The cochlea as an independent neuroendocrine organ: expression and possible roles of a local hypothalamic-pituitary-adrenal axis-equivalent signaling system.

摘要: A key property possessed by the mammalian cochlea is its ability to dynamically alter own sensitivity. Because hair cells and ganglion are prone damage following exposure loud sound, extant mechanisms limiting cochlear include modulation involving both mechanical (via outer cell motility) neural signaling inner cell-ganglion synapses) steps of peripheral auditory processing. Feedback systems such as that embodied olivocochlear system can sensitivity, but respond only after stimulus encoding, allowing potentially damaging sounds impact ear before sensitivity adjusted. Less well characterized potential cellular involved in protection against metabolic stress resultant damage. Although pharmacological manipulation may hold some promise for attenuating damage, targeting this still allow occur does not depend on a fully functional feedback loop mitigation. Thus, understanding endogenous lead new strategies therapies prevention consequent hearing loss. We have recently discovered novel molecularly equivalent classic hypothalamic-pituitary-adrenal (HPA) axis. This HPA-equivalent functions balance susceptibility noise-induced loss, also protects insults resulting from exposures ototoxic drugs. represent local response designed mitigate arising various types insult.