Rationale Electrophysiological studies show that systemic nicotine narrows frequency receptive fields and increases gain in neural responses to characteristic frequency stimuli. We postulated that nicotine enhances related auditory processing in humans. Objectives The main hypothesis was that nicotine improves auditory performance. A secondary hypothesis was that the degree of nicotine-induced improvement depends on the individual's baseline performance. Methods Young (18-27 years old), normal-hearing nonsmokers received nicotine (Nicorette gum, 6mg) or placebo gum in a singleblind, randomized, crossover design. Subjects performed four experiments involving tone-in-noise detection, temporal gap detection, spectral ripple discrimination, and selective auditory attention before and after treatment. The perceptual differences between posttreatment nicotine and placebo conditions were measured and analyzed as a function of the pre-treatment baseline performance.Results Nicotine significantly improved performance in the more difficult tasks of tone-in-noise detection and selective attention (effect size = − 0.3) but had no effect on relatively easier tasks of temporal gap detection and spectral ripple discrimination. The two tasks showing significant nicotine effects further showed no baseline-dependent improvement. Conclusions Nicotine improves auditory performance in difficult listening situations. The present results support future investigation of nicotine effects in clinical populations with auditory processing deficits or reduced cholinergic activation.

Cochlear implant (CI) listeners have difficulty understanding speech in complex listening environments. This deficit is thought to be largely due to peripheral encoding problems arising from current spread, which results in wide peripheral filters. In normal hearing (NH) listeners, central processing contributes to segregation of speech from competing sounds. We tested the hypothesis that basic central processing abilities are retained in post-lingually deaf CI listeners, but processing is hampered by degraded input from the periphery. In eight CI listeners, we measured auditory nerve compound action potentials to characterize peripheral filters. Then, we measured psychophysical detection thresholds in the presence of multi-electrode maskers placed either inside (peripheral masking) or outside (central masking) the peripheral filter. This was intended to distinguish peripheral from central contributions to signal detection. Introduction of temporal asynchrony between the signal and masker improved signal detection in both peripheral and central masking conditions for all CI listeners. Randomly varying components of the masker created spectral-variance cues, which seemed to benefit only two out of eight CI listeners. Contrastingly, the spectral-variance cues improved signal detection in all five NH listeners who listened to our CI simulation. Together these results indicate that widened peripheral filters significantly hamper central processing of spectral-variance cues but not of temporal cues in post-lingually deaf CI listeners. As indicated by two CI listeners in our study, however, post-lingually deaf CI listeners may retain some central processing abilities similar to NH listeners.

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Auditory neuropathy affects synaptic encoding or neural conduction of signals in the cochlea or the auditory nerve. Subjects with auditory neuropathy poorly recognize speech in noise which correlates with poor temporal processing. The integrity of temporal processes in the auditory system can be assessed with detection of just-noticeable differences in gap between sounds. Disorder in the auditory periphery appears to alter the precise timing or latency of synchronous neural discharges important for temporal coding. However, the relative contribution of auditory nerve activities to central temporal processing is unknown. Auditory neuropathy produced significantly worse than normal gap detection within a frequency but normal gap detection between different frequencies. No correlation between same- and different-frequency gap detection supports two temporal processes: a peripheral mechanism dependent on overlapping nerve fibers mediating same-frequency gaps and a central mechanism dependent on cross-correlated activity of non-overlapping fibers mediating different-frequency gaps. The fast, peripheral mechanism enables temporal acuity on the order of milliseconds and is likely limited by neural synchrony, the amount of total nerve activity, or both, whereas the sluggish, central mechanism is likely limited by switching time between perceptual channels on the order of a hundred milliseconds. The results demonstrate auditory nerve activities limit peripheral but not central temporal acuity.