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dc.contributor.author
Murthy, Vidya
dc.contributor.author
Taranda, Julian
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Elgoyhen, Ana Belen
dc.contributor.author
Vetter, Douglas E.
dc.date.available
2019-07-16T16:16:28Z
dc.date.issued
2009-12
dc.identifier.citation
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
dc.identifier.issn
1932-8451
dc.identifier.uri
http://hdl.handle.net/11336/79625
dc.description.abstract
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.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
John Wiley & Sons Inc
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Acetylcholine Receptors
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Alpha9 Nachr
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Cochlea
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Olivocochlear System
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Synapse Development
dc.subject.classification
Bioquímica y Biología Molecular
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Ciencias Biológicas
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CIENCIAS NATURALES Y EXACTAS
dc.title
Activity of nAChRs containing α9 subunits modulates synapse stabilization via bidirectional signaling programs
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-07-11T19:22:09Z
dc.journal.volume
69
dc.journal.number
14
dc.journal.pagination
931-949
dc.journal.pais
Estados Unidos
dc.journal.ciudad
Hoboken
dc.description.fil
Fil: Murthy, Vidya. Tufts University School of Medicine; Eslovaquia
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Fil: 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; Eslovaquia
dc.description.fil
Fil: 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; Argentina
dc.description.fil
Fil: Vetter, Douglas E.. Tufts University School of Medicine; Eslovaquia
dc.journal.title
Developmental Neurobiology
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819290/
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1002/dneu.20753
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/dneu.20753
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