Efferent control of cochlear inner hair cell responses in the guinea‐pig.

Brown, M. Christian; Nuttall, A. L.

doi:10.1113/jphysiol.1984.sp015396

Cited by 173 publications

(78 citation statements)

References 37 publications

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“…This is most likely caused by a decrease in the endocochlear potential, arising from a shunt in current through the OHC when the medial system is activated (Housley and Ashmore, 1991;Blanchet et al, 2000). The reduced endocochlear potential causes hyperpolarization of the inner hair cells and a reduction of the spontaneous neurotransmitter release onto the auditory afferent fibers, reducing spontaneous firing of the afferents (Brown and Nuttall, 1984;Sewell, 1984).…”

Section: Discussionmentioning

confidence: 99%

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Mulders

Seluakumaran²,

Robertson³

2010

Journal of Neuroscience

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Animal models have demonstrated that mild hearing loss caused by acoustic trauma results in spontaneous hyperactivity in the central auditory pathways. This hyperactivity has been hypothesized to be involved in the generation of tinnitus, a phantom auditory sensation. We have recently shown that such hyperactivity, recorded in the inferior colliculus, is still dependent on cochlear neural output for some time after recovery (up to 6 weeks). We have now studied the capacity of an intrinsic efferent system, i.e., the olivocochlear system, to alter hyperactivity. This system is known to modulate cochlear neural output. Anesthetized guinea pigs were exposed to a loud sound and after 2 or 3 weeks of recovery, single-neuron recordings in inferior colliculus were made to confirm hyperactivity. Olivocochlear axons were electrically stimulated and effects on cochlear neural output and on highly spontaneous neurons in inferior colliculus were assessed. Olivocochlear stimulation suppressed spontaneous hyperactivity in the inferior colliculus. This result is in agreement with our earlier finding that hyperactivity can be modulated by altering cochlear neural output. Interestingly, the central suppression was generally much larger and longer lasting than reported previously for primary afferents. Blockade of the intracochlear effects of olivocochlear system activation eliminated some but not all of the effects observed on spontaneous activity, suggesting also a central component to the effects of stimulation. More research is needed to investigate whether these central effects of olivocochlear efferent stimulation are due to central intrinsic circuitry or to coactivation of central efferent collaterals to the cochlear nucleus.

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Section: Discussionmentioning

confidence: 99%

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Mulders

Seluakumaran²,

Robertson³

2010

Journal of Neuroscience

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“…It is well known that the medial efferent system inhibits the auditory nerve responses by reducing the basilar membrane motion [16,17] . Both basilar membrane motion alterations and reductions in neurotransmitter release by the inner hair cells because of efferent inhibition cause both an elevation in ART and a reduction in amplitude with contralateral noise [18] . It has been reported that efferent system functioning can be assessed using the contralateral suppression of acoustic reflexes [9] ; however, no other researchers have attempted to determine the effects of contralateral noise on acoustic reflex latency (ARL) measurements.…”

Section: Introductionmentioning

confidence: 99%

Effect of Contralateral Noise on Acoustic Reflex Latency Measures

Prabhu

Divyashree²,

Neeraja³

et al. 2016

Int Adv Otol

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OBJECTIVE:The present study was conducted to determine the effect of contralateral broadband noise on acoustic reflex latency (ARL). MATERIALS and METHODS:Acoustic reflex latency changes for 10 and 90% on-and off-time acoustic reflexes with contralateral broadband noise were measured in 30 adults with normal hearing. RESULTS:The results of the study demonstrate that there was a latency prolongation for reflex on-time (10 and 90%) and latency reduction for reflex off-time (10 and 90%). This effect was seen for 500, 1000, and 2000 Hz reflex-eliciting signals. The results also showed that there was no effect of gender on latency changes in acoustic reflexes. CONCLUSIONS:Latency changes may explain efferent auditory system mechanisms used for the protection of the cochlea and improvement in speech perception. Thus, contralateral changes of ARL can serve as an additional tool to assess the efferent system functioning.

