Document Detail

The cochlea as an independent neuroendocrine organ: expression and possible roles of a local hypothalamic-pituitary-adrenal axis-equivalent signaling system.
MedLine Citation:
PMID:  22484018     Owner:  NLM     Status:  MEDLINE    
A key property possessed by the mammalian cochlea is its ability to dynamically alter its own sensitivity. Because hair cells and ganglion cells are prone to damage following exposure to loud sound, extant mechanisms limiting cochlear damage include modulation involving both the mechanical (via outer hair cell motility) and neural signaling (via inner hair cell-ganglion cell synapses) steps of peripheral auditory processing. Feedback systems such as that embodied by the olivocochlear system can alter sensitivity, but respond only after stimulus encoding, allowing potentially damaging sounds to impact the inner ear before sensitivity is adjusted. Less well characterized are potential cellular signaling systems involved in protection against metabolic stress and resultant damage. Although pharmacological manipulation of the olivocochlear system may hold some promise for attenuating cochlear damage, targeting this system may still allow damage to occur that does not depend on a fully functional feedback loop for its mitigation. Thus, understanding endogenous cell signaling systems involved in cochlear protection may lead to new strategies and therapies for prevention of cochlear damage and consequent hearing loss. We have recently discovered a novel cochlear signaling system that is molecularly equivalent to the classic hypothalamic-pituitary-adrenal (HPA) axis. This cochlear HPA-equivalent system functions to balance auditory sensitivity and susceptibility to noise-induced hearing loss, and also protects against cellular metabolic insults resulting from exposures to ototoxic drugs. This system may represent a local cellular response system designed to mitigate damage arising from various types of insult.
Johnvesly Basappa; Christine E Graham; Sevin Turcan; Douglas E Vetter
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2012-03-29
Journal Detail:
Title:  Hearing research     Volume:  288     ISSN:  1878-5891     ISO Abbreviation:  Hear. Res.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-06-08     Completed Date:  2012-10-10     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  7900445     Medline TA:  Hear Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  3-18     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier B.V. All rights reserved.
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MeSH Terms
Auditory Pathways / metabolism
Cochlea / drug effects,  metabolism*,  pathology
Feedback, Physiological
Glucocorticoids / metabolism
Hearing Loss, Noise-Induced / metabolism,  pathology,  prevention & control
Hypothalamo-Hypophyseal System / metabolism*
Noise / adverse effects
Pituitary-Adrenal System / metabolism*
Receptors, Corticotropin-Releasing Hormone / metabolism
Signal Transduction* / drug effects
Grant Support
Reg. No./Substance:
0/Glucocorticoids; 0/Receptors, Corticotropin-Releasing Hormone

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