Survival of cochlear sensory epithelial cells may be regulated by inhibitor of differentiation-1 (Id1) and the N-methyl-D-aspartic acid (NMDA) receptor. However, it is unclear whether Id1 and the NMDA receptor are involved in the radiation-mediated survival of rat cochlear sensory epithelial cells. Here, we show that the percentage of apoptotic cells increased, the percentage of cells in the S phase decreased, Id1 mRNA and protein expression decreased and the NMDA receptor subtype 2B (NR2B) mRNA and protein level increased in OC1 cells after radiation. Cells infected with the Id1 gene exhibited higher Id1 mRNA and protein levels and lower NR2B mRNA and protein levels than the control cells. In contrast, after transfection of the Id1 siRNA into OC1 cells, Id1 mRNA and protein expression decreased and NR2B mRNA and protein expression increased relative to that of the control group. Additionally, treatment with ifenprodil for 24 h before radiation reduced apoptosis and increased the percentage of cells in the S phase. Our results suggest that Id1 and NR2B might regulate the survival of OC1 cells following radiation.
BackgroundTinnitus can interfere with a patient’s speech discrimination, but whether tinnitus itself or the accompanying sensorineural hearing loss (SNHL) causes this interference is still unclear. We analyzed event-related electroencephalograms (EEGs) to observe auditory-related brain function and explore the possible effects of SNHL on auditory processing in tinnitus patients.MethodsSpeech discrimination scores (SDSs) were recorded in 21 healthy control subjects, 24 tinnitus patients, 24 SNHL patients, and 27 patients with both SNHL and tinnitus. EEGs were collected under an oddball paradigm. Then, the mismatch negativity (MMN) amplitude and latency, the clustering coefficient and average path length of the whole network in the tinnitus and SNHL groups were compared with those in the control group. Additionally, we analyzed the intergroup differences in functional connectivity among the primary auditory cortex (AC), parahippocampal gyrus (PHG), and inferior frontal gyrus (IFG).ResultsSNHL patients with or without tinnitus had lower SDSs than the control subjects. Compared with control subjects, tinnitus patients with or without SNHL had decreased MMN amplitudes, and SNHL patients had longer MMN latencies. Tinnitus patients without SNHL had a smaller clustering coefficient and a longer whole-brain average path length than the control subjects. SNHL patients with or without tinnitus had a smaller clustering coefficient and a longer average path length than patients with tinnitus alone. The connectivity strength from the AC to the PHG and IFG was lower on the affected side in tinnitus patients than that in control subjects; the connectivity strength from the PHG to the IFG was also lower on the affected side in tinnitus patients than that in control subjects. However, the connectivity strength from the IFG to the AC was stronger in tinnitus patients than that in the control subjects. In SNHL patients with or without tinnitus, these changes were magnified.ConclusionChanges in auditory processing in tinnitus patients do not influence SDSs. Instead, SNHL might cause the activity of the AC, PHG and IFG to change, resulting in impaired speech recognition in tinnitus patients with SNHL.
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