Electrically evoked auditory nerve responses in the cochlea with normal outer hair cells

As hybrid cochlear implant devices are increasingly used for restoring hearing in patients with residual hearing, it is important to understand electrically evoked responses in cochleae having functional hair cells. To test the hypothesis that extracochlear electrical stimulation (EES) from sinusoidal current can provoke an auditory nerve response with normal frequency selectivity, the EES-evoked compound action potential(ECAP) was investigated in this study. Brief sinusoidal electrical currents, delivered via a round window electrode, were used to evoke ECAP. The ECAP waveform was observed to be the same as the acoustically evoked CAP(ACAP), except for a shorter latency. The input/output and intensity/latency functions of ACAPs and ECAPs were also similar. The maximum acoustic masking for both ACAP and ECAP occurred near probe frequencies. Since the masked tuning curve of a CAP reflects the frequency selectivity of neural excitation, these data demonstrate a highly specific activation of the auditory nerve, which would result in high degree of frequency selectivity. This frequency selectivity likely results from the cochlear traveling wave caused by electrically stimulated outer hair cells.

Cochlear function after selective spiral ganglion cells degeneration induced by ouabain

Background Ouabain, a cardiac glycoside that specifically binds to Na/K-ATPase and inhibits its activity, was applied to gerbils to develop a method for studying auditory neuropathy. Methods Ouabain was applied to the round window of the cochlea in each gerbil by using a piece of gelfoam with 3 μl or 24 μl （1 mmol/L） ouabain solution. The changes of the threshold of auditory brainstem response, cochlear function round window electrocochleography, as well as the morphological changes of the spiral ganglion cells of the cochlea were observed after application of ouabain for 24 hours or 96 hours. Results In ouabain treated gerbils, auditory brainstem response and compound action potential thresholds showed either elevation or no response at all. However, the thresholds of cochlear microphonic and distortion product otoacoustic emissions were not affected. Degeneration and necrosis of some spiral ganglion cells in ears with applications of ouabain （24 hours, 3 μl, 1 mmol/L; 96 hours, 24 μl, 1 mmol/L ouabain）. The number of spiral ganglion cells was decreased （24 hours, 3 μl, 1 mmol/L ouabain） or near to a total loss （96 hours, 24 μl, 1 mmol/L ouabain）.Conclusions These results indicate a high degree of independence between the spiral ganglion ceils and the outer hair cell systems in the cochlear transduction mechanism. The method used in this study would provide a valuable tool for studying auditory neuropathy.

Prophylactic effect of Ca^(2+)-deficient artificial perilymph perfusion on noise-induced hearing loss

Objective To investigate the prophylactic effect of low calcium concentration perilymph on noise-induced hearing loss. Methods Forty guinea pigs with normal hearing weighing 250-350 g were assigned to five groups (8 in each group): (1) Ca2+-deficient perilymph perfusion (CDP) for 2 h; (2) white noise (120 dB SPL) exposure (WNE) only for 1 h, (3) combination of calcium-deficient perilymph perfusion and white noise (120 dB SPL) exposure (WNE+CDP); (4) normal artificial perilymph (NAP) perfusion for 2 h; and (5) white noise exposure + normal artificial perilymph perfusion (WNE+NAP) for 2 h. Compound action potentials (CAP) evoked by click was recorded from round window every 15 min. The cochleae from 5 animals in each group were examined with scanning electron microscope. Results The CAP for group 1 experienced a threshold shift (TS) of 15-26 dB, while group 2 yielded a 46-59 dB TS and group 3 a 37-45 dB TS; no threshold shift occurred in group 4. The CAP TS in group 5 was 33-64 dB. The CAP TS of group 3 was less than that of group 2. After one hour of noise exposure, the CAP TS of group 3 were 45.92±2.90 dB and 59.30±3.95dB in group 2. There were significant differences (P<0.05) between groups 3 and 2. The CAP TS of group 3 was less than that of group 5 at the points of 1, 1.5 and 2 h after noise exposure. There was a significant difference between groups 3 and 5 (P<0.01). Stereocilia of 89 OHC3 were in disarray in five cochleae after noise exposure in group 2. The cuticular plates of 8 OHC2,3 sank and the stereocilia became fused in only one animal cochlea after noise exposure in group 3 combined with low calcium perilymph perfusion. Conclusions Low calcium concentration appears to participate in preventing noise-induced hearing loss and the rising of calcium concentrations in inner hair cells after noise exposure, which may have been due to the opening of calcium channels in inner hair cells during noise exposure. The mechanism of the prophylactic effect might be caused by a lower calcium concentration in inner hair cells in the cochlea attenuating the influence of noise exposure on hearing loss; calcium deficient perilymph perfusion prevented calcium accumulation in inner hair cells of the cochlea. The motility of the OHCs might be partially inhibited by low calcium concentration that reduced noise-induced hearing loss in turn.