Behavioral Gap Detection Research Articles

Contributions of Hearing Loss and Traumatic Brain Injury to Blast-Induced Cortical Parvalbumin Neuron Loss and Auditory Processing Deficits.

Auditory processing disorder is the most common problem affecting veterans after blast exposure, but the distinct impacts of blast-related traumatic brain injury and blast-related hearing loss are unknown. Independently, both hearing loss and blast exposure affect the entire auditory processing pathway at the molecular and physiological levels. Here, we identified distinct changes to the primary auditory cortex (AI) and temporal processing in mice following blast exposure both with and without protected hearing. Our results show that blast-exposure alone activated microglia in AI, but hearing loss was required for reductions in the density of parvalbumin-expressing interneurons. Although blast exposure impaired the temporal following response, these impairments were more severe with concurrent unilateral hearing loss, further resulting in impairments in behavioral gap detection. Taken together, these results indicate that protecting hearing during blast exposure can prevent most impairments to auditory processing but does not fully protect temporal processing.

Within- and across-frequency temporal processing and speech perception in cochlear implant users.

Cochlear implant (CI) recipient's speech perception performance is highly variable and is influenced by temporal processing abilities. Temporal processing is commonly assessed using a behavioral task that requires the participant to detect a silent gap with the pre- and post-gap stimuli of the same frequency (within-frequency gap detection) or of different frequencies (across-frequency gap detection). The purpose of the study was to evaluate behavioral and electrophysiological measures of within- and across-frequency temporal processing and their correlations with speech perception performance in CI users. Participants included 11 post-lingually deafened adult CI users (n = 15 ears; Mean Age = 50.2 yrs) and 11 age- and gender-matched normal hearing (NH) individuals (n = 15 ears; Mean Age = 49.0 yrs). Speech perception was assessed with Consonant-Nucleus-Consonant Word Recognition (CNC), Arizona Biomedical Sentence Recognition (AzBio), and Bamford-Kowal-Bench Speech-in-Noise Test (BKB-SIN) tests. Within- and across-frequency behavioral gap detection thresholds (referred to as the GDTwithin and GDTacross) were measured using an adaptive, two-alternative, forced-choice procedure. Cortical auditory evoked potentials (CAEPs) were elicited using within- and across-frequency gap stimuli under four gap duration conditions (no gap, GDT, sub-threshold GDT, and supra-threshold GDT). Correlations among speech perception, GDTs, and CAEPs were examined. CI users had poorer speech perception scores compared to NH listeners (p < 0.05), but the GDTs were not different between groups (p > 0.05). Compared to NH peers, CI users showed increased N1 latency in the CAEPs evoked by the across-frequency gap stimuli (p < 0.05). No group difference was observed for the CAEPs evoked by the within-frequency gap (p > 0.05). Three CI ears showing the longest GDTwithin also showed the poorest performance in speech in noise. The within-frequency CAEP increased in amplitude with the increase of gap duration; while the across-frequency CAEP displayed a similar amplitude for all gap durations. There was a significant correlation between speech scores and within-frequency CAEP measures for the supra-threshold GDT condition, with CI users with poorer speech performance having a smaller N1-P2 amplitude and longer N1 latency. No correlations were found among GDTacross, speech perception, and across-frequency CAEP measures. Within- and across-frequency gap detection may involve different neural mechanisms. The within-frequency gap detection task can help identify CI users with poor speech performance for rehabilitation. The within-frequency CAEP is a better predictor for speech perception performance than the across-frequency CAEP.

A genetically identified population of layer 4 neurons in auditory cortex that contributes to pre-pulse inhibition of the acoustic startle response.

