Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling.

摘要: Severe noise-induced damage to the inner ear leads auditory nerve fiber degeneration thereby reducing neural input cochlear nucleus (CN). Paradoxically, this a significant increase in spontaneous activity CN which has been linked tinnitus, hyperacusis and pain. The biological mechanisms that lead an increased are largely unknown, but could arise from changes glutamatergic or GABAergic neurotransmission neuroinflammation. To test hypothesis, we unilaterally exposed rats for 2h 126dB SPL narrow band noise centered at 12kHz. Hearing loss measured by brainstem responses exceeded 55dB 6 32kHz. mRNA was harvested 14 28days post-exposure qRT-PCR analysis performed on 168 genes involved inflammation, neuropathic pain neurotransmission. Expression levels of Slc17a6 Gabrg3, excitation inhibition respectively, were significantly post-exposure, suggesting possible role hyperactivity associated with tinnitus hyperacusis. In inflammatory array, exposure upregulated expression four pain/inflammatory genes, Tlr2, Oprd1, Kcnq3 Ntrk1 decreased two more Ccl12 Il1β. Pain/inflammatory gene via signaling may induce sterile pain, microglial activation migration fibers trigeminal, cuneate vestibular nuclei into CN. These contribute somatic otalgia.