Auditory Research publications

Primary auditory cortex (A1) exhibits a tonotopic representation of characteristic frequency (CF). The receptive field properties of A1 neurons emerge from a combination of thalamic inputs and intracortical connections. However, the mechanisms that guide growth of these inputs during development and shape receptive field properties remain largely unknown. We previously showed that Eph family proteins help establish tonotopy in the auditory brainstem. Moreover, other studies have shown that these proteins shape topography in visual and somatosensory cortices. Here, we examined the contribution of Eph proteins to cortical organization of CF, response thresholds and sharpness of frequency tuning. We examined mice with null mutations in EphB2 and EphB3, as these mice show significant changes in auditory brainstem connectivity. We mapped A1 using local field potential recordings in adult EphB2(-/-);EphB3(-/-) and EphB3(-/-) mice, and in a central A1 location inserted a 16-channel probe to measure tone-evoked current-source density (CSD) profiles. Based on the shortest-latency current sink in the middle layers, which reflects putative thalamocortical input, we determined frequency receptive fields and sharpness of tuning (Q(20)) for each recording site. While both mutant mouse lines demonstrated increasing CF values from posterior to anterior A1 similar to wild type mice, we found that the double mutant mice had significantly lower Q(20) values than either EphB3(-/-) mice or wild type mice, indicating broader tuning. In addition, we found that the double mutants had significantly higher CF thresholds and longer onset latency at threshold than mice with wild type EphB2. These results demonstrate that EphB receptors influence auditory cortical responses, and suggest that EphB signaling has multiple functions in auditory system development.

Recent evidence indicates the existence of pyramidal cells (PCs) and interneurons with nontrivial tuning characteristics for sound attributes in the primary auditory cortex (A1) of mammals. These neurons are functionally distributed into layers and sparsely organized at a small scale. However, their topological locations at a large scale in A1 have not yet been investigated. Furthermore, these neurons are usually classified from fine maps of attribute-dependent spiking activity, and not much attention is paid to population postsynaptic potentials related to their activity. We used extracellular recordings obtained from multiple sites in A1 of adult rats to determine neuronal codifiers for sound attributes defined by coarse representations of the population dose–response curves. We demonstrated that these codifiers, majorly involving PCs, are heterogeneously distributed along A1. Spiking activity in these neurons during stimulation was correlated to β (12–25 Hz) and low γ (25–70 Hz) postsynaptic oscillations in the infragranular layer, whereas in the supragranular layer, better correlations were found with high γ (70–170 Hz) oscillations. The time-frequency analysis of the postsynaptic potentials showed a transient broadband power increase in all layers after the stimulus onset that was followed by a sustained high γ oscillation in the supragranular layer, fluctuations in the laminar content of the low-frequency oscillations, and a global attenuation in the low-frequency powers after the stimulus offset that happened together with a long-lasting strengthening of the β oscillations. We concluded that, for rats, sounds are codified in A1 by segregated networks of specialized PCs whose postsynaptic activity impinges on the emergence of sparse/dense spiking patterns.

Sensory pathways process behaviorally relevant signals in various contexts and therefore have to adapt to differing background conditions. Depending on changes in signal statistics, this adjustment might be a combination of two fundamental computational operations: subtractive adaptation shifting a neuron's threshold and divisive gain control scaling its sensitivity. The cricket auditory system has to deal with highly stereotyped conspecific songs at low carrier frequencies, and likely much more variable predator signals at high frequencies. We proposed that due to the differences between the two signal classes, the operation that is implemented by adaptation depends on the carrier frequency. We aimed to identify the biophysical basis underlying the basic computational operations of subtraction and division. We performed in vivo intracellular and extracellular recordings in a first-order auditory interneuron (AN2) that is active in both mate recognition and predator avoidance. We demonstrated subtractive shifts at the carrier frequency of conspecific songs and division at the predator-like carrier frequency. Combined application of current injection and acoustic stimuli for each cell allowed us to demonstrate the subtractive effect of cell-intrinsic adaptation currents. Pharmacological manipulation enabled us to demonstrate that presynaptic inhibition is most likely the source of divisive gain control. We showed that adjustment to the sensory context can depend on the class of signals that are relevant to the animal. We further revealed that presynaptic inhibition is a simple mechanism for divisive operations. Unlike other proposed mechanisms, it is widely available in the sensory periphery of both vertebrates and invertebrates.