A fundamental task faced by the auditory system is the detection of events that are signaled by fluctuations in sound. Spiking in auditory cortical neurons is critical for sound detection, but the causal roles of specific cell types and circuits are still mostly unknown. Here we tested the role of a genetically identified population of layer 4 auditory cortical neurons in sound detection. We measured sound detection using a common variant of pre-pulse inhibition of the acoustic startle response, in which a silent gap in background noise acts as a cue that attenuates startle. We used a Gpr26-Cre driver line, which we found expressed predominantly in layer 4 of auditory cortex. Photostimulation of these cells, which were responsive to gaps in noise, was sufficient to attenuate the startle reflex. Photosuppression of these cells reduced neural responses to gaps throughout cortex, and impaired behavioral gap detection. These data demonstrate that cortical Gpr26 neurons are both necessary and sufficient for top–down modulation of the acoustic startle reflex, and are thus likely to be involved in sound detection.

A Layer 3→5 Circuit in Auditory Cortex That Contributes to Pre-pulse Inhibition of the Acoustic Startle Response.

While connectivity within sensory cortical circuits has been studied extensively, how these connections contribute to perception and behavior is not well understood. Here we tested the role of a circuit between layers 3 and 5 of auditory cortex in sound detection. We measured sound detection using a common variant of pre-pulse inhibition of the acoustic startle response, in which a silent gap in background noise acts as a cue that attenuates startle. We used the Nr5a-Cre driver line, which we found drove expression in the auditory cortex restricted predominantly to layer 3. Photoactivation of these cells evoked short-latency, highly reliable spiking in downstream layer 5 neurons, and attenuated startle responses similarly to gaps in noise. Photosuppression of these cells did not affect behavioral gap detection. Our data provide the first demonstration that direct activation of auditory cortical neurons is sufficient to attenuate the acoustic startle response, similar to the detection of a sound.

Comparison of Silent Gap in Noise Cortical Auditory Evoked Potentials in Matched Tinnitus and No-Tinnitus Control Subjects.

Purpose Previous research suggests the existence of gap detection impairments because of tinnitus. The current study aimed to determine whether there was objective evidence of gap impairment in individuals with tinnitus by recording silent gap in white noise cortical auditory evoked potentials (CAEPs) in a chronic tinnitus group and a no-tinnitus group. The results were compared to previous gap-evoked potential and behavioral gap detection studies. Method Chronic tinnitus and no-tinnitus groups were formed by matching pairs of subjects ( n = 26) based on age, gender, and hearing thresholds. Behaviorally determined gap detection thresholds were used to define the electrophysiological gap duration conditions of subthreshold, threshold, and suprathreshold gaps in white noise. Amplitude, latency, and area of the CAEP were analyzed by group and condition using mixed-model analyses of variance. Results Across all participants, as the duration of the gap increased, amplitude and area of the CAEP increased. There were no significant differences by tinnitus status between groups for any outcome measures, except for a significant interaction between group and gap duration for P1 latency. Conclusions Silent gap-evoked CAEPs can be recorded in adults with and without tinnitus. Amplitude and area were sensitive to gap duration across groups; latency was not. Contrary to hypotheses, there was little evidence supporting differences in gap-evoked CAEPs between the tinnitus and control groups. Stimulus and other factors that may have contributed to the lack of a group difference in the current study are discussed, as well as implications for future studies of objective measures of tinnitus perception. Supplemental Material https://doi.org/10.23641/asha.7822601.

Acoustic change complex for frequency changes

Purpose: Acoustic change complex (ACC) reflects brain’s capacity to discriminate the acoustic features present in the signal, hence serves as an index of discrimination capacity. ACC for intensity changes and gaps-in-noise have consistently shown that the ACC threshold is consistent with behavioral intensity discrimination and gap detection thresholds. While, the ACC threshold for frequency change is found to be highly variable. The present study was carried out to investigate the agreement between behavioral frequency discrimination threshold and the ACC threshold for frequency change.Methods: Ten young adults with normal hearing in both ears participated in the study. The ACC was elicited using frequency changing tones, with a frequency change of 5, 10, 25, 50, 100 and 200 Hz.Results: The present study showed that a greater frequency change is required to elicit the ACC compared to behavioral discrimination threshold. In most of the participants, a frequency change greater than 50 Hz was required to elicit the ACC. Magnitude of frequency change had effect on latency and amplitude of peaks of the ACC, amplitude was higher and latency was shorter for greater frequency change.Conclusion: ACC threshold for frequency change does not resemble behavioral discrimination threshold and is variable across participants.

