Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochlea

Autores
Vattino, Lucas Gabriel; Ballestero, Jimena Andrea; Maison, Stéphane F.; Di Guilmi, Mariano Nicolás; Taranda, Julian; Liberman, Charles M.; Fuchs, Paul A.; Katz, Eleonora; Elgoyhen, Ana Belen
Año de publicación
2018
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Gain control of the auditory system operates at multiple levels. Cholinergic medial olivocochlear (MOC) fibers that originate in the brainstem and make direct synaptic contacts at the base of the outer hair cells (OHCs) are the final targets of several feedback loops from both the periphery and higher processing cen ters. Efferent activation inhibits somatic electromotil ity of OHCs, an active amplification system within the mammalian cochlea. This is mediated by the activa tion of a calcium permeable α9α10 ionotropic cho linergic nicotinic receptor (nAChR) functionally cou pled to calcium activated SK potassium channels. The strength of cochlear inhibition is driven by the rate of MOC activity and short term facilitation at the MOC OHC synapse (Ballestero et al., 2011).The present work shows that a knockin mouse with a mutation in the α9α10 nAChR (L9’;T) with increased channel gating (Taranda et al., 2009) greatly prolongs hair cell evoked inhibitory postsynaptic currents (IPSCs). Long-term presynaptic compensatory mechanisms lead to reduced quantum content (IHC wt =1.29 ± 0.21; L9’;T= 0.83 ± 0.12, n=5- 6. OHC wt =0.23 ± 0.04, L9’;T = 0.14 ± 0.02, n=12-15). However, upon high frequency stimulation of MOC-OHC synapses, L9’;T mice exhibited more facilitation leading to greatly prolonged synaptic responses (S2 /S1- 40Hz: wt = 1.37 ± 0.16, L9’;T = 3.47 ± 0.44, n = 6-8, p< 0.05). At the cochlear physiology level, these synaptic changes were matched by a longer time course of efferent MOC suppression of DPOAEs. Thus, the maximal suppres sive effect of electrical shocks (70-s, 200 Hz) at the base of the IVth ventricle was doubled both at 16 (p < 0.01) and 22 kHz (p < 0.05), reached much more slowly (16 kHz: wt = 5.3 ± 1.0 s, L9’;T = 30.8 ± 4.1 s; 22 kHz: wt = 1.5 ± 0.4 s, L9’;T = 44.1 ± 3.1 s) and persisted for a longer time after the shocks for both 16 and 22 kHz in L9’;T mice (> 5 min) as compared to their wt littermates (≤1 s). These results indicate that the properties of the MOC-OHC synapse directly determine the efficacy of the MOC feedback to the cochlea being a main player in the “gain control” of the auditory periphery.
Fil: Vattino, Lucas Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Ballestero, Jimena Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Maison, Stéphane F.. Harvard Medical School; Estados Unidos
Fil: Di Guilmi, Mariano Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Taranda, Julian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Liberman, Charles M.. Harvard Medical School; Estados Unidos
Fil: Fuchs, Paul A.. University Johns Hopkins; Estados Unidos
Fil: Katz, Eleonora. 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 Ciencias Exactas y Naturales; Argentina
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. Instituto de Farmacología; Argentina
41St Annual MidWinter Meeting
San Diego
Estados Unidos
Association for Research in Otolaryngology
Materia
SISTEMA EFERENTE OLIVOCOCLEAR
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/154581
Acceder
id CONICETDig_4135b24767e9d38bfae35190c76b112c
oai_identifier_str oai:ri.conicet.gov.ar:11336/154581
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochleaVattino, Lucas GabrielBallestero, Jimena AndreaMaison, Stéphane F.Di Guilmi, Mariano NicolásTaranda, JulianLiberman, Charles M.Fuchs, Paul A.Katz, EleonoraElgoyhen, Ana BelenSISTEMA EFERENTE OLIVOCOCLEARhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Gain control of the auditory system operates at multiple levels. Cholinergic medial olivocochlear (MOC) fibers that originate in the brainstem and make direct synaptic contacts at the base of the outer hair cells (OHCs) are the final targets of several feedback loops from both the periphery and higher processing cen ters. Efferent activation inhibits somatic electromotil ity of OHCs, an active amplification system within the mammalian cochlea. This is mediated by the activa tion of a calcium permeable α9α10 ionotropic cho linergic nicotinic receptor (nAChR) functionally cou pled to calcium activated SK potassium channels. The strength of cochlear inhibition is driven by the rate of MOC activity and short term facilitation at the MOC OHC synapse (Ballestero et al., 2011).The present work shows that a knockin mouse with a mutation in the α9α10 nAChR (L9’;T) with increased channel gating (Taranda et al., 2009) greatly prolongs hair cell evoked inhibitory postsynaptic currents (IPSCs). Long-term presynaptic compensatory mechanisms lead to reduced quantum content (IHC wt =1.29 ± 0.21; L9’;T= 0.83 ± 0.12, n=5- 6. OHC wt =0.23 ± 0.04, L9’;T = 0.14 ± 0.02, n=12-15). However, upon high frequency stimulation of MOC-OHC synapses, L9’;T mice exhibited more facilitation leading to greatly prolonged synaptic responses (S2 /S1- 40Hz: wt = 1.37 ± 0.16, L9’;T = 3.47 ± 0.44, n = 6-8, p< 0.05). At the cochlear physiology level, these synaptic changes were matched by a longer time course of efferent MOC suppression of DPOAEs. Thus, the maximal suppres sive effect of electrical shocks (70-s, 200 Hz) at the base of the IVth ventricle