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dc.contributor.author
Bachman, Julia L.
dc.contributor.author
Kitcher, Siân R.
dc.contributor.author
Vattino, Lucas Gabriel
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dc.contributor.author
Beaulac, Holly J.
dc.contributor.author
Chaves, M. Grace
dc.contributor.author
Hernandez Rivera, Israel
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Katz, Eleonora
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dc.contributor.author
Wedemeyer, Carolina
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dc.contributor.author
Weisz, Catherine J. C.
dc.date.available
2024-07-25T12:40:17Z
dc.date.issued
2024-03
dc.identifier.citation
Bachman, Julia L.; Kitcher, Siân R.; Vattino, Lucas Gabriel; Beaulac, Holly J.; Chaves, M. Grace; et al.; GABAergic synapses between auditory efferent neurons and type II spiral ganglion afferent neurons in the mouse cochlea; Cold Spring Harbor Laboratory Press; BioRxiv; 2024; 3-2024; 1-34
dc.identifier.issn
2692-8205
dc.identifier.uri
http://hdl.handle.net/11336/240852
dc.description.abstract
Cochlear outer hair cells (OHCs) are electromotile and are implicated in mechanisms ofamplification of responses to sound that enhance sound sensitivity and frequency tuning. Theysend information to the brain through glutamatergic synapses onto a small subpopulation ofneurons of the ascending auditory nerve, the type II spiral ganglion neurons (SGNs). The OHCsynapses onto type II SGNs are sparse and weak, suggesting that type II SGNs respond primarilyto loud and possibly damaging levels of sound. OHCs also receive innervation from the brainthrough the medial olivocochlear (MOC) efferent neurons. MOC neurons are cholinergic yetexert an inhibitory effect on auditory function as they are coupled to alpha9/alpha10 nicotinicacetylcholine receptors (nAChRs) on OHCs, which leads to calcium influx that gates SKpotassium channels. The net hyperpolarization exerted by this efferent synapse reduces OHCactivity-evoked electromotility and is implicated in cochlear gain control, protection againstacoustic trauma, and attention. MOC neurons also label for markers of gamma-aminobutyric acid(GABA) and GABA synthesis. GABAB autoreceptor (GABABR) activation by GABA releasedfrom MOC terminals has been demonstrated to reduce ACh release, confirming importantnegative feedback roles for GABA. However, the full complement of GABAergic activity in thecochlea is not currently understood, including the mechanisms that regulate GABA release fromMOC axon terminals, whether GABA diffuses from MOC axon terminals to other postsynapticcells, and the location and function of GABAA receptors (GABAARs). Previous electronmicroscopy studies suggest that MOC neurons form contacts onto several other cell types in thecochlea, but whether these contacts form functional synapses, and what neurotransmitters areemployed, are unknown. Here we use immunohistochemistry, optical neurotransmitter imagingand patch-clamp electrophysiology from hair cells, afferent dendrites, and efferent axons todemonstrate that in addition to presynaptic GABABR autoreceptor activation, MOC efferentaxon terminals release GABA onto type II SGN afferent dendrites with postsynaptic activitymediated by GABAARs. This synapse may have multiple roles including developmentalregulation of cochlear innervation, fine tuning of OHC activity, or providing feedback to thebrain about MOC and OHC activity.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Cold Spring Harbor Laboratory Press
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dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
GABA
dc.subject
TYPE II
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EFFERENTS
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COCHLEA
dc.subject.classification
Bioquímica y Biología Molecular
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
GABAergic synapses between auditory efferent neurons and type II spiral ganglion afferent neurons in the mouse cochlea
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2024-06-04T14:49:14Z
dc.journal.volume
2024
dc.journal.pagination
1-34
dc.journal.pais
Estados Unidos
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dc.description.fil
Fil: Bachman, Julia L.. National Institutes of Health; Estados Unidos
dc.description.fil
Fil: Kitcher, Siân R.. National Institutes of Health; Estados Unidos
dc.description.fil
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
dc.description.fil
Fil: Beaulac, Holly J.. National Institutes of Health; Estados Unidos
dc.description.fil
Fil: Chaves, M. Grace. National Institutes of Health; Estados Unidos. Eaton Peabody Laboratories; Estados Unidos. Harvard Medical School; Estados Unidos
dc.description.fil
Fil: Hernandez Rivera, Israel. National Institutes of Health; Estados Unidos
dc.description.fil
Fil: Katz, Eleonora. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
dc.description.fil
Fil: Wedemeyer, Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
dc.description.fil
Fil: Weisz, Catherine J. C.. National Institutes of Health; Estados Unidos
dc.journal.title
BioRxiv
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.biorxiv.org/content/10.1101/2024.03.28.587185v1.full
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1101/2024.03.28.587185
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