Brief Stimulus Exposure Fully Remediates Temporal Processing Deficits Induced by Early Hearing Loss

In childhood, partial hearing loss can produce prolonged deficits in speech perception and temporal processing. However, early therapeutic interventions targeting temporal processing may improve later speech-related outcomes. Gap detection is a measure of auditory temporal resolution that relies on the auditory cortex (ACx), and early auditory deprivation alters intrinsic and synaptic properties in the ACx. Thus, early deprivation should induce deficits in gap detection, which should be reflected in ACx gap sensitivity. We tested whether earplugging-induced, early transient auditory deprivation in male and female Mongolian gerbils caused correlated deficits in behavioral and cortical gap detection, and whether these could be rescued by a novel therapeutic approach: brief exposure to gaps in background noise. Two weeks after earplug removal, animals that had been earplugged from hearing onset throughout auditory critical periods displayed impaired behavioral gap detection thresholds (GDTs), but this deficit was fully reversed by three 1 h sessions of exposure to gaps in noise. In parallel, after earplugging, cortical GDTs increased because fewer cells were sensitive to short gaps, and gap exposure normalized this pattern. Furthermore, in deprived animals, both first-spike latency and first-spike latency jitter increased, while spontaneous and evoked firing rates decreased, suggesting that deprivation causes a wider range of perceptual problems than measured here. These cortical changes all returned to control levels after gap exposure. Thus, brief stimulus exposure, perhaps in a salient context such as the unfamiliar placement into a testing apparatus, rescued impaired gap detection and may have potential as a remediation tool for general auditory processing deficits.SIGNIFICANCE STATEMENT Hearing loss in early childhood leads to impairments in auditory perception and language processing that can last well beyond the restoration of hearing sensitivity. Perceptual deficits can be improved by training, or by acoustic enrichment in animal models, but both approaches involve extended time and effort. Here, we used a novel remediation technique, brief periods of auditory stimulus exposure, to fully remediate cortical and perceptual deficits in gap detection induced by early transient hearing loss. This technique also improved multiple cortical response properties. Rescue by this efficient exposure regime may have potential as a therapeutic tool to remediate general auditory processing deficits in children with perceptual challenges arising from early hearing loss.

Noise Trauma-Induced Behavioral Gap Detection Deficits Correlate with Reorganization of Excitatory and Inhibitory Local Circuits in the Inferior Colliculus and Are Prevented by Acoustic Enrichment.

Hearing loss leads to a host of cellular and synaptic changes in auditory brain areas that are thought to give rise to auditory perception deficits such as temporal processing impairments, hyperacusis, and tinnitus. However, little is known about possible changes in synaptic circuit connectivity that may underlie these hearing deficits. Here, we show that mild hearing loss as a result of brief noise exposure leads to a pronounced reorganization of local excitatory and inhibitory circuits in the mouse inferior colliculus. The exact nature of these reorganizations correlated with the presence or absence of the animals' impairments in detecting brief sound gaps, a commonly used behavioral sign for tinnitus in animal models. Mice with gap detection deficits (GDDs) showed a shift in the balance of synaptic excitation and inhibition that was present in both glutamatergic and GABAergic neurons, whereas mice without GDDs showed stable excitation-inhibition balances. Acoustic enrichment (AE) with moderate intensity, pulsed white noise immediately after noise trauma prevented both circuit reorganization and GDDs, raising the possibility of using AE immediately after cochlear damage to prevent or alleviate the emergence of central auditory processing deficits.SIGNIFICANCE STATEMENT Noise overexposure is a major cause of central auditory processing disorders, including tinnitus, yet the changes in synaptic connectivity underlying these disorders remain poorly understood. Here, we find that brief noise overexposure leads to distinct reorganizations of excitatory and inhibitory synaptic inputs onto glutamatergic and GABAergic neurons and that the nature of these reorganizations correlates with animals' impairments in detecting brief sound gaps, which is often considered a sign of tinnitus. Acoustic enrichment immediately after noise trauma prevents circuit reorganizations and gap detection deficits, highlighting the potential for using sound therapy soon after cochlear damage to prevent the development of central processing deficits.

