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10.1016/j.cub.2015.01.009 http://scihub22266oqcxt.onion/10.1016/j.cub.2015.01.009 C4348215!4348215!25639244     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Curr+Biol 2015 ; 25 (5): 606-12 Nephropedia Template TP {{tp|p=25639244|t=2015. A Non-canonical Pathway from Cochlea to Brain Signals Tissue-damaging Noise |pdf=|usr=}}{{25639244}} gab.com Text A Non-canonical Pathway from Cochlea to Brain Signals Tissue-damaging Noise JO: Curr Biol http://www.kidney.de/pget.php?&tw=1&pmid=25639244 #FOAvip Intense noise damages the cochlear organ of Corti, particularly the outer hair cells (OHCs)[1], however this epithelium is not innervated by nociceptors of somatosensory ganglia, which detect damage elsewhere in the body. The only sensory neurons innervating the organ of Corti originate from the spiral ganglion, roughly 95% of which innervate exclusively inner hair cells (IHCs)[2-4]. Upon sound stimulation, IHCs release glutamate to activate AMPA-type receptors on these myelinated type-I neurons, which carry the neuronal signals to the cochlear nucleus. The remaining spiral ganglion cells (type-IIs) are unmyelinated and contact OHCs[2-4]. Their function is unknown. Using immunoreactivity to cFos, we documented neuronal activation in the brainstem of Vglut3?/? mice, in which the canonical auditory pathway (activation of type-I afferents by glutamate released from inner hair cells) is silenced[5, 6]. In these deaf mice, we found responses to noxious noise, that damages hair cells, but not to innocuous noise, in neurons of the cochlear nucleus, but not in the vestibular or trigeminal nuclei. This response originates in the cochlea and not in other areas also stimulated by intense noise (middle ear and vestibule) as it was absent in CD1 mice with selective cochlear degeneration but normal vestibular and somatosensory function. These data imply the existence of an alternative neuronal pathway from cochlea to brainstem that is activated by tissue-damaging noise and does not require glutamate release from IHCs. This detection of noise-induced tissue damage, possibly by type-II cochlear afferents, represents a novel form of sensation we term auditory nociception. Twit Text FOAVip A Non-canonical Pathway from Cochlea to Brain Signals Tissue-damaging Noise ????Curr Biol http://www.kidney.de/pget.php?&tw=1&pmid=25639244 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25639244 #FOAvip English Wikipedia <ref>{{Cite pmid|25639244}}</ref> A Non-canonical Pathway from Cochlea to Brain Signals Tissue-damaging Noise #MMPMID25639244 Flores EN; Duggan A; Madathany T; Hogan AK; Márquez F; Kumar G; Seal R; Edwards R; Liberman MC; García-Añoveros J Curr Biol 2015[Mar]; 25 (5): 606-12 PMID25639244show ga Intense noise damages the cochlear organ of Corti, particularly the outer hair cells (OHCs)[1], however this epithelium is not innervated by nociceptors of somatosensory ganglia, which detect damage elsewhere in the body. The only sensory neurons innervating the organ of Corti originate from the spiral ganglion, roughly 95% of which innervate exclusively inner hair cells (IHCs)[2-4]. Upon sound stimulation, IHCs release glutamate to activate AMPA-type receptors on these myelinated type-I neurons, which carry the neuronal signals to the cochlear nucleus. The remaining spiral ganglion cells (type-IIs) are unmyelinated and contact OHCs[2-4]. Their function is unknown. Using immunoreactivity to cFos, we documented neuronal activation in the brainstem of Vglut3?/? mice, in which the canonical auditory pathway (activation of type-I afferents by glutamate released from inner hair cells) is silenced[5, 6]. In these deaf mice, we found responses to noxious noise, that damages hair cells, but not to innocuous noise, in neurons of the cochlear nucleus, but not in the vestibular or trigeminal nuclei. This response originates in the cochlea and not in other areas also stimulated by intense noise (middle ear and vestibule) as it was absent in CD1 mice with selective cochlear degeneration but normal vestibular and somatosensory function. These data imply the existence of an alternative neuronal pathway from cochlea to brainstem that is activated by tissue-damaging noise and does not require glutamate release from IHCs. This detection of noise-induced tissue damage, possibly by type-II cochlear afferents, represents a novel form of sensation we term auditory nociception. äA Non-canonical Pathway from Cochlea to Brain Signals Tissue-damaging (epmc).pdf DeepDyve Pubget Overpricing