Adolescent smoking is associated with auditory-cognitive deficits and structural alterations to auditory thalamocortical systems, suggesting that higher auditory function is vulnerable to nicotine exposure during adolescence. Although nicotinic acetylcholine receptors (nAChRs) regulate thalamocortical processing in adults, it is not known whether they regulate processing at earlier ages since their expression pattern changes throughout postnatal development. Here we investigate nicotinic regulation of tone-evoked current source density (CSD) profiles in mouse primary auditory cortex from just after hearing onset until adulthood. At the youngest ages, systemic nicotine did not affect CSD profiles. However, beginning in early adolescence nicotine enhanced characteristic frequency (CF)-evoked responses in layers 2–4 by enhancing thalamocortical, early intracortical, and late intracortical response components. Nicotinic responsiveness developed rapidly and peaked over the course of adolescence, then declined thereafter. Generally, responsiveness in females developed more quickly, peaked earlier, and declined more abruptly and fully than in males. In contrast to the enhancement of CF-evoked responses, nicotine suppressed shorter-latency intracortical responses to spectrally distant (non-CF) stimuli while enhancing longer-latency responses. Intracortical infusion of nAChR antagonists showed that enhancement of CF-evoked intracortical processing involves α4β2*, but not α7, nAChRs, whereas both receptor subtypes regulate non-CF-evoked late intracortical responses. Notably, antagonist effects in females implied regulation by endogenous acetylcholine. Thus, nicotinic regulation of cortical processing varies with age and sex, with peak effects during adolescence that may contribute to the vulnerability of adolescents to smoking.

Animal experiments suggest that chronic tinnitus ("ringing in the ears") may result from processes that overcompensate for lost afferent input. Abnormally elevated spontaneous neural activity has been found in the dorsal cochlear nucleus (DCN) of animals with psychophysical evidence of tinnitus. However, it has also been reported that DCN ablation fails to reduce established tinnitus. Since other auditory areas have been implicated in tinnitus, the role of the DCN is unresolved. The apparently conflicting electrophysiological and lesion data can be reconciled if the DCN serves as a necessary trigger zone rather than a chronic generator of tinnitus. The present experiment used lesion procedures identical to those that failed to decrease pre-existing tinnitus. The exception was that lesions were done prior to tinnitus induction. Young adult rats were trained and tested using a psychophysical procedure shown to detect tinnitus. Tinnitus was induced by a single unilateral high-level noise exposure. Consistent with the trigger hypothesis, bilateral dorsal DCN lesions made before high-level noise exposure prevented the development of tinnitus. A protective effect stemming from disruption of the afferent pathway could not explain the outcome because unilateral lesions ipsilateral to the noise exposure did not prevent tinnitus and unilateral lesions contralateral to the noise exposure actually exacerbated the tinnitus. The DCN trigger mechanism may involve plastic circuits that, through loss of inhibition, or upregulation of excitation, increase spontaneous neural output to rostral areas such as the inferior colliculus. The increased drive could produce persistent pathological changes in the rostral areas, such as high-frequency bursting and decreased interspike variance, that comprise the chronic tinnitus signal.

Cochlear implant listeners receive auditory stimulation through amplitude-modulated electric pulse trains. Auditory nerve studies in animals demonstrate qualitatively different patterns of firing elicited by low versus high pulse rates, suggesting that stimulus pulse rate might influence the transmission of temporal information through the auditory pathway. We tested in awake guinea pigs the temporal acuity of auditory cortical neurons for gaps in cochlear implant pulse trains. Consistent with results using anesthetized conditions, temporal acuity improved with increasing pulse rates. Unlike the anesthetized condition, however, cortical neurons responded in the awake state to multiple distinct features of the gap-containing pulse trains, with the dominant features varying with stimulus pulse rate. Responses to the onset of the trailing pulse train (Trail-ON) provided the most sensitive gap detection at 1,017 and 4,069 pulse-per-second (pps) rates, particularly for short (25 ms) leading pulse trains. In contrast, under conditions of 254 pps rate and long (200 ms) leading pulse trains, a sizeable fraction of units demonstrated greater temporal acuity in the form of robust responses to the offsets of the leading pulse train (Lead-OFF). Finally, TONIC responses exhibited decrements in firing rate during gaps, but were rarely the most sensitive feature. Unlike results from anesthetized conditions, temporal acuity of the most sensitive units was nearly as sharp for brief as for long leading bursts. The differences in stimulus coding across pulse rates likely originate from pulse rate-dependent variations in adaptation in the auditory nerve. Two marked differences from responses to acoustic stimulation were: first, Trail-ON responses to 4,069 pps trains encoded substantially shorter gaps than have been observed with acoustic stimuli; and second, the Lead-OFF gap coding seen for <15 ms gaps in 254 pps stimuli is not seen in responses to sounds. The current results may help to explain why moderate pulse rates around 1,000 pps are favored by many cochlear implant listeners.