Temporal gap and amplitude modulation detection evaluated using the electrically evoked auditory change complex in patients with auditory brainstem implants

This study aims to objectively evaluate temporal processing capabilities using the electrically evoked auditory change complex (eACC) in patients with auditory brainstem implants (ABIs). Study participants include seven Cochlear Nucleus 24M ABI recipients (six children and one adult). All children received ABIs due to cochlear nerve deficiency and the adult recipient was diagnosed with neurofibromatosis type II (NF-2). The speech processor was bypassed and electrical stimulus was a biphasic pulse train directly sent through individual electrodes of the ABI. Gap durations tested in this study ranged from 4 to 256 ms. Amplitude modulation frequency was 10 Hz. Modulation depths tested in this study ranged from 1% to 99%. Behavioral gap detection thresholds were also obtained for two participants. The eACCs were evoked by temporal gaps and amplitude modulations. The shortest gap duration and the smallest amplitude modulation depth that can be used to evoke the eACC vary across study participants and across stimulating electrodes within individual participants. These preliminary data also suggest that the temporal gap detection primarily depends on subcortical auditory neural structures. The eACC can be used to objectively evaluate temporal processing capabilities in both adult and pediatric ABI recipients.

Electrophysiological gap detection thresholds: effects of age and comparison with a behavioral measure.

Temporal processing ability has been linked to speech understanding ability and older adults often complain of difficulty understanding speech in difficult listening situations. Temporal processing can be evaluated using gap detection procedures. There is some research showing that gap detection can be evaluated using an electrophysiological procedure. However, there is currently no research establishing gap detection threshold using the N1-P2 response. The purposes of the current study were to 1) determine gap detection thresholds in younger and older normal-hearing adults using an electrophysiological measure, 2) compare the electrophysiological gap detection threshold and behavioral gap detection threshold within each group, and 3) investigate the effect of age on each gap detection measure. This study utilized an older adult group and younger adult group to compare performance on an electrophysiological and behavioral gap detection procedure. The subjects in this study were 11 younger, normal-hearing adults (mean = 22 yrs) and 11 older, normal-hearing adults (mean = 64.36 yrs). All subjects completed an adaptive behavioral gap detection procedure in order to determine their behavioral gap detection threshold (BGDT). Subjects also completed an electrophysiologic gap detection procedure to determine their electrophysiologic gap detection threshold (EGDT). Older adults demonstrated significantly larger gap detection thresholds than the younger adults. However, EGDT and BGDT were not significantly different in either group. The mean difference between EGDT and BGDT for all subjects was 0.43 msec. Older adults show poorer gap detection ability when compared to younger adults. However, this study shows that gap detection thresholds can be measured using evoked potential recordings and yield results similar to a behavioral measure.

Gap Detection in School-Age Children and Adults: Effects of Inherent Envelope Modulation and the Availability of Cues Across Frequency

