Редактирование: UCN3

Urocortin-3 precursor (Stresscopin) (Urocortin III) (Ucn III) [SPC]

==Publications==

{{medline-entry
|title=Urocortin 3 signalling in the auditory brainstem aids recovery of hearing after reversible noise-induced threshold shift.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31270820
|abstract=Ongoing, moderate noise exposure does not instantly damage the auditory system but may cause lasting deficits, such as elevated thresholds and accelerated ageing of the auditory system. The neuromodulatory peptide urocortin-3 ([[UCN3]]) is involved in the body's recovery from a stress response, and is also expressed in the cochlea and the auditory brainstem. Lack of [[UCN3]] facilitates age-induced hearing loss and causes permanently elevated auditory thresholds following a single 2 h noise exposure at moderate intensities. Outer hair cell function in mice lacking [[UCN3]] is unaffected, so that the observed auditory deficits are most likely due to inner hair cell function or central mechanisms. Highly specific, rather than ubiquitous, expression of [[UCN3]] in the brain renders it a promising candidate for designing drugs to ameliorate stress-related auditory deficits, including recovery from acoustic trauma. Environmental acoustic noise is omnipresent in our modern society, with sound levels that are considered non-damaging still causing long-lasting or permanent changes in the auditory system. The small neuromodulatory peptide urocortin-3 ([[UCN3]]) is the endogenous ligand for corticotropin-releasing factor receptor type 2 and together they are known to play an important role in stress recovery. [[UCN3]] expression has been observed in the auditory brainstem, but its role remains unclear. Here we describe the detailed distribution of [[UCN3]] expression in the murine auditory brainstem and provide evidence that [[UCN3]] is expressed in the synaptic region of inner hair cells in the cochlea. We also show that mice with deficient [[UCN3]] signalling experience premature ageing of the auditory system starting at an age of 4.7 months with significantly elevated thresholds of auditory brainstem responses ([[ABR]]s) compared to age-matched wild-type mice. Following a single, 2 h exposure to moderate (84 or 94 dB SPL) noise, [[UCN3]]-deficient mice exhibited significantly larger shifts in [[ABR]] thresholds combined with maladaptive recovery. In wild-type mice, the same noise exposure did not cause lasting changes to auditory thresholds. The presence of [[UCN3]]-expressing neurons throughout the auditory brainstem and the predisposition to hearing loss caused by preventing its normal expression suggests [[UCN3]] as an important neuromodulatory peptide in the auditory system's response to loud sounds.
|mesh-terms=* Aging
* Animals
* Auditory Threshold
* Evoked Potentials, Auditory, Brain Stem
* Female
* Hair Cells, Auditory, Outer
* Hearing Loss, Noise-Induced
* Male
* Mice
* Mice, Inbred C57BL
* Mice, Knockout
* Mice, Transgenic
* Noise
* Signal Transduction
* Urocortins
|keywords=* Corticotropin-releasing hormone receptor
* DPOAEs
* acoustic trauma
* ageing
* auditory brainstem responses
* neuropeptide
* stress recovery
* urocortin
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6852351
}}