Efferent pathways modulate hyperactivity in inferior colliculus

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 suc...

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Main Authors: Mulders, W.H.A.M., Seluakumaran, K., Robertson, D.
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Published: Soc Neuroscience 2010
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Online Access:http://eprints.um.edu.my/12687/
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spelling my.um.eprints.126872015-02-11T06:34:25Z http://eprints.um.edu.my/12687/ Efferent pathways modulate hyperactivity in inferior colliculus Mulders, W.H.A.M. Seluakumaran, K. Robertson, D. Q Science (General) 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).Wehave 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. Soc Neuroscience 2010 Article PeerReviewed Mulders, W.H.A.M. and Seluakumaran, K. and Robertson, D. (2010) Efferent pathways modulate hyperactivity in inferior colliculus. Journal of Neuroscience, 30 (28). pp. 9578-9587.
institution Universiti Malaya
building UM Library
collection Institutional Repository
continent Asia
country Malaysia
content_provider Universiti Malaya
content_source UM Research Repository
url_provider http://eprints.um.edu.my/
topic Q Science (General)
spellingShingle Q Science (General)
Mulders, W.H.A.M.
Seluakumaran, K.
Robertson, D.
Efferent pathways modulate hyperactivity in inferior colliculus
description 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).Wehave 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.
format Article
author Mulders, W.H.A.M.
Seluakumaran, K.
Robertson, D.
author_facet Mulders, W.H.A.M.
Seluakumaran, K.
Robertson, D.
author_sort Mulders, W.H.A.M.
title Efferent pathways modulate hyperactivity in inferior colliculus
title_short Efferent pathways modulate hyperactivity in inferior colliculus
title_full Efferent pathways modulate hyperactivity in inferior colliculus
title_fullStr Efferent pathways modulate hyperactivity in inferior colliculus
title_full_unstemmed Efferent pathways modulate hyperactivity in inferior colliculus
title_sort efferent pathways modulate hyperactivity in inferior colliculus
publisher Soc Neuroscience
publishDate 2010
url http://eprints.um.edu.my/12687/
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score 13.211869