The present study evaluated the effects of inherent envelope modulation and the availability of cues across frequency on behavioral gap detection with noise-band stimuli in school-age children. Listeners were 34 normal-hearing children (ages 5.2-15.6 years) and 12 normal-hearing adults (ages 18.5-28.8 years). Stimuli were continuous bands of noise centered on 2000 Hz, either 1000- or 25-Hz wide. In addition to Gaussian noise at these bandwidths, there were conditions using 25-Hz-wide noise bands modified to either accentuate or minimize inherent envelope modulation (staccato and low-fluctuation noise, respectively). Within the 25-Hz-wide conditions, adults' gap detection thresholds were highest in the staccato, lower in the Gaussian, and lowest in the low-fluctuation noise. Similar trends were evident in children's thresholds, although inherent envelope modulation had a smaller effect on children than on adults. Whereas adults' thresholds were comparable for the 1000-Hz-wide Gaussian and 25-Hz-wide low-fluctuation stimulus, children's performance converged on adults' performance at a younger age for the 1000-Hz-wide Gaussian stimulus. Results are consistent with the idea that children are less susceptible to the disruptive effects of inherent envelope modulation than adults when detecting a gap in a narrow-band noise. Further, the ability to use spectrally distributed gap detection cues appears to mature relatively early in childhood.

N1-P2 Recordings to Gaps in Broadband Noise

Normal temporal processing is important for the perception of speech in quiet and in difficult listening situations. Temporal resolution is commonly measured using a behavioral gap detection task, where the patient or subject must participate in the evaluation process. This is difficult to achieve with subjects who cannot reliably complete a behavioral test. However, recent research has investigated the use of evoked potential measures to evaluate gap detection. The purpose of the current study was to record N1-P2 responses to gaps in broadband noise in normal hearing young adults. Comparisons were made of the N1 and P2 latencies, amplitudes, and morphology to different length gaps in noise in an effort to quantify the changing responses of the brain to these stimuli. It was the goal of this study to show that electrophysiological recordings can be used to evaluate temporal resolution and measure the influence of short and long gaps on the N1-P2 waveform. This study used a repeated-measures design. All subjects completed a behavioral gap detection procedure to establish their behavioral gap detection threshold (BGDT). N1-P2 waveforms were recorded to the gap in a broadband noise. Gap durations were 20 msec, 2 msec above their BGDT, and 2 msec. These durations were chosen to represent a suprathreshold gap, a near-threshold gap, and a subthreshold gap. Fifteen normal-hearing young adult females were evaluated. Subjects were recruited from the local university community. Latencies and amplitudes for N1 and P2 were compared across gap durations for all subjects using a repeated-measures analysis of variance. A qualitative description of responses was also included. Most subjects did not display an N1-P2 response to a 2 msec gap, but all subjects had present clear evoked potential responses to 20 msec and 2+ msec gaps. Decreasing gap duration toward threshold resulted in decreasing waveform amplitude. However, N1 and P2 latencies remained stable as gap duration changed. N1-P2 waveforms can be elicited by gaps in noise in young normal-hearing adults. The responses are present as low as 2 msec above behavioral gap detection thresholds (BGDT). Gaps that are below BGDT do not generally evoke an electrophysiological response. These findings indicate that when a waveform is present, the gap duration is likely above their BGDT. Waveform amplitude is also a good index of gap detection, since amplitude decreases with decreasing gap duration. Future studies in this area will focus on various age groups and individuals with auditory disorders.

Human evoked cortical activity to silent gaps in noise: effects of age, attention, and cortical processing speed.

