Bilateral Dorsal Cochlear Nucleus Lesions Prevent Acoustic-Trauma Induced Tinnitus in an Animal Model

Animal experiments suggest that chronic tinnitus (“ringing in the ears”) may result from processes that overcompensate for lost afferent input. Abnormally elevated spontaneous neural activity has been found in the dorsal cochlear nucleus (DCN) of animals with psychophysical evidence of tinnitus. How...

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Bibliographic Details
Published in:	Journal of the Association for Research in Otolaryngology Vol. 13; no. 1; pp. 55 - 66
Main Authors:	Brozoski, Thomas Jeffrey, Wisner, Kurt W., Sybert, Lauren T., Bauer, Carol A.
Format:	Journal Article
Language:	English
Published:	New York Springer-Verlag 01-02-2012 Springer Nature B.V
Subjects:	Acoustic Stimulation - methods Action Potentials - physiology Animals Auditory Threshold - physiology Catheter Ablation Cochlear Nucleus - pathology Cochlear Nucleus - physiopathology Denervation - methods Disease Models, Animal Evoked Potentials, Auditory, Brain Stem - physiology Functional Laterality - physiology Male Medicine Medicine & Public Health Neurobiology Neurosciences Noise - adverse effects Otorhinolaryngology Rats Rats, Long-Evans Tinnitus Tinnitus - pathology Tinnitus - physiopathology Tinnitus - prevention & control hearing disorder auditory brainstem trigger zone prevention
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Summary:	Animal experiments suggest that chronic tinnitus (“ringing in the ears”) may result from processes that overcompensate for lost afferent input. Abnormally elevated spontaneous neural activity has been found in the dorsal cochlear nucleus (DCN) of animals with psychophysical evidence of tinnitus. However, it has also been reported that DCN ablation fails to reduce established tinnitus. Since other auditory areas have been implicated in tinnitus, the role of the DCN is unresolved. The apparently conflicting electrophysiological and lesion data can be reconciled if the DCN serves as a necessary trigger zone rather than a chronic generator of tinnitus. The present experiment used lesion procedures identical to those that failed to decrease pre-existing tinnitus. The exception was that lesions were done prior to tinnitus induction. Young adult rats were trained and tested using a psychophysical procedure shown to detect tinnitus. Tinnitus was induced by a single unilateral high-level noise exposure. Consistent with the trigger hypothesis, bilateral dorsal DCN lesions made before high-level noise exposure prevented the development of tinnitus. A protective effect stemming from disruption of the afferent pathway could not explain the outcome because unilateral lesions ipsilateral to the noise exposure did not prevent tinnitus and unilateral lesions contralateral to the noise exposure actually exacerbated the tinnitus. The DCN trigger mechanism may involve plastic circuits that, through loss of inhibition, or upregulation of excitation, increase spontaneous neural output to rostral areas such as the inferior colliculus. The increased drive could produce persistent pathological changes in the rostral areas, such as high-frequency bursting and decreased interspike variance, that comprise the chronic tinnitus signal.
ISSN:	1525-3961 1438-7573
DOI:	10.1007/s10162-011-0290-3