Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs

Although the synaptogenic program for cholinergic synapses of the neuromuscular junction is well known, little is known of the identity or dynamic expression patterns of proteins involved in non-neuromuscular nicotinic synapse development. We have previously demonstrated abnormal presynaptic termina...

Descripción completa

Detalles Bibliográficos
Autores: Murthy, Vidya, Taranda, Julian, Elgoyhen, Ana Belen, Vetter, Douglas E.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2009
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/79625
Acceso en línea:http://hdl.handle.net/11336/79625
Access Level:acceso abierto
Palabra clave:ACETYLCHOLINE RECEPTORS
ALPHA9 NACHR
COCHLEA
OLIVOCOCHLEAR SYSTEM
SYNAPSE DEVELOPMENT
https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
id AR_2eec35d30dfbc33dc22a23bc1394c06d
oai_identifier_str oai:ri.conicet.gov.ar:11336/79625
network_acronym_str AR
network_name_str Argentina
repository_id_str
dc.title.none.fl_str_mv Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs
title Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs
spellingShingle Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs
Murthy, Vidya
ACETYLCHOLINE RECEPTORS
ALPHA9 NACHR
COCHLEA
OLIVOCOCHLEAR SYSTEM
SYNAPSE DEVELOPMENT
https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
title_short Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs
title_full Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs
title_fullStr Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs
title_full_unstemmed Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs
title_sort Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs
dc.creator.none.fl_str_mv Murthy, Vidya
Taranda, Julian
Elgoyhen, Ana Belen
Vetter, Douglas E.
author Murthy, Vidya
author_facet Murthy, Vidya
Taranda, Julian
Elgoyhen, Ana Belen
Vetter, Douglas E.
author_role author
author2 Taranda, Julian
Elgoyhen, Ana Belen
Vetter, Douglas E.
author2_role author
author
author
dc.subject.none.fl_str_mv ACETYLCHOLINE RECEPTORS
ALPHA9 NACHR
COCHLEA
OLIVOCOCHLEAR SYSTEM
SYNAPSE DEVELOPMENT
https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
topic ACETYLCHOLINE RECEPTORS
ALPHA9 NACHR
COCHLEA
OLIVOCOCHLEAR SYSTEM
SYNAPSE DEVELOPMENT
https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
description Although the synaptogenic program for cholinergic synapses of the neuromuscular junction is well known, little is known of the identity or dynamic expression patterns of proteins involved in non-neuromuscular nicotinic synapse development. We have previously demonstrated abnormal presynaptic terminal morphology following loss of nicotinic acetylcholine receptor (nAChR) α9 subunit expression in adult cochleae. However, the molecular mechanisms underlying these changes have remained obscure. To better understand synapse formation and the role of cholinergic activity in the synaptogenesis of the inner ear, we exploit the nAChR α9 subunit null mouse. In this mouse, functional acetylcholine (ACh) neurotransmission to the hair cells is completely silenced. Results demonstrate a premature, effusive innervation to the synaptic pole of the outer hair cells in α9 null mice coinciding with delayed expression of cell adhesion proteins during the period of effusive contact. Collapse of the ectopic innervation coincides with an age-related hyperexpression pattern in the null mice. In addition, we document changes in expression of presynaptic vesicle recycling/trafficking machinery in the α9 null mice that suggests a bidirectional information flow between the target of the neural innervation (the hair cells) and the presynaptic terminal that is modified by hair cell nAChR activity. Loss of nAChR activity may alter transcriptional activity, as CREB binding protein expression is decreased coincident with the increased expression of N-Cadherin in the adult α9 null mice. Finally, by using mice expressing the nondesensitizing α9 L90T point mutant nAChR subunit, we show that increased nAChR activity drives synaptic hyperinnervation. © 2009 Wiley Periodicals, Inc.
publishDate 2009
dc.date.none.fl_str_mv 2009-12
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/11336/79625
Murthy, Vidya; Taranda, Julian; Elgoyhen, Ana Belen; Vetter, Douglas E.; Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs; John Wiley & Sons Inc; Developmental Neurobiology; 69; 14; 12-2009; 931-949
1932-8451
CONICET Digital
CONICET
url http://hdl.handle.net/11336/79625
identifier_str_mv Murthy, Vidya; Taranda, Julian; Elgoyhen, Ana Belen; Vetter, Douglas E.; Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs; John Wiley & Sons Inc; Developmental Neurobiology; 69; 14; 12-2009; 931-949
1932-8451
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819290/
info:eu-repo/semantics/altIdentifier/doi/10.1002/dneu.20753
info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/dneu.20753
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv John Wiley & Sons Inc
publisher.none.fl_str_mv John Wiley & Sons Inc
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1799195814917046272
spelling Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programsMurthy, VidyaTaranda, JulianElgoyhen, Ana BelenVetter, Douglas E.ACETYLCHOLINE RECEPTORSALPHA9 NACHRCOCHLEAOLIVOCOCHLEAR SYSTEMSYNAPSE DEVELOPMENThttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Although the synaptogenic program for cholinergic synapses of the neuromuscular junction is well known, little is known of the identity or dynamic expression patterns of proteins involved in non-neuromuscular nicotinic synapse development. We have previously demonstrated abnormal presynaptic terminal morphology following loss of nicotinic acetylcholine receptor (nAChR) α9 subunit expression in adult cochleae. However, the molecular mechanisms underlying these changes have remained obscure. To better understand synapse formation and the role of cholinergic activity in the synaptogenesis of the inner ear, we exploit the nAChR α9 subunit null mouse. In this mouse, functional acetylcholine (ACh) neurotransmission to the hair cells is completely silenced. Results demonstrate a premature, effusive innervation to the synaptic pole of the outer hair cells in α9 null mice coinciding with delayed expression of cell adhesion proteins during the period of effusive contact. Collapse of the ectopic innervation coincides with an age-related hyperexpression pattern in the null mice. In addition, we document changes in expression of presynaptic vesicle recycling/trafficking machinery in the α9 null mice that suggests a bidirectional information flow between the target of the neural innervation (the hair cells) and the presynaptic terminal that is modified by hair cell nAChR activity. Loss of nAChR activity may alter transcriptional activity, as CREB binding protein expression is decreased coincident with the increased expression of N-Cadherin in the adult α9 null mice. Finally, by using mice expressing the nondesensitizing α9 L90T point mutant nAChR subunit, we show that increased nAChR activity drives synaptic hyperinnervation. © 2009 Wiley Periodicals, Inc.Fil: Murthy, Vidya. Tufts University School of Medicine; EslovaquiaFil: Taranda, Julian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina. Tufts University School of Medicine; EslovaquiaFil: Elgoyhen, Ana Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Farmacología; ArgentinaFil: Vetter, Douglas E.. Tufts University School of Medicine; EslovaquiaJohn Wiley & Sons Inc2009-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/79625Murthy, Vidya; Taranda, Julian; Elgoyhen, Ana Belen; Vetter, Douglas E.; Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs; John Wiley & Sons Inc; Developmental Neurobiology; 69; 14; 12-2009; 931-9491932-8451CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819290/info:eu-repo/semantics/altIdentifier/doi/10.1002/dneu.20753info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/dneu.20753info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2024-05-08T14:04:45Zoai:ri.conicet.gov.ar:11336/79625instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982024-05-08 14:04:45.544CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
score 15.811543

Similares en LA Referencia