The goal of this study was to examine the degree to which age-related differences in early or automatic levels of auditory processing and attention-related processes explain age-related differences in auditory temporal processing. We hypothesized that age-related differences in attention and cognition compound age-related differences at automatic levels of processing, contributing to the robust age effects observed during challenging listening tasks. We examined age-related and individual differences in cortical event-related potential (ERP) amplitudes and latencies, processing speed, and gap detection from 25 younger and 25 older adults with normal hearing. ERPs were elicited by brief silent periods (gaps) in an otherwise continuous broadband noise and were measured under two listening conditions, passive and active. During passive listening, participants ignored the stimulus and read quietly. During active listening, participants button pressed each time they detected a gap. Gap detection (percent detected) was calculated for each gap duration during active listening (3, 6, 9, 12, and 15 msec). Processing speed was assessed using the Purdue Pegboard Test and the Connections Test. Repeated measures analyses of variance assessed effects of age on gap detection, processing speed, and ERP amplitudes and latencies. An "attention modulation" construct was created using linear regression to examine the effects of attention while controlling for age-related differences in auditory processing. Pearson correlation analyses assessed the extent to which attention modulation, ERPs, and processing speed predicted behavioral gap detection. Older adults had significantly poorer gap detection and slower processing speed than younger adults. Even after adjusting for poorer gap detection, the neurophysiological response to gap onset was atypical in older adults with reduced P2 amplitudes and virtually absent N2 responses. Moreover, individual differences in attention modulation of P2 response latencies and N2 amplitudes predicted gap detection and processing speed in older adults. That is, older adults with P2 latencies that decreased and N2 amplitudes that increased with active listening had faster processing speed and better gap detection than those older adults whose P2 latencies increased and N2 amplitudes decreased with attention. The results from the present study are broadly consistent with previous findings that older adults exhibit significantly poorer gap detection than younger adults in challenging tasks. Even after adjusting for poorer gap detection, older and younger adults showed robust differences in their electrophysiological responses to sound offset. Furthermore, the degree to which attention modulated the ERP was associated with individual variation in measures of processing speed and gap detection. Taken together, these results suggest an age-related deficit in early or automatic levels of auditory temporal processing and that some older adults may be less able to compensate for declines in processing by attending to the stimulus. These results extend our previous findings and support the hypothesis that age-related differences in cognitive or attention-related processing, including processing speed, contribute to an age-related decrease in gap detection.

Age-related changes in glycine receptor subunit composition and binding in dorsal cochlear nucleus

Age-related hearing loss, presbycusis, can be thought of, in part, as a slow progressive peripheral deafferentation. Previous studies suggest that certain deficits seen in presbycusis may partially result from functional loss of the inhibitory neurotransmitter glycine in dorsal cochlear nucleus (DCN). The present study assessed age-related behavioral gap detection changes and neurochemical changes of postsynaptic glycine receptor (GlyRs) subunits and their anchoring protein gephyrin in fusiform cells of young (7–11 months) and aged (28–33 months) Fischer brown Norway (FBN) rats. Aged rats showed significantly (20–30 dB) elevated auditory brainstem-evoked response thresholds across all tested frequencies and worse gap detection ability compared to young FBN rats. In situ hybridization and quantitative immunocytochemistry were used to measure GlyR subunit message and protein levels. There were significant age-related increases in the α 1 subunit message with significant age-related decreases in α 1 subunit protein. Gephyrin message and protein showed significant increases in aged DCN fusiform cells. The pharmacologic consequences of these age-related subunit changes were assessed using [ 3H] strychnine binding. In support of the age-related decrease of α 1 subunit protein levels in DCN, there was a significant age-related decrease in the total number of GlyR binding sites with no significant change in affinity. These age-related changes may reflect an effort to reestablish a homeostatic balance between excitation and inhibition impacting on DCN fusiform cells by downregulation of inhibitory function in the face of an age-related loss of peripheral input. Age-related decrease in presynaptic glycine release results in altered subunit composition and this may correlate with loss of temporal coding of the aged fusiform cell in DCN. The previously reported role for gephyrin in retrograde intracellular receptor subunit trafficking could contribute to the α 1 decrease in the face of increased message.

Kv1.1 channel subunits are not necessary for high temporal acuity in behavioral and electrophysiological gap detection

