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For the duration of each and every period, the animals were treated with a systemic injection (300 mg/ kg/day) of SS and DPOAEs have been measured 2-hours post administration. Changes in DPOAE amplitudes were nor-Review of salicylate-induced hearing loss, neurotoxicity, tinnitus and neuropathophysiologyFig. 1. Schematic of mean DPOAE amplitudes plotted as a function of L1 intensity pre- salicylate treatment, 1 h post-salicylate remedy, and 2 h post salicylate treatment (300 mg/kg i.p.). Frequencies (4, 5.three, eight, 11, 16, 20 kHz) indicated above every single panel represent 2f1-f2. Acute systemic salicylate administration considerably decreased DPOAE amplitudes in low (four, five.3, 8, and 11 kHz) and higher (20 kHz) frequencies but not at mid (16 kHz) frequencies. ( P=0.01, P=0.001, ns=not substantial).malised to pre-treatment amplitudes. For the duration of each treatment periods, DPOAE amplitudes have been drastically reduced. Having said that, every single treatment period was followed by a significant rebound enhancement of DPOAE amplitudes when compared with pre-treatment amplitudes 5. There was no modify in DPOAE amplitudes soon after a long duration treatment with salicylate at By position by way of the moderate levels (200 mg/kg/day, 5 days a week, for three weeks) 5. Interestingly, chronic salicylate therapy increases prestin mRNA expression. Adult guinea pigs received a systemic injection of SS (200-250mg/kg) twice every day for 2 weeks. Prestin mRNA expression progressively enhanced following daily administrations. Western blots indicated a rise in the prestin protein 31. 4 weeks right after cessation of SS treatment prestin mRNA levels returned to regular 31. These outcomes indicate that as a result of chronic higher doses of salicylate, the electromotile function of your OHCs is enhanced, leading to greater cochlear amplification. Some have hypothesised that tinnitus could be generated because of an imbalance involving IHC and OHC activity 32. The up-regulation in prestin observed within the O.The incoming sound 26. Salicylate impacts the OHC electromotility response by displacing chloride and binding to the anion inding web sites on prestin, suppressing the amplification properties on the cochlea 23. Sodium salicylate (SS) causes a frequency-dependent reduction in DPOAE 12. Figure 1 shows the mean DPOAE input/output (I/O) response of 6 Sprague-Dawley rats beneath ketamine/xylazine (50/6 mg/kg) anaesthesia. Before SS remedy all six frequencies (2f1-f2= 4, five.three, 8, 11, 16, 20 kHz) showed robust responses. Nevertheless, two hours post injection (300 mg/kg, i.p.), DPOAEs decreased drastically in the low frequencies (2f1-f2 11 kHz) and higher frequencies (2f1-f2 >16 kHz) but had significantly less influence around the mid frequencies (2f1-f2 11 -20 kHz) 12. Whilst salicylate triggered a substantial reduction in DPOAEs indicating a sensory hearing loss, animal behavioural models have also indicated that this dose reliably induces tinnitus 3 27-29. The significant reduction in low and higher frequency responses could lead to mid-frequency expansion of the tonotopic map of your AC. Interestingly, animal models have indicated that salicylate induced a mid-frequency perception of tinnitus 30, consistent using the frequency-dependent reduction in DPOAE 12. Chronic effects Chronic salicylate treatment also influences the motor protein prestin. Chronic treatment with SS enhanced DPOAE amplitudes and triggered an up-regulation in prestin mRNA and protein expression five 31.