was doubled both at 16 (p < 0.01) and 22 kHz (p < 0.05), reached much more slowly (16 kHz: wt = 5.3 ± 1.0 s, L9’;T = 30.8 ± 4.1 s; 22 kHz: wt = 1.5 ± 0.4 s, L9’;T = 44.1 ± 3.1 s) and persisted for a longer time after the shocks for both 16 and 22 kHz in L9’;T mice (> 5 min) as compared to their wt littermates (≤1 s). These results indicate that the properties of the MOC-OHC synapse directly determine the efficacy of the MOC feedback to the cochlea being a main player in the “gain control” of the auditory periphery.Fil: Vattino, Lucas Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Ballestero, Jimena Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Maison, Stéphane F.. Harvard Medical School; Estados UnidosFil: Di Guilmi, Mariano Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Taranda, Julian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Liberman, Charles M.. Harvard Medical School; Estados UnidosFil: Fuchs, Paul A.. University Johns Hopkins; Estados UnidosFil: Katz, Eleonora. 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 Ciencias Exactas y Naturales; ArgentinaFil: 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. Instituto de Farmacología; Argentina41St Annual MidWinter MeetingSan DiegoEstados UnidosAssociation for Research in OtolaryngologyAssociation for Research in Otolaryngology2018info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/154581Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochlea; 41St Annual MidWinter Meeting; San Diego; Estados Unidos; 2018; 1-30742-3152CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://aro.org/wp-content/uploads/2020/09/2018_ARO_Abstracts_ALL_PAGES.pdfInternacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:54:26Zoai:ri.conicet.gov.ar:11336/154581instacron: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:34982025-09-29 09:54:27.181CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochlea
title Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochlea
spellingShingle Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochlea
Vattino, Lucas Gabriel
SISTEMA EFERENTE OLIVOCOCLEAR
title_short Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochlea
title_full Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochlea
title_fullStr Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochlea
title_full_unstemmed Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochlea
title_sort Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochlea
dc.creator.none.fl_str_mv Vattino, Lucas Gabriel
Ballestero, Jimena Andrea
Maison, Stéphane F.
Di Guilmi, Mariano Nicolás
Taranda, Julian
Liberman, Charles M.
Fuchs, Paul A.
Katz, Eleonora
Elgoyhen, Ana Belen
author Vattino, Lucas Gabriel
author_facet Vattino, Lucas Gabriel
Ballestero, Jimena Andrea
Maison, Stéphane F.
Di Guilmi, Mariano Nicolás
Taranda, Julian
Liberman, Charles M.
Fuchs, Paul A.
Katz, Eleonora
Elgoyhen, Ana Belen
author_role author
author2 Ballestero, Jimena Andrea
Maison, Stéphane F.
Di Guilmi, Mariano Nicolás
Taranda, Julian
Liberman, Charles M.
Fuchs, Paul A.
Katz, Eleonora
Elgoyhen, Ana Belen
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv SISTEMA EFERENTE OLIVOCOCLEAR
topic SISTEMA EFERENTE OLIVOCOCLEAR
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Gain control of the auditory system operates at multiple levels. Cholinergic medial olivocochlear (MOC) fibers that originate in the brainstem and make direct synaptic contacts at the base of the outer hair cells (OHCs) are the final targets of several feedback loops from both the periphery and higher processing cen ters. Efferent activation inhibits somatic electromotil ity of OHCs, an active amplification system within the mammalian cochlea. This is mediated by the activa tion of a calcium permeable α9α10 ionotropic cho linergic nicotinic receptor (nAChR) functionally cou pled to calcium activated SK potassium channels. The strength of cochlear inhibition is driven by the rate of MOC activity and short term facilitation at the MOC OHC synapse (Ballestero et al., 2011).The present work shows that a knockin mouse with a mutation in the α9α10 nAChR (L9’;T) with increased channel gating (Taranda et al., 2009) greatly prolongs hair cell evoked inhibitory postsynaptic currents (IPSCs). Long-term presynaptic compensatory mechanisms lead to reduced quantum content (IHC wt =1.29 ± 0.21; L9’;T= 0.83 ± 0.12, n=5- 6. OHC wt =0.23 ± 0.04, L9’;T = 0.14 ± 0.02, n=12-15). However, upon high frequency stimulation of MOC-OHC synapses, L9’;T mice exhibited more facilitation leading to greatly prolonged synaptic responses (S2 /S1- 40Hz: wt = 1.37 ± 0.16, L9’;T = 3.47 ± 0.44, n = 6-8, p< 0.05). At the cochlear physiology level, these synaptic changes were matched by a longer time course of efferent MOC suppression of DPOAEs. Thus, the maximal suppres sive effect of electrical shocks (70-s, 200 Hz) at the base of the IVth ventricle was doubled both at 16 (p < 0.01) and 22 kHz (p < 0.05), reached much more slowly (16 kHz: wt = 5.3 ± 1.0 s, L9’;T = 30.8 ± 4.1 s; 22 kHz: wt = 1.5 ± 0.4 s, L9’;T = 44.1 ± 3.1 s) and persisted for a longer time after the shocks for both 16 and 22 kHz in L9’;T mice (> 5 min) as compared to their wt littermates (≤1 s). These results indicate that the properties of the MOC-OHC synapse directly determine the efficacy of the MOC feedback to the cochlea being a main player in the “gain control” of the auditory periphery.