The Kv1.1 potassium channel subunit, encoded by the Kcna1 gene, is heavily expressed in the auditory brainstem and is thought to have a critical role in producing the high temporal precision of action potentials characteristic of the auditory system. Our intent was to determine whether temporal acuity was reduced in Kcna1 null-mutant (−/−) mice, compared to wild-type (+/+) and heterozygotic mice (+/−), as measured by the encoding of gaps in the inferior colliculus by near-field auditory evoked potentials (NFAEP) or behavioral gap detection (BGD) using a prepulse inhibition paradigm. NFAEPs were collected at 40, 60 and 80 dB SPL with gap durations from 0.5 to 64 ms. BGD data were collected using silent gaps in 70 dB noise from 1 to 15 ms in duration. There were no systematic effects of Kcna1 genotype on NFAEP recovery functions, NFAEP latencies, or the time constant for BGD, but there was a small reduction in asymptotic prepulse inhibition for the longest gap stimuli in −/− mice. Gap thresholds were approximately 1–2 ms across genotypes, stimulus conditions, and paradigms. These data suggest that the neural pathways encoding behaviorally relevant, rapid auditory temporal fluctuations are not limited by the absence of Kv1.1 expression.

Temporal resolution in young and elderly subjects as measured by mismatch negativity and a psychoacoustic gap detection task

Objectives: The speech understanding difficulties of elderly persons with age-related hearing loss may be related in part to reduced auditory temporal resolution. To investigate the effects of aging on temporal resolution, the electrophysiological and psychoacoustic detection thresholds for a very short silent gap within a pure tone were determined, and the relation between the two test results was examined. Methods: Behavioral gap detection thresholds were determined in 10 young and 10 elderly normally hearing subjects using an adaptive test procedure. To elicit mismatch negativity (MMN), deviant stimuli with gap durations varying from 6 to 24 ms in 3 ms steps were presented in separate test blocks. Results: There were no significant differences in the psychoacoustic gap detection thresholds between young and elderly subjects. In contrast, longer gaps were needed to elicit MMN in elderly subjects. They also had significantly reduced MMN peak amplitudes, increased MMN peak latencies, a significantly smaller P2 amplitude and longer P2 latency in their responses to the standard stimulus when compared to the same measures in young subjects. Conclusions: Processing of basic temporal stimulus features in elderly subjects is considerably more reduced at the preattentive level (as indicated by MMN), than when attention is directed to the task (as indicated by the psychoacoustic results).

Mismatch negativity and psychoacoustic measures of gap detection in normally hearing subjects

Temporal auditory processing deficits are thought to play an important role in some pathologies of speech understanding difficulties. The purposes of the present study were to determine whether short silent gaps within a pure tone can be used to elicit mismatch negativity (MMN) as an objective measure of temporal resolution, and to investigate the relation between MMN and performance on a behavioral gap-detection task. The stimuli used for both tasks were 1-kHz sinusoids presented in a low-pass masking noise. Behavioral gap-detection thresholds were determined using an adaptive three-alternative forced-choice procedure. To elicit MMN, a series of deviant stimuli with varying gap durations was generated and presented in an oddball paradigm among standard stimuli without a gap. Only the gaps larger than the mean behavioral gap-detection threshold evoked a clear MMN. There was no clear relation between psychoacoustic and MMN thresholds.

Neural correlates of behavioral gap detection in the inferior colliculus of the young CBA mouse.

The gap detection paradigm is frequently used in psychoacoustics to characterize the temporal acuity of the auditory system. Neural responses to silent gaps embedded in white-noise carriers, were obtained from mouse inferior colliculus (IC) neurons and the results compared to behavioral estimates of gap detection. Neural correlates of gap detection were obtained from 78 single neurons located in the central nucleus of the IC. Minimal gap thresholds (MGTs) were computed from single-unit gap functions and were found to be comparable, 1-2 ms, to the behavioral gap threshold (2 ms). There was no difference in MGTs for units in which both carrier intensities were collected. Single unit responses were classified based on temporal discharge patterns to steady-state noise bursts. Onset and primary-like units had the shortest mean MGTs (2.0 ms), followed by sustained units (4.0 ms) and phasic-off units (4.2 ms). The longest MGTs were obtained for inhibitory neurons (x = 14 ms). Finally, the time-course of behavioral and neurophysiological gap functions were found to be in good agreement. The results of the present study indicate the neural code necessary for behavioral gap detection is present in the temporal discharge patterns of the majority of IC neurons.