The cochlea as an independent neuroendocrine organ: Expression and possible roles of a local hypothalamic-pituitary-adrenal axis-equivalent signaling system Journal Article
| Authors: | Basappa, J.; Graham, C. E.; Turcan, S.; Vetter, D. E. |
| Article Title: | The cochlea as an independent neuroendocrine organ: Expression and possible roles of a local hypothalamic-pituitary-adrenal axis-equivalent signaling system |
| Abstract: | 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. © 2012 Elsevier B.V. |
| Keywords: | signal transduction; protein expression; review; nonhuman; protein function; animals; neuromodulation; risk factor; regulatory mechanism; mammal; glucocorticoid; cellular stress response; disease predisposition; cell protection; feedback, physiological; nerve cell; cell motility; hearing loss; dendrite; neuroprotection; glucocorticoids; ototoxicity; hypothalamus hypophysis adrenal system; synapse; protein defect; cochlea; corticotropin; corticotropin releasing factor; hormone action; noise; steroidogenesis; hypothalamo-hypophyseal system; pituitary-adrenal system; hair cell; glutamate ammonia ligase; auditory stimulation; nerve cell lesion; neuroendocrine system; endocrine function; corticotropin releasing factor receptor 1; corticotropin releasing factor receptor 2; glutamate receptor 2; glutamate receptor 4; acoustic nerve fiber; auditory feedback; auditory nervous system; cochlea injury; corticosteroid release; inner ear disease; metabolic stress; olivocochlear system; sound intensity; auditory pathways; hearing loss, noise-induced; receptors, corticotropin-releasing hormone |
| Journal Title: | Hearing Research |
| Volume: | 288 |
| Issue: | 1-2 |
| ISSN: | 0378-5955 |
| Publisher: | Elsevier B.V. |
| Date Published: | 2012-06-01 |
| Start Page: | 3 |
| End Page: | 18 |
| Language: | English |
| DOI: | 10.1016/j.heares.2012.03.007 |
| PROVIDER: | scopus |
| PMCID: | PMC3371174 |
| PUBMED: | 22484018 |
| DOI/URL: | |
| Notes: | --- - "Export Date: 2 July 2012" - "CODEN: HERED" - "Source: Scopus" |