Fil: Vattino, Lucas Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Ballestero, Jimena Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Maison, Stéphane F.. Harvard Medical School; Estados Unidos
Fil: Di Guilmi, Mariano Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Taranda, Julian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Liberman, Charles M.. Harvard Medical School; Estados Unidos
Fil: Fuchs, Paul A.. University Johns Hopkins; Estados Unidos
Fil: Katz, Eleonora. 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 Ciencias Exactas y Naturales; Argentina
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. Instituto de Farmacología; Argentina
41St Annual MidWinter Meeting
San Diego
Estados Unidos
Association for Research in Otolaryngology
description Gain control of the auditory system operates at multiple levels. Cholinergic medial olivocochlear (MOC) fibers that originate in the brainstem and make direct synaptic contacts at the base of the outer hair cells (OHCs) are the final targets of several feedback loops from both the periphery and higher processing cen ters. Efferent activation inhibits somatic electromotil ity of OHCs, an active amplification system within the mammalian cochlea. This is mediated by the activa tion of a calcium permeable α9α10 ionotropic cho linergic nicotinic receptor (nAChR) functionally cou pled to calcium activated SK potassium channels. The strength of cochlear inhibition is driven by the rate of MOC activity and short term facilitation at the MOC OHC synapse (Ballestero et al., 2011).The present work shows that a knockin mouse with a mutation in the α9α10 nAChR (L9’;T) with increased channel gating (Taranda et al., 2009) greatly prolongs hair cell evoked inhibitory postsynaptic currents (IPSCs). Long-term presynaptic compensatory mechanisms lead to reduced quantum content (IHC wt =1.29 ± 0.21; L9’;T= 0.83 ± 0.12, n=5- 6. OHC wt =0.23 ± 0.04, L9’;T = 0.14 ± 0.02, n=12-15). However, upon high frequency stimulation of MOC-OHC synapses, L9’;T mice exhibited more facilitation leading to greatly prolonged synaptic responses (S2 /S1- 40Hz: wt = 1.37 ± 0.16, L9’;T = 3.47 ± 0.44, n = 6-8, p< 0.05). At the cochlear physiology level, these synaptic changes were matched by a longer time course of efferent MOC suppression of DPOAEs. Thus, the maximal suppres sive effect of electrical shocks (70-s, 200 Hz) at the base of the IVth ventricle was doubled both at 16 (p < 0.01) and 22 kHz (p < 0.05), reached much more slowly (16 kHz: wt = 5.3 ± 1.0 s, L9’;T = 30.8 ± 4.1 s; 22 kHz: wt = 1.5 ± 0.4 s, L9’;T = 44.1 ± 3.1 s) and persisted for a longer time after the shocks for both 16 and 22 kHz in L9’;T mice (> 5 min) as compared to their wt littermates (≤1 s). These results indicate that the properties of the MOC-OHC synapse directly determine the efficacy of the MOC feedback to the cochlea being a main player in the “gain control” of the auditory periphery.
publishDate 2018
dc.date.none.fl_str_mv 2018
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
Reunión
Journal
http://purl.org/coar/resource_type/c_5794
info:ar-repo/semantics/documentoDeConferencia
status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/154581
Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochlea; 41St Annual MidWinter Meeting; San Diego; Estados Unidos; 2018; 1-3
0742-3152
CONICET Digital
CONICET
url http://hdl.handle.net/11336/154581
identifier_str_mv Enhanced hair cell postsynaptic responses alter release from presynaptic efferent neurons to prolong inhibition of the cochlea; 41St Annual MidWinter Meeting; San Diego; Estados Unidos; 2018; 1-3
0742-3152
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://aro.org/wp-content/uploads/2020/09/2018_ARO_Abstracts_ALL_PAGES.pdf
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.coverage.none.fl_str_mv Internacional
dc.publisher.none.fl_str_mv Association for Research in Otolaryngology
publisher.none.fl_str_mv Association for Research in Otolaryngology
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
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
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