Short-term synaptic plasticity regulates the level of olivocochlear inhibition to auditory hair cells

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In the mammalian inner ear, the gain control of auditory inputs is exerted by medial olivocochlear (MOC) neurons that innervate cochlear outer hair cells (OHCs). OHCs mechanically amplify the incoming sound waves by virtue of their electromotile properties while the MOC system reduces the gain of au...

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Autores principales:	Ballestero, J., de San Martín, J.Z., Goutman, J., Elgoyhen, A.B., Fuchs, P.A., Katz, E.
Formato:	Artículo publishedVersion
Lenguaje:	Inglés
Publicado:	2011
Materias:	alpha9alpha10 nicotinic acetylcholine receptor calcium activated potassium channel nicotinic receptor SK2 channel unclassified drug animal tissue article brain nerve cell cochlea controlled study electrostimulation facilitation female hair cell inhibitory postsynaptic potential male medial olivocochlear neuron mouse nerve cell plasticity neurotransmitter release newborn nonhuman presynaptic facilitation priority journal synaptic transmission temporal summation Acoustic Stimulation Animals Animals, Newborn Biophysics Chelating Agents Cochlea Cochlear Nerve Egtazic Acid Electric Stimulation Female Glycine Agents Hair Cells, Auditory Indoles Inhibitory Postsynaptic Potentials Male Mice Mice, Inbred BALB C Neural Inhibition Patch-Clamp Techniques Peptides Serotonin Antagonists Sodium Channel Blockers Strychnine Synapses Temperature Tetrodotoxin Time Factors
Acceso en línea:	http://hdl.handle.net/20.500.12110/paper_02706474_v31_n41_p14763_Ballestero
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