We recently demonstrated that sub-chronic low-dose kanamycin (KM, 300 mg/kg sc, 2×/day, 10 days) dramatically reduces permanent noise-induced hearing loss (NIHL) and hair cell loss in 1 month old CBA/J mice (Fernandez et al., 2010, J. Assoc. Res. Otolaryngol. 11, 235-244). Protection by KM remained for at least 48 h after the last dose, and appeared to involve a cumulative effect of multiple doses as part of a preconditioning process. The first month of life lies within the early 'sensitive period' for both cochlear noise and ototoxic injury in mice, and CBA/J mice appear exquisitely vulnerable to noise during this period (Ohlemiller et al., 2011; Hearing Res. 272, 13-20). From our initial data, we could not rule out 1) that less rigorous treatment protocols than the intensive one we applied may be equally-or more-protective; 2) that protection by KM is tightly linked to processes unique to the sensitive period for noise or ototoxins; or 3) that protection by KM is exclusive to CBA/J mice. The present experiments address these questions by varying the number and timing of fixed doses (300 mg/kg sc) of KM, as well as the age at treatment in CBA/J mice. We also tested for protection in young C57BL/6J (B6) mice. We find that nearly complete protection against at least 2 h of intense (110 dB SPL) broadband noise can be observed in CBA/J mice at least for ages up to 1 year. Reducing dosing frequency to as little as once every other day (a four-fold decrease in dosing frequency) appeared as protective as twice per day. However, reducing the number of doses to just 1 or 2, followed by noise 24 or 48 h later greatly reduced protection. Notably, hearing thresholds and hair cells in young B6 mice appeared completely unprotected by the same regimen that dramatically protects CBA/J mice. We conclude that protective effects of KM against NIHL in CBA/J mice can be engaged by a wide range of dosing regimens, and are not exclusive to the sensitive period for noise or ototoxins. While we cannot presently judge the generality of protection across genetic backgrounds, it appears not to be universal, since B6 showed no benefit. Classical genetic approaches based on CBA/J × B6 crosses may reveal loci critical to protective cascades engaged by kanamycin and perhaps other preconditioners. Their human analogs may partly determine who is at elevated risk of acquired hearing loss.

Aberrant, lesion-induced neuroplastic changes in the auditory pathway are believed to give rise to the phantom sound of tinnitus. Noise-induced cochlear damage can induce extensive fiber growth and synaptogenesis in the cochlear nucleus, but it is currently unclear if these changes are linked to tinnitus. To address this issue, we unilaterally exposed nine rats to narrow-band noise centered at 12 kHz at 126 dB sound pressure level (SPL) for 2 h and sacrificed them 10 weeks later for evaluation of synaptic plasticity (growth-associated protein 43 [GAP-43] expression) in the cochlear nucleus. Noise-exposed rats along with three age-matched controls were screened for tinnitus-like behavior with gap prepulse inhibition of the acoustic startle (GPIAS) before, 1-10 days after, and 8-10 weeks after the noise exposure. All nine noise-exposed rats showed similar patterns of severe hair cell loss at high- and mid-frequency regions in the exposed ear. Eight of the nine showed strong up-regulation of GAP-43 in auditory nerve fibers and pronounced shrinkage of the ventral cochlear nucleus (VCN) on the noise-exposed side, and strong up-regulation of GAP-43 in the medial ventral VCN, but not in the lateral VCN or the dorsal cochlear nucleus. GAP-43 up-regulation in VCN was significantly greater in Noise-No-Tinnitus rats than in Noise-Tinnitus rats. One Noise-No-Tinnitus rat showed no up-regulation of GAP-43 in auditory nerve fibers and only little VCN shrinkage, suggesting that auditory nerve degeneration plays a role in tinnitus generation. Our results suggest that noise-induced tinnitus is suppressed by strong up-regulation of GAP-43 in the medial VCN. GAP-43 up-regulation most likely originates from medial olivocochlear neurons. Their increased excitatory input on inhibitory neurons in VCN may possibly reduce central hyperactivity and tinnitus.

We have studied eye-head coordination in nonhuman primates with acoustic targets after finding that they are unable to make accurate saccadic eye movements to targets of this type with the head restrained. Three male macaque monkeys with experience in localizing sounds for rewards by pointing their gaze to the perceived location of sources served as subjects. Visual targets were used as controls. The experimental sessions were configured to minimize the chances that the subject would be able to predict the modality of the target as well as its location and time of presentation. The data show that eye and head movements are coordinated differently to generate gaze shifts to acoustic targets. Chiefly, the head invariably started to move before the eye and contributed more to the gaze shift. These differences were more striking for gaze shifts of <20–25° in amplitude, to which the head contributes very little or not at all when the target is visual. Thus acoustic and visual targets trigger gaze shifts with different eye-head coordination. This, coupled to the fact that anatomic evidence involves the superior colliculus as the link between auditory spatial processing and the motor system, suggests that separate signals are likely generated within this midbrain structure.

