Objective The objective of this study was to describe the auditory evoked response to silent gaps for a group of older adults using stimulus conditions identical to those used in psychophysical studies of gap detection. Design The P1-N1-P2 response to the onsets of stimuli (markers) defining a silent gap for within-channel (spectrally identical markers) and across-channel (spectrally different markers) conditions was examined using four perceptually-equated gap durations. Study Sample A group of 24 older adults (mean age = 63 years) with normal hearing or minimal hearing loss participated. Results Older adults exhibited neural activation patterns that were qualitatively different and more frontally oriented than those observed in a previous study (Lister et al., 2007) of younger listeners. Older adults showed longer P2 latencies and larger P1 amplitudes than younger adults, suggesting relatively slower neural travel time and altered auditory inhibition/arousal by irrelevant stimuli. Conclusion Older adults appeared to recruit later-occurring T-complex-like generators for gap processing, compared to earlier-occurring T-complex-like generators by the younger group. Early and continued processing of channel cues with later processing of gap cues may represent the inefficiency of the aging auditory system and may contribute to poor speech understanding in noisy, real-world listening environments.

Objectives-The objective of this study was to describe the cortical evoked response to silent gaps in a group of young adults with normal hearing using stimulus conditions identical to those used in psychophysical studies of gap detection. Specifically, we sought to examine the P1-N1-P2 auditory evoked response to the onsets of stimuli (markers) defining a silent gap for withinchannel (spectrally identical markers) and across-channel (spectrally different markers) conditions using four perceptually-equated gap durations. It was hypothesized that (1) P1, N1, and P2 would be present and consistent for 1st marker (before the gap) onsets; (2) for within-channel markers, P1, N1, and P2 would be present for 2nd marker (after the gap) onsets only when the gap was of a duration equal to or larger than the behaviorally measured gap detection threshold; and (3) for the across-channel conditions, P1, N1, and P2 would be present for 2nd marker onsets regardless of gap duration. This is expected due to the additional cue of frequency change following the gap.Design-Twelve young adults (mean age 26 years) with normal hearing participated. Withinchannel and across-channel gap detection thresholds were determined using an adaptive psychophysical procedure. Next, cortical auditory evoked potentials (P1-N1-P2) were recorded with a 32-channel Neuro-scan™ electroencephalogram system using within-channel and acrosschannel markers identical to those used for the psychophysical task and four perceptually weighted gap durations: (1) individual listener's gap detection threshold; (2) above gap detection threshold; (3) below gap detection threshold; and (4) a 1-ms gap identical to the gap in the standard interval of the psychophysical task. P1-N1-P2 peak latencies and amplitudes were analyzed using repeated-measures analyses of variance. A temporal-spatial principal component analysis was also conducted.Results-The latency of P2 and the amplitude of P1, N1, and P2 were significantly affected by the acoustic characteristics of the 2nd marker as well as the duration of the gap. Larger amplitudes and shorter latencies were generally found for the conditions in which the acoustic cues were most salient (e.g., across-channel markers, 1st markers, large gap durations). Interestingly, the temporal-spatial principal component analysis revealed activity elicited by gap durations equal to gap detection threshold in the latency regions of 167 and 183 ms for temporal-parietal and rightfrontal spatial locations.Address for correspondence: Jennifer Lister, Department of Communication Sciences and Disorders, University of South Florida, 4202 E. Fowler Ave. PCD 1017, Tampa, FL 33620. jlister@cas.usf.edu.. HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptConclusions-The cortical response to a silent gap is unique to specific marker characteristics and gap durations among young adults with normal hearing. Specifically, when the onset of the 2nd marker is perceptually salient, the amplitude of the P1-N1-P2 re...

Studies suggest that reduced cognitive control due to nicotine withdrawal may have a critical role in promoting tobacco use. The P3 family of event-related brain potential (ERP) components is thought to serve as markers of cognitive control processes. Unfortunately, existing research that examines the effects of nicotine deprivation on P3 amplitude has been marred by small sample sizes and other design limitations. The present study sought to determine the effects of nicotine deprivation on P3b and P3a amplitudes, which index task relevant target detection and orienting responses to novelty, respectively. A secondary aim was to examine self-reported trait cognitive control as a moderator of nicotine deprivation-induced reductions in P3b and P3a amplitudes. In all, 121 nicotine-dependent smokers attended two experimental sessions following 12-h smoking/nicotine deprivation. In a counterbalanced manner, participants smoked nicotine cigarettes during one session and placebo cigarettes during the other session. Findings indicated that nicotine deprivation reduced P3b amplitude (po0.00001) during a three-stimulus oddball task independent of trait cognitive control. In contrast, nicotine deprivation reduced P3a only among participants who scored lower on measures of trait cognitive control. Implications for conceptualizing risk for nicotine dependence, and its treatment, are discussed.

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