1 and the regulatory α2δ, γ and β subunits. Molecular and functional studies have revealed which α1 subunit gene...

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Autores principales: Pagani, Mario Rafael, Uchitel, Osvaldo Daniel
Publicado: 2004
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03064522_v123_n1_p75_Pagani
http://hdl.handle.net/20.500.12110/paper_03064522_v123_n1_p75_Pagani
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spelling paper:paper_03064522_v123_n1_p75_Pagani2023-06-08T15:31:13Z Differential expression of α1 and β subunits of voltage dependent Ca2+ channel at the neuromuscular junction of normal and P/Q Ca2+ channel knockout mouse Pagani, Mario Rafael Uchitel, Osvaldo Daniel Ataxia Denervation Immunostaining Neuromuscular junction Synaptic transmission calcium channel calcium channel P type calcium channel Q type calcium ion alpha chain animal experiment animal tissue article beta chain calcium cell level controlled study fluorescence gene overexpression genotype immunocytochemistry knockout mouse mouse muscle denervation neuromuscular synapse nonhuman nucleotide sequence pathology priority journal protein expression wild type Voltage-dependent calcium channels (VDCC) have a key role in neuronal function transforming the voltage signals into intracellular calcium signals. They are composed of the pore-forming α1 and the regulatory α2δ, γ and β subunits. Molecular and functional studies have revealed which α1 subunit gene product is the molecular constituent of each class of native calcium channel (L, N, P/Q, R and T type). Electrophysiological and immunocytochemical studies have suggested that at adult mouse motor nerve terminal (MNT) only P/Q type channels, formed by α1A subunit, mediate evoked transmitter release. The generation of α1A-null mutant mice offers an opportunity to study the expression and localization of calcium channels at a synapse with complete loss of P/Q calcium channel. We have investigated the expression and localization of VDCCs α1 and β subunits at the wild type (WT) and knockout (KO) mouse neuromuscular junction (NMJ) using fluorescence immunocytochemistry. The α1A subunit was observed only at WT NMJ and was absent at denervated muscles and at KO NMJ. The subunits α1B, α1D and α1E were also present at WT NMJ and they were over- expressed at KO NMJ suggesting a compensatory expression due to the lack of the α1A. On the other hand, the β1b, β2a and β4 were present at the same levels in both genotypes. The presence of other types of VDCC at WT NMJ indicate that they may play other roles in the signaling process which have not been elucidated and also shows that other types of VDCC are able to substitute the α1A subunit, P/Q channel under certain pathological conditions. © 2003 IBRO. Published by Elsevier Ltd. All rights reserved. Fil:Pagani, R. 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. 2004 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03064522_v123_n1_p75_Pagani http://hdl.handle.net/20.500.12110/paper_03064522_v123_n1_p75_Pagani
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Ataxia
Denervation
Immunostaining
Neuromuscular junction
Synaptic transmission
calcium channel
calcium channel P type
calcium channel Q type
calcium ion
alpha chain
animal experiment
animal tissue
article
beta chain
calcium cell level
controlled study
fluorescence
gene overexpression
genotype
immunocytochemistry
knockout mouse
mouse
muscle denervation
neuromuscular synapse
nonhuman
nucleotide sequence
pathology
priority journal
protein expression
wild type
spellingShingle Ataxia
Denervation
Immunostaining
Neuromuscular junction
Synaptic transmission
calcium channel
calcium channel P type
calcium channel Q type
calcium ion
alpha chain
animal experiment
animal tissue
article
beta chain
calcium cell level
controlled study
fluorescence
gene overexpression
genotype
immunocytochemistry
knockout mouse
mouse
muscle denervation
neuromuscular synapse
nonhuman
nucleotide sequence
pathology
priority journal
protein expression
wild type
Pagani, Mario Rafael
Uchitel, Osvaldo Daniel
Differential expression of α1 and β subunits of voltage dependent Ca2+ channel at the neuromuscular junction of normal and P/Q Ca2+ channel knockout mouse
topic_facet Ataxia
Denervation
Immunostaining
Neuromuscular junction
Synaptic transmission
calcium channel
calcium channel P type
calcium channel Q type
calcium ion
alpha chain
animal experiment
animal tissue
article
beta chain
calcium cell level
controlled study
fluorescence
gene overexpression
genotype
immunocytochemistry
knockout mouse
mouse
muscle denervation
neuromuscular synapse
nonhuman
nucleotide sequence
pathology
priority journal
protein expression
wild type
description Voltage-dependent calcium channels (VDCC) have a key role in neuronal function transforming the voltage signals into intracellular calcium signals. They are composed of the pore-forming α1 and the regulatory α2δ, γ and β subunits. Molecular and functional studies have revealed which α1 subunit gene product is the molecular constituent of each class of native calcium channel (L, N, P/Q, R and T type). Electrophysiological and immunocytochemical studies have suggested that at adult mouse motor nerve terminal (MNT) only P/Q type channels, formed by α1A subunit, mediate evoked transmitter release. The generation of α1A-null mutant mice offers an opportunity to study the expression and localization of calcium channels at a synapse with complete loss of P/Q calcium channel. We have investigated the expression and localization of VDCCs α1 and β subunits at the wild type (WT) and knockout (KO) mouse neuromuscular junction (NMJ) using fluorescence immunocytochemistry. The α1A subunit was observed only at WT NMJ and was absent at denervated muscles and at KO NMJ. The subunits α1B, α1D and α1E were also present at WT NMJ and they were over- expressed at KO NMJ suggesting a compensatory expression due to the lack of the α1A. On the other hand, the β1b, β2a and β4 were present at the same levels in both genotypes. The presence of other types of VDCC at WT NMJ indicate that they may play other roles in the signaling process which have not been elucidated and also shows that other types of VDCC are able to substitute the α1A subunit, P/Q channel under certain pathological conditions. © 2003 IBRO. Published by Elsevier Ltd. All rights reserved.
author Pagani, Mario Rafael
Uchitel, Osvaldo Daniel
author_facet Pagani, Mario Rafael
Uchitel, Osvaldo Daniel
author_sort Pagani, Mario Rafael
title Differential expression of α1 and β subunits of voltage dependent Ca2+ channel at the neuromuscular junction of normal and P/Q Ca2+ channel knockout mouse
title_short Differential expression of α1 and β subunits of voltage dependent Ca2+ channel at the neuromuscular junction of normal and P/Q Ca2+ channel knockout mouse
title_full Differential expression of α1 and β subunits of voltage dependent Ca2+ channel at the neuromuscular junction of normal and P/Q Ca2+ channel knockout mouse
title_fullStr Differential expression of α1 and β subunits of voltage dependent Ca2+ channel at the neuromuscular junction of normal and P/Q Ca2+ channel knockout mouse
title_full_unstemmed Differential expression of α1 and β subunits of voltage dependent Ca2+ channel at the neuromuscular junction of normal and P/Q Ca2+ channel knockout mouse
title_sort differential expression of α1 and β subunits of voltage dependent ca2+ channel at the neuromuscular junction of normal and p/q ca2+ channel knockout mouse
publishDate 2004
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03064522_v123_n1_p75_Pagani
http://hdl.handle.net/20.500.12110/paper_03064522_v123_n1_p75_Pagani
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