Linked Life Data

8790735

Source:http://linkedlifedata.com/resource/pubmed/id/8790735

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1996-12-4
pubmed:abstractText
Otoacoustic emissions (OAEs) are considered to originate from active cochlear processes involving the outer hair cells (OHC). These emissions are suppressed by activity in the efferent olivocochlear bundle (OCB) and following OHC damage caused by noise exposure or ototoxic drugs. Temporary enhancement of OAEs may occur following noise exposure, and permanent enhancement of emissions has been associated with primary afferent dysfunction in the auditory system. This suggests that there are active adaptation processes in the cochlea exist that could potentially compensate for loss of afferent input. We have used the anti-cancer drug carboplatin to induce selective inner hair cell (IHC) lesions in the cochleae of chinchilla and measured the elevation of auditory thresholds that occurred using brainstem responses (ABR). Following carboplatin treatment click evoked otoacoustic emissions (CEOAEs) were amplified from cochlear frequency regions, which demonstrated extensive IHC damage but apparently normal OHCs. These results support the theory that OHCs cells are involved in the production of these cochlear emissions but also provides further evidence that active adaptation processes exist in the cochlea. It is postulated that loss of afferent input reduces the activity in the medial efferent OCB resulting in de-suppression of OHC contractility. Enhanced OHC contractility could then produce amplification of CEOAEs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0001-6489
pubmed:author
pubmed:issnType
Print
pubmed:volume
116
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
374-81
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Otoacoustic emission amplification after inner hair cell damage.
pubmed:affiliation
Department of Otolaryngology-Head and Neck Surgery, Wolverhampton Hospital, U.K.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't