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PubMed · 2240997

[Cochlear physiology and physiopathology. Recent data].

Abstract

Our concept of cochlear physiology has changed so drastically over the last decade that most classical textbooks have become obsolete. This bibliographical inadequacy regarding the functioning of the normal cochlea is particularly disturbing when it comes to addressing patho-physiology problems (hearing loss or tinnitus). What drastic changes have there been, that can justify such need for information updating? These relate primarily to the role of one the two types of sensory cells of the cochlea; i.e., the outer hair cells (or OHC). These cells are endowed with contractile properties and react to tonal impulse by modifying the vibration of the cochlear partition. This "active mechanism" response provokes a localized amplification of the vibration imparting to these classical sensory transducers, or inner hair cells (IHC), their optimal frequency sensitivity and discrimination properties. This new concept alone would suffice to justify our present topic. We chose, however, to insert a general presentation of cochlear physiology, the intent of which is to briefly review the classical data and to analyze in some depth the issues that have drastically changed our knowledge.

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BibTeXRIS

R Pujol. 1990. [Cochlear physiology and physiopathology. Recent data].. https://pubmed.ncbi.nlm.nih.gov/2240997/

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A model of peripherally developing hearing loss and tinnitus based on the role of hypoxia and ischemia.

The incidence of sensorineural hearing loss often caused by direct damage to the cochlear hair cells is by far more frequent and more serious than disorders affecting the external ear or the middle ear. Mechanisms that are discussed to be relevant for the genesis of tinnitus and acquired hearing impairment are hair cell loss, signal transduction disturbances in the region of the outer and inner hair cells and the spiral ganglion, impairment of cochlear blood flow, mechanical disturbance, and hypoxia and ischemia. The present model surveys the possible cellular and molecular biological causes of peripherally developing hearing loss and tinnitus. In particular, the paper discusses the roles of hypoxia and ischemia in the cochlea and in the etiology of the neurosensory types of tinnitus. Peripheral origins of hearing disturbances and tinnitus may be: (a) damage to the stereocilia and the tip links, (b) dysfunction of potassium channels or (c) modification of the glutamate release. Moreover, the hypoxia inducible factor-1 may have an important role to play as a key transcription factor in the cells' adaptation to hypoxia and ischemia. An impairment of the cochlear blood flow may be induced by the expression of target genes like nitrogen monoxide synthase and endothelin-1 resulting in tinnitus. The paper discusses consequences resulting from the present model for the medical treatment of peripherally developing tinnitus and hearing loss.

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