Noradrenergic and serotonergic projections to the superior olive: potential for modulation of olivocochlear neurons

Woods, Charles I.; Azeredo, William J.

doi:10.1016/s0006-8993(99)01541-3

Cited by 44 publications

(37 citation statements)

References 44 publications

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“…6B) is consistent with studies showing (1) noradrenergic terminals (from the locus coeruleus) on the cell bodies of medial olivocochlear neurons (Mulders and Robertson 2005a;Thompson and Schofield 2000;Woods and Azeredo 1999) and (2) largely excitatory effects of catecholamines on olivocochlear cells in slice preparations (Wang and Robertson 1997). In our olivocochlear assay, the size of efferent effects, i.e., the change in DPOAE amplitudes, is proportional to the change in discharge rates in olivocochlear fibers elicited by the shocks.…”

Section: Adrenergic Signaling and Vulnerability To Acoustic Injurysupporting

confidence: 90%

“…Pharmacological evidence for adrenergic modulation of K + secretion in the stria via β 1 receptors has further strengthened the idea that circulating, or locally synthesized, catecholamines may also be important in cochlear function and dysfunction (Schimanski et al 2001). Secondly, in addition to direct inner ear effects via adrenergic projections from the peripheral sympathetic chain to the cochlea, central adrenergic projections from the locus coeruleus to the olivocochlear (OC) efferent system (Mulders and Robertson 2005a, b;Woods and Azeredo 1999) may also modulate cochlear function, or responses to stress, indirectly by modulating the strength of this soundevoked feedback pathway. Indeed, the peculiar phenomenon whereby destruction of the contralateral cochlea protects the ipsilateral ear from subsequent acoustic overstimulation (Rajan and Johnstone 1989) could arise from "stress"-induced activation of the olivocochlear reflex via its central adrenergic inputs.…”

Section: Introductionmentioning

confidence: 99%

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Mice Lacking Adrenergic Signaling Have Normal Cochlear Responses and Normal Resistance to Acoustic Injury but Enhanced Susceptibility to Middle-Ear Infection

Maison

Larsen

et al. 2010

JARO

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The vasculature and neurons of the inner ear receive adrenergic innervation from the cervical sympathetic chain, and adrenergic receptors may be expressed by cells of the organ of Corti and stria vascularis, despite a lack of direct sympathetic innervation. To assess the functional role of adrenergic signaling in the auditory periphery, we studied mice with targeted deletion of the gene for dopamine β-hydroxylase (DBH), which catalyzes the conversion of dopamine to noradrenaline; thus, these mutant mice have no measurable adrenaline or noradrenaline. Dbh −/− mice were more susceptible to spontaneous middle-ear infection than their control littermates, consistent with a role for sympathetics in systemic and/or local immune response. At 6-8 weeks of age, cochlear thresholds and suprathreshold responses assessed by auditory brainstem responses and distortion product otoacoustic emissions, as well as light-microscopic morphology, were indistinguishable from controls, if ears with conductive hearing loss were eliminated. Dbh −/− mice were no more susceptible to acoustic injury than controls, despite prior reports that sympathectomy reduces noise damage. Dbh −/− mice showed enhancement of shock-evoked olivocochlear suppression of cochlear responses, which may arise from the loss of adrenergic inputs to olivocochlear neurons in the brainstem. However, adrenergic modulation of olivocochlear efferents does not mediate the protective effect of contralateral cochlear destruction on ipsilateral response to acoustic overexposure.

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Section: Adrenergic Signaling and Vulnerability To Acoustic Injurysupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Mice Lacking Adrenergic Signaling Have Normal Cochlear Responses and Normal Resistance to Acoustic Injury but Enhanced Susceptibility to Middle-Ear Infection

Maison

Larsen

et al. 2010

JARO

View full text Add to dashboard Cite

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“…Also, we found early labeling of vestibular efferent neurons, which are scattered in the dorsal pontine region (Strutz 1982) and which may have previously been counted as raphe labeling. Immunohistochemical studies show that noradrenaline-containing and serotoninergic varicosities contact both MOC and LOC neurons (Thompson and Thompson 1995;Woods and Azeredo 1999;Mulders and Robertson 2000b). The source of the serotoninergic innervation is probably the dorsal raphe and reticular neurons, and the source of the noradrenergic innervation is the locus coeruleus in the rat (Mulders and Robertson 2001) and the subcoerulean nucleus in the guinea pig (Mulders and Robertson 2005b).…”

Section: Inputs From the Cortex And Other Centersmentioning

confidence: 99%

Identification of Inputs to Olivocochlear Neurons Using Transneuronal Labeling with Pseudorabies Virus (PRV)

Brown

Mukerji

Drottar

et al. 2013

JARO

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Olivocochlear (OC) neurons respond to sound and provide descending input that controls processing in the cochlea. The identities of neurons in the pathways providing inputs to OC neurons are incompletely understood. To explore these pathways, the retrograde transneuronal tracer pseudorabies virus (Bartha strain, expressing green fluorescent protein) was used to label OC neurons and their inputs in guinea pigs. Labeling of OC neurons began 1 day after injection into the cochlea. On day 2 (and for longer survival times), transneuronal labeling spread to the cochlear nucleus, inferior colliculus, and other brainstem areas. There was a correlation between the numbers of these transneuronally labeled neurons and the number of labeled medial (M) OC neurons, suggesting that the spread of labeling proceeds mainly via synapses on MOC neurons. In the cochlear nucleus, the transneuronally labeled neurons were multipolar cells including the subtype known as planar cells. In the central nucleus of the inferior colliculus, transneuronally labeled neurons were of two principal types: neurons with disc-shaped dendritic fields and neurons with dendrites in a stellate pattern. Transneuronal labeling was also observed in pyramidal cells in the auditory cortex and in centers not typically associated with the auditory pathway such as the pontine reticular formation, subcoerulean nucleus, and the pontine dorsal raphe. These data provide information on the identity of neurons providing input to OC neurons, which are located in auditory as well as non-auditory centers.

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“…Also serotonin often coexists with GABA in the inferior colliculus and both acting in the suppression of fearful and aversive behavior 41 . Furthermore, descending serotonergic projections from Raphe nucleus may also modulate superior olive neurons 42 , the generators of ABR wave III 43 . These results are consistent with the results of Shulman & Kisiel 44 .…”

Section: Electrophysiological Recordings Associated With Tinnitus Rimentioning

confidence: 99%

Alterations in early auditory evoked potentials and brainstem transmission time associated with tinnitus residual inhibition induced by auditory electrical stimulation

Mahmoudian¹,

Lenarz²,

Esser³

et al. 2013

The International Tinnitus Journal

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Noradrenergic and serotonergic projections to the superior olive: potential for modulation of olivocochlear neurons

Cited by 44 publications

References 44 publications

Mice Lacking Adrenergic Signaling Have Normal Cochlear Responses and Normal Resistance to Acoustic Injury but Enhanced Susceptibility to Middle-Ear Infection

Mice Lacking Adrenergic Signaling Have Normal Cochlear Responses and Normal Resistance to Acoustic Injury but Enhanced Susceptibility to Middle-Ear Infection

Identification of Inputs to Olivocochlear Neurons Using Transneuronal Labeling with Pseudorabies Virus (PRV)

Alterations in early auditory evoked potentials and brainstem transmission time associated with tinnitus residual inhibition induced by auditory electrical stimulation

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