Intracortical microstimulation (ICMS), which has shown promise in the visual, auditory and somatosensory systems as a platform for sensory prostheses, typically relies on charged balanced, symmetric, biphasic stimulation. However, neural stimulation models as well as experiments conducted in cochlear implant users have suggested that charge balanced asymmetric pulses could generate lower detection thresholds for stimulation in terms of charge per phase. For this study, rats were chronically implanted with microelectrode arrays unilaterally in their right auditory cortex and then trained to detect ICMS delivered through a single electrode site in order to determine their behavioral threshold. This model was used in two experiments. The first experiment addressed the effect of lead phase direction, asymmetry, and phase duration on detection threshold. The second experiment fixed the cathode phase duration at 123 μs and varied only the phase asymmetry and lead phase direction. Taken together, the results of these experiments suggest that, for ICMS, the primary determinant of threshold level is cathode phase duration, and that asymmetry provides no significant advantage when compared to symmetric, cathode leading pulses. However, symmetric anode leading pulses of less than or equal to 205 μs per phase consistently showed higher thresholds when compared to all other pulses of equal cathode phase duration.

It is well known that ethacrynic acid (EA) can potentiate the ototoxicity of aminoglycoside antibiotics (AmAn) such as kanamycin (KM), if they were applied at the same time. Currently, to create the model of EA-KM-induced cochlear lesion in rats, adult rats received a single injection of EA (75 mg/kg, intravenous injection), or followed immediately by KM (500 mg/kg, intramuscular injection). The hearing function was assessed by auditory brainstem response (ABR) measurement in response to click and/or tone bursts at 4, 8, 12, 16, 20, 24, and 32 kHz. The static microcirculation status in the stria vascularis after a single EA injection was evaluated with eosin staining. The pathological changes in cochlear and vestibular hair cells were also quantified after co-administration of EA and KM. After a single EA injection, blood flow in vessels supplying the stria vascularis rapidly diminished. However, the blood supply to the cochlear lateral wall partially recovered 5 h after EA treatment. Threshold changes in ABR were basically parallel to the microcirculation changes in stria vascularis after single EA treatment. Importantly, disposable co-administration of EA and KM resulted in a permanent hearing loss and severe damage to the cochlear hair cells, but spared the vestibular hair cells. Since the cochlear lateral wall is the important part of the blood-cochlea barrier, EA-induced anoxic damage to the epithelium of stria vascularis may enhance the entry of KM to the cochlea. Thus, experimental animal model of selective cochlear damage with normal vestibular systems can be reliably created through co-administration of EA and KM.

Performance evaluation is a critical feature of motor learning. In the vocal system, it requires the integration of auditory feedback signals with vocal motor commands. The network activity that supports such integration is unknown, but it has been proposed that vocal performance evaluation occurs offline. Recording from NIf, a sensorimotor structure in the avian song system, we show that short bouts of singing in adult male zebra finches ( Taeniopygia guttata ) induce persistent increases in firing activity and coherent oscillations in the fast gamma range (90–150 Hz). Single units are strongly phase locked to these oscillations, which can last up to 30 s, often outlasting vocal activity by an order of magnitude. In other systems, oscillations often are triggered by events or behavioral tasks but rarely outlast the event that triggered them by more than 1 s. The present observations are the longest reported gamma oscillations triggered by an isolated behavioral event. In mammals, gamma oscillations have been associated with memory consolidation and are hypothesized to facilitate communication between brain regions. We suggest that the timing and persistent nature of NIf's fast gamma oscillations make them well suited to facilitate the integration of auditory and vocal motor traces associated with vocal performance evaluation.

The primary auditory cortex (A1) is involved in sound localization. A consistent observation in A1 is a clustered representation of binaural properties, but how spatial tuning varies within binaural clusters is unknown. Here, this issue was addressed in A1 of the pallid bat, a species that relies on passive hearing (as opposed to echolocation) to localize prey. Evidence is presented for systematic representations of sound azimuth within two binaural clusters in the pallid bat A1: the binaural inhibition (EI) and peaked (P) binaural interaction clusters. The representation is not a “point-to-point” space map as seen in the superior colliculus, but is in the form of a systematic increase in the area of activated cortex as azimuth changes from ipsilateral to contralateral locations. The underlying substrate in the EI cluster is a systematic representation of the medial boundary of azimuth receptive fields. The P cluster is activated mostly for sounds near the midline, providing a spatial acoustic fovea. Activity in the P cluster falls off systematically as the sