Organization of Olivocochlear Neurons in the Cat Studied with the Retrograde Tracer Cholera Toxin-B

Warr, W. Bruce; Boche, Jo Beck; Ye, Ye; Kim, Duck O.

doi:10.1007/s10162-002-2046-6

Cited by 20 publications

(19 citation statements)

References 28 publications

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“…Since the ␣9 and ␣10 subunits of the nicotinic acetylcholine receptor are specific for the medial system (Vetter et al, 1999;Lustig, 2006), the blockade by strychnine perfusion would not alter any lateral effects on primary afferents. However, activation of the lateral system by electrical stimulation at the floor of the IVth ventricle has never been confirmed and is considered unlikely in view of the unmyelinated axons of the lateral system (Brown, 1987;Warr et al, 2002).…”

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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“…Although the number of TH-positive neurons in the LSO is small, it is well known that at least one class of LSO neurons (termed shell neurons, in the rat) travel long distances within the cochlea, project with numerous bifurcations, and end with many terminal boutons. These neurons have been well described in the guinea pig (Brown 1987), rat (Vetter andMugnaini 1992;Warr et al 1997;Warr andBoche 2003), chinchilla (Azeredo et al 1999), and hamster (Sanchez-Gonzalez et al 2003), and may exist in the cat as well (Warr et al 2002). Although it has not been definitively shown that TH-positive neurons in the cochlea fall within this bifurcating class of neurons, Niu et al (2004) argue that the dense TH staining they previously observed in the cochlea (Niu and Canlon 2002) is clearly consistent with bifurcating distribution given the small number of TH-positive neurons in the LSO.…”

Section: Figmentioning

confidence: 94%

Disruption of Lateral Olivocochlear Neurons via a Dopaminergic Neurotoxin Depresses Sound-Evoked Auditory Nerve Activity

Prell

Hälsey

Hughes

et al. 2005

JARO

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We applied the dopaminergic (DA) neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the guinea pig cochlear perilymph. Immunolabeling of lateral olivocochlear (LOC) neurons using antibodies against synaptophysin was reduced after the MPTP treatment. In contrast, labeling of the medial olivocochlear innervation remained intact. As after brainstem lesions of the lateral superior olive (LSO), the site of origin of the LOC neurons, the main effect of disrupting LOC innervation of the cochlea via MPTP was a depression of the amplitude of the compound action potential (CAP). CAP amplitude depression was similar to that produced by LSO lesions. Latency of the N1 component of the CAP, and distortion product otoacoustic emission amplitude and adaptation were unchanged by the MPTP treatment. This technique for selectively lesioning descending LOC efferents provides a new opportunity for examining LOC modulation of afferent activity and behavioral measures of perception.

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“…MOC dendrites are extensive (Adams 1983;White and Warr 1983;Osen et al 1984;Vetter and Mugnaini 1992;Warr et al 2002;Sánchez-González et al 2003). The remaining panels show averaged staining for two knockouts and two wild types in B medial edge, C dorsal edge, D lateral edge, and E core.…”

Section: Oc Somata and Dendritesmentioning

confidence: 99%

Olivocochlear Neuron Central Anatomy Is Normal in α9 Knockout Mice

Brown

Vetter

2008

JARO

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Olivocochlear (OC) neurons were studied in a transgenic mouse with deletion of the α9 nicotinic acetylcholine receptor subunit. In this α9 knockout mouse, the peripheral effects of OC stimulation are lacking and the peripheral terminals of OC neurons under outer hair cells have abnormal morphology. To account for this mouse's apparently normal hearing, it has been proposed to have central compensation via collateral branches to the cochlear nucleus. We tested this idea by staining OC neurons for acetylcholinesterase and examining their morphology in knockout mice, wild-type mice of the same background strain, and CBA/CaJ mice. Knockout mice had normal OC systems in terms of numbers of OC neurons, dendritic patterns, and numbers of branches to the cochlear nucleus. The branch terminations were mainly to edge regions and to a lesser extent the core of the cochlear nucleus, and were similar among the strains in terms of the distribution and staining density. These data demonstrate that there are no obvious changes in the central morphology of the OC neurons in α9 knockout mice and make less attractive the idea that there is central compensation for deletion of the peripheral receptor in these mice.

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Organization of Olivocochlear Neurons in the Cat Studied with the Retrograde Tracer Cholera Toxin-B

Cited by 20 publications

References 28 publications

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Disruption of Lateral Olivocochlear Neurons via a Dopaminergic Neurotoxin Depresses Sound-Evoked Auditory Nerve Activity

Olivocochlear Neuron Central Anatomy Is Normal in α9 Knockout Mice

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