Afferent innervation of outer and inner hair cells is normal in neonatally de-efferented cats

Liberman, M. Charles; O'Grady, Daniel F.; Dodds, Leslie W.; McGee, JoAnn; Walsh, Edward J.

doi:10.1002/1096-9861(20000717)423:1<132::aid-cne11>3.0.co;2-7

Cited by 22 publications

(11 citation statements)

References 48 publications

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“…This change cannot be accounted for based on the weight of the animals because weight did not differ significantly between control and α9KO mice (P50 control: 21.5 ± 0.8 g, P50 α9KO: 21.8 ± 0.8 g; p = 0.80, Student's t- test). In addition, cochlear compound action potential (CAP) threshold sensitivity is unchanged in α9KO mice (Vetter et al, 1999; He et al, 2004), and chronic de-efferentation does not affect afferent innervation of either IHCs or OHCs (Liberman et al, 2000). Thus, it is unlikely that changes in the cochlea or in auditory nerve activity are responsible for the reduced ASR amplitudes in α9KO mice.…”

Section: Resultsmentioning

confidence: 99%

Mice Lacking the Alpha9 Subunit of the Nicotinic Acetylcholine Receptor Exhibit Deficits in Frequency Difference Limens and Sound Localization

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Lauer

Kandler

2017

Front. Cell. Neurosci.

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Sound processing in the cochlea is modulated by cholinergic efferent axons arising from medial olivocochlear neurons in the brainstem. These axons contact outer hair cells in the mature cochlea and inner hair cells during development and activate nicotinic acetylcholine receptors composed of α9 and α10 subunits. The α9 subunit is necessary for mediating the effects of acetylcholine on hair cells as genetic deletion of the α9 subunit results in functional cholinergic de-efferentation of the cochlea. Cholinergic modulation of spontaneous cochlear activity before hearing onset is important for the maturation of central auditory circuits. In α9KO mice, the developmental refinement of inhibitory afferents to the lateral superior olive is disturbed, resulting in decreased tonotopic organization of this sound localization nucleus. In this study, we used behavioral tests to investigate whether the circuit anomalies in α9KO mice correlate with sound localization or sound frequency processing. Using a conditioned lick suppression task to measure sound localization, we found that three out of four α9KO mice showed impaired minimum audible angles. Using a prepulse inhibition of the acoustic startle response paradigm, we found that the ability of α9KO mice to detect sound frequency changes was impaired, whereas their ability to detect sound intensity changes was not. These results demonstrate that cholinergic, nicotinic α9 subunit mediated transmission in the developing cochlear plays an important role in the maturation of hearing.

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Section: Resultsmentioning

confidence: 99%

Mice Lacking the Alpha9 Subunit of the Nicotinic Acetylcholine Receptor Exhibit Deficits in Frequency Difference Limens and Sound Localization

Clause

Lauer

Kandler

2017

Front. Cell. Neurosci.

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“…Severing the efferent supply of newborn cats altered afferent response properties (Walsh et al, 1998) but not cochlear afferent innervation, (Liberman et al, 2000) although previous efforts did show elevated afferent innervation to OHCs (Pujol and Carlier, 1982). While potentially revealing, surgical ablation presents substantial experimental challenges.…”

Section: Effect Of Altering Moc Efferent Function or Innervationmentioning

confidence: 90%

Modulation of hair cell efferents

Wersinger

Fuchs

2011

Hearing Research

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Outer hair cells (OHCs) amplify the sound-evoked motion of the basilar membrane to enhance acoustic sensitivity and frequency selectivity. Medial olivocochlear (MOC) efferents inhibit OHCs to reduce the sound-evoked response of cochlear afferent neurons. OHC inhibition occurs through the activation of postsynaptic α9α10 nicotinic receptors tightly coupled to calcium-dependent SK2 channels that hyperpolarize the hair cell. MOC neurons are cholinergic but a number of other neurotransmitters and neuromodulators have been proposed to participate in efferent transmission, with emerging evidence for both pre-and postsynaptic effects. Cochlear inhibition in vivo is maximized by repetitive activation of the efferents, reflecting facilitation and summation of transmitter release onto outer hair cells. This review summarizes recent studies on cellular and molecular mechanisms of cholinergic inhibition and the regulation of those molecular components, in particular the involvement of intracellular calcium. Facilitation at the efferent synapse is compared in a variety of animals, as well as other possible mechanisms of modulation of ACh release. These results suggest that short-term plasticity contributes to effective cholinergic inhibition of hair cells.

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“…However, we have previously described that ChAT immunolabelling is absent under the IHCs and OHCs in the mid-turn mouse cochlea until P3 [12], and no significant TMRD labelling of the efferent fibres occurred until P6, by which time the transient type I afferent synapses were retracting. Moreover, efferent terminals are not required for the normal development of cochlear afferent innervation [51]. Therefore the transient ribbon synapses formed on OHCs between P0 and P3 are unlikely to reflect the formation of efferent synapses.…”

Section: Discussionmentioning

confidence: 99%

Synaptic profiles during neurite extension, refinement and retraction in the developing cochlea

et al. 2012

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BackgroundDuring development, excess synapses form between the central and peripheral nervous systems that are then eliminated to achieve correct connectivity. In the peripheral auditory system, the developing type I spiral ganglion afferent fibres undergo a dramatic re-organisation, initially forming connections with both sensory inner hair cells (IHCs) and outer hair cells (OHCs). The OHC connections are then selectively eliminated, leaving sparse innervation by type II afferent fibres, whilst the type I afferent synapses with IHCs are consolidated.ResultsWe examined the molecular makeup of the synaptic contacts formed onto the IHCs and OHCs during this period of afferent fibre remodelling. We observed that presynaptic ribbons initially form at all the afferent neurite contacts, i.e. not only at the expected developing IHC-type I fibre synapses but also at OHCs where type I fibres temporarily contact. Moreover, the transient contacts forming onto OHCs possess a broad set of pre- and postsynaptic proteins, suggesting that functional synaptic connections are formed prior to the removal of type I fibre innervation. AMPA-type glutamate receptor subunits were transiently observed at the base of the OHCs, with their downregulation occurring in parallel with the withdrawal of type I fibres, dispersal of presynaptic ribbons, and downregulation of the anchoring proteins Bassoon and Shank. Conversely, at developing type I afferent IHC synapses, the presence of pre- and postsynaptic scaffold proteins was maintained, with differential plasticity in AMPA receptor subunits observed and AMPA receptor subunit composition changing around hearing onset.ConclusionsOverall our data show a differential balance in the patterns of synaptic proteins at developing afferent IHC versus OHC synapses that likely reflect their stable versus transient fates.

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Afferent innervation of outer and inner hair cells is normal in neonatally de-efferented cats

Cited by 22 publications

References 48 publications

Mice Lacking the Alpha9 Subunit of the Nicotinic Acetylcholine Receptor Exhibit Deficits in Frequency Difference Limens and Sound Localization

Mice Lacking the Alpha9 Subunit of the Nicotinic Acetylcholine Receptor Exhibit Deficits in Frequency Difference Limens and Sound Localization

Modulation of hair cell efferents

Synaptic profiles during neurite extension, refinement and retraction in the developing cochlea

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