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spelling	paperaa:paper_02706474_v31_n41_p14763_Ballestero2023-06-12T16:47:16Z Short-term synaptic plasticity regulates the level of olivocochlear inhibition to auditory hair cells J. Neurosci. 2011;31(41):14763-14774 Ballestero, J. de San Martín, J.Z. Goutman, J. Elgoyhen, A.B. Fuchs, P.A. Katz, E. alpha9alpha10 nicotinic acetylcholine receptor calcium activated potassium channel nicotinic receptor SK2 channel unclassified drug animal tissue article brain nerve cell cochlea controlled study electrostimulation facilitation female hair cell inhibitory postsynaptic potential male medial olivocochlear neuron mouse nerve cell plasticity neurotransmitter release newborn nonhuman presynaptic facilitation priority journal synaptic transmission temporal summation Acoustic Stimulation Animals Animals, Newborn Biophysics Chelating Agents Cochlea Cochlear Nerve Egtazic Acid Electric Stimulation Female Glycine Agents Hair Cells, Auditory Indoles Inhibitory Postsynaptic Potentials Male Mice Mice, Inbred BALB C Neural Inhibition Patch-Clamp Techniques Peptides Serotonin Antagonists Sodium Channel Blockers Strychnine Synapses Temperature Tetrodotoxin Time Factors In the mammalian inner ear, the gain control of auditory inputs is exerted by medial olivocochlear (MOC) neurons that innervate cochlear outer hair cells (OHCs). OHCs mechanically amplify the incoming sound waves by virtue of their electromotile properties while the MOC system reduces the gain of auditory inputs by inhibiting OHC function. How this process is orchestrated at the synaptic level remains unknown. In the present study, MOC firing was evoked by electrical stimulation in an isolated mouse cochlear preparation, while OHCs postsynaptic responses were monitored by whole-cell recordings. These recordings confirmed that electrically evoked IPSCs (eIPSCs) are mediated solely by α9β10 nAChRs functionally coupled to calcium-activated SK2 channels. Synaptic release occurred with low probability when MOC-OHC synapses were stimulated at 1 Hz. However, as the stimulation frequency was raised, the reliability of release increased due to presynaptic facilitation. In addition, the relatively slow decay of eIPSCs gave rise to temporal summation at stimulation frequencies >10 Hz. The combined effect of facilitation and summation resulted in a frequency-dependent increase in the average amplitude of inhibitory currents in OHCs. Thus, we have demonstrated that short-term plasticity is responsible for shaping MOC inhibition and, therefore, encodes the transfer function from efferent firing frequency to the gain of the cochlear amplifier. © 2011 the authors. Fil:Ballestero, J. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Goutman, J. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Katz, E. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2011 info:eu-repo/semantics/article info:ar-repo/semantics/artículo info:eu-repo/semantics/publishedVersion application/pdf eng info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_02706474_v31_n41_p14763_Ballestero
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
language	Inglés
orig_language_str_mv	eng
topic	alpha9alpha10 nicotinic acetylcholine receptor calcium activated potassium channel nicotinic receptor SK2 channel unclassified drug animal tissue article brain nerve cell cochlea controlled study electrostimulation facilitation female hair cell inhibitory postsynaptic potential male medial olivocochlear neuron mouse nerve cell plasticity neurotransmitter release newborn nonhuman presynaptic facilitation priority journal synaptic transmission temporal summation Acoustic Stimulation Animals Animals, Newborn Biophysics Chelating Agents Cochlea Cochlear Nerve Egtazic Acid Electric Stimulation Female Glycine Agents Hair Cells, Auditory Indoles Inhibitory Postsynaptic Potentials Male Mice Mice, Inbred BALB C Neural Inhibition Patch-Clamp Techniques Peptides Serotonin Antagonists Sodium Channel Blockers Strychnine Synapses Temperature Tetrodotoxin Time Factors
spellingShingle	alpha9alpha10 nicotinic acetylcholine receptor calcium activated potassium channel nicotinic receptor SK2 channel unclassified drug animal tissue article brain nerve cell cochlea controlled study electrostimulation facilitation female hair cell inhibitory postsynaptic potential male medial olivocochlear neuron mouse nerve cell plasticity neurotransmitter release newborn nonhuman presynaptic facilitation priority journal synaptic transmission temporal summation Acoustic Stimulation Animals Animals, Newborn Biophysics Chelating Agents Cochlea Cochlear Nerve Egtazic Acid Electric Stimulation Female Glycine Agents Hair Cells, Auditory Indoles Inhibitory Postsynaptic Potentials Male Mice Mice, Inbred BALB C Neural Inhibition Patch-Clamp Techniques Peptides Serotonin Antagonists Sodium Channel Blockers Strychnine Synapses Temperature Tetrodotoxin Time Factors Ballestero, J. de San Martín, J.Z. Goutman, J. Elgoyhen, A.B. Fuchs, P.A. Katz, E. Short-term synaptic plasticity regulates the level of olivocochlear inhibition to auditory hair cells
topic_facet	alpha9alpha10 nicotinic acetylcholine receptor calcium activated potassium channel nicotinic receptor SK2 channel unclassified drug animal tissue article brain nerve cell cochlea controlled study electrostimulation facilitation female hair cell inhibitory postsynaptic potential male medial olivocochlear neuron mouse nerve cell plasticity neurotransmitter release newborn nonhuman presynaptic facilitation priority journal synaptic transmission temporal summation Acoustic Stimulation Animals Animals, Newborn Biophysics Chelating Agents Cochlea Cochlear Nerve Egtazic Acid Electric Stimulation Female Glycine Agents Hair Cells, Auditory Indoles Inhibitory Postsynaptic Potentials Male Mice Mice, Inbred BALB C Neural Inhibition Patch-Clamp Techniques Peptides Serotonin Antagonists Sodium Channel Blockers Strychnine Synapses Temperature Tetrodotoxin Time Factors
description	In the mammalian inner ear, the gain control of auditory inputs is exerted by medial olivocochlear (MOC) neurons that innervate cochlear outer hair cells (OHCs). OHCs mechanically amplify the incoming sound waves by virtue of their electromotile properties while the MOC system reduces the gain of auditory inputs by inhibiting OHC function. How this process is orchestrated at the synaptic level remains unknown. In the present study, MOC firing was evoked by electrical stimulation in an isolated mouse cochlear preparation, while OHCs postsynaptic responses were monitored by whole-cell recordings. These recordings confirmed that electrically evoked IPSCs (eIPSCs) are mediated solely by α9β10 nAChRs functionally coupled to calcium-activated SK2 channels. Synaptic release occurred with low probability when MOC-OHC synapses were stimulated at 1 Hz. However, as the stimulation frequency was raised, the reliability of release increased due to presynaptic facilitation. In addition, the relatively slow decay of eIPSCs gave rise to temporal summation at stimulation frequencies >10 Hz. The combined effect of facilitation and summation resulted in a frequency-dependent increase in the average amplitude of inhibitory currents in OHCs. Thus, we have demonstrated that short-term plasticity is responsible for shaping MOC inhibition and, therefore, encodes the transfer function from efferent firing frequency to the gain of the cochlear amplifier. © 2011 the authors.
format	Artículo Artículo publishedVersion
author	Ballestero, J. de San Martín, J.Z. Goutman, J. Elgoyhen, A.B. Fuchs, P.A. Katz, E.
author_facet	Ballestero, J. de San Martín, J.Z. Goutman, J. Elgoyhen, A.B. Fuchs, P.A. Katz, E.
author_sort	Ballestero, J.
title	Short-term synaptic plasticity regulates the level of olivocochlear inhibition to auditory hair cells
title_short	Short-term synaptic plasticity regulates the level of olivocochlear inhibition to auditory hair cells
title_full	Short-term synaptic plasticity regulates the level of olivocochlear inhibition to auditory hair cells
title_fullStr	Short-term synaptic plasticity regulates the level of olivocochlear inhibition to auditory hair cells
title_full_unstemmed	Short-term synaptic plasticity regulates the level of olivocochlear inhibition to auditory hair cells
title_sort	short-term synaptic plasticity regulates the level of olivocochlear inhibition to auditory hair cells
publishDate	2011
url	http://hdl.handle.net/20.500.12110/paper_02706474_v31_n41_p14763_Ballestero
work_keys_str_mv	AT ballesteroj shorttermsynapticplasticityregulatesthelevelofolivocochlearinhibitiontoauditoryhaircells AT desanmartinjz shorttermsynapticplasticityregulatesthelevelofolivocochlearinhibitiontoauditoryhaircells AT goutmanj shorttermsynapticplasticityregulatesthelevelofolivocochlearinhibitiontoauditoryhaircells AT elgoyhenab shorttermsynapticplasticityregulatesthelevelofolivocochlearinhibitiontoauditoryhaircells AT fuchspa shorttermsynapticplasticityregulatesthelevelofolivocochlearinhibitiontoauditoryhaircells AT katze shorttermsynapticplasticityregulatesthelevelofolivocochlearinhibitiontoauditoryhaircells
_version_	1769810334806179840

Short-term synaptic plasticity regulates the level of olivocochlear inhibition to auditory hair cells

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