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“…Lateral olivocochlear (LOC) neurons have cell bodies in or around the lateral superior olive and project to afferent fibers near inner hair cells (Warr and Guinan, 1979;Liberman, 1980;Liberman and Brown, 1986;Brown, 1987;Vetter and Mugnaini, 1992;Maison et al, 2003). Cholinergic MOC endings in the cochlea exert their effects by means of a nicotinic receptor (Vetter et al, 1999;Elgoyhen et al, 2001Elgoyhen et al, , 2003 that influences outer hair cell function and alters cochlear responses (Wiederhold and Kiang, 1970;Mountain, 1980;Siegel and Kim, 1982;Brown and Nuttall, 1984). For instance, activation of MOC neurons alters distortion product otoacoustic emissions (DPOAEs), causing rapid amplitude changes in the first several hundred milliseconds after primary-tone onset (Liberman et al, 1996;Kujawa and Liberman, 2001).…”

Section: Introductionmentioning

confidence: 99%

Medial olivocochlear reflex interneurons are located in the posteroventral cochlear nucleus: A kainic acid lesion study in guinea pigs

Venecia

Liberman

Guinan

et al. 2005

J of Comparative Neurology

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The medial olivocochlear (MOC) reflex arc is probably a three-neuron pathway consisting of type I spiral ganglion neurons, reflex interneurons in the cochlear nucleus, and MOC neurons that project to the outer hair cells of the cochlea. We investigated the identity of MOC reflex interneurons in the cochlear nucleus by assaying their regional distribution using focal injections of kainic acid. Our reflex metric was the amount of change in the distortion product otoacoustic emission (at 2f 1 -f 2 ) just after onset of the primary tones. This metric for MOC reflex strength has been shown to depend on an intact reflex pathway. Lesions involving the posteroventral cochlear nucleus (PVCN), but not the other subdivisions, produced long-term decreases in MOC reflex strength. The degree of cell loss within the dorsal part of the PVCN was a predictor of whether the lesion affected MOC reflex strength. We suggest that multipolar cells within the PVCN have the distribution and response characteristics appropriate to be the MOC reflex interneurons. Keywordshearing; outer hair cell; otoacoustic emission; superior oliveThe auditory system contains several descending pathways (Spangler and Warr, 1991), of which the best-studied is the olivocochlear (OC) efferents. OC neurons reside in the superior olivary complex and project to the cochlea (Fig. 1). The OC system is divided into two subsystems (reviewed by Warr, 1992;. Medial olivocochlear (MOC) neurons have cell bodies in the medial part of the superior olivary complex and project to outer hair cells. Lateral olivocochlear (LOC) neurons have cell bodies in or around the lateral superior olive and project to afferent fibers near inner hair cells (Warr and Guinan, 1979;Liberman, 1980;Liberman and Brown, 1986;Brown, 1987;Vetter and Mugnaini, 1992;Maison et al., 2003). Cholinergic MOC endings in the cochlea exert their effects by means of a nicotinic receptor (Vetter et al., 1999;Elgoyhen et al., 2001Elgoyhen et al., , 2003 that influences outer hair cell function and alters cochlear responses (Wiederhold and Kiang, 1970;Mountain, 1980;Siegel and Kim, 1982;Brown and Nuttall, 1984). For instance, activation of MOC neurons alters distortion product otoacoustic emissions (DPOAEs), causing rapid amplitude changes in the first several hundred milliseconds after primary-tone onset (Liberman et al., 1996;Kujawa and Liberman, 2001). The functional role of this sound-evoked feedback system may include adjusting *Correspondence to: M. Christian Brown, Eaton-Peabody Laboratory, Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, MA 02114. E-mail: mcb@epl.meei.harvard.edu. Grant sponsor: National Institute on Deafness and Other Communication Disorders; Grant number: RO1 DC 01089; Grant number: RO1 DC 00188; Grant number: P30 DC05209; Grant number: T32 DC00020-11; Grant sponsor: Triological Society. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript cochlear gain, reducing effects of masking noise, and protecting the ear from acous...

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Efferent control of cochlear inner hair cell responses in the guinea‐pig.

Cited by 173 publications

References 37 publications

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Effect of Contralateral Noise on Acoustic Reflex Latency Measures

Medial olivocochlear reflex interneurons are located in the posteroventral cochlear nucleus: A kainic acid lesion study in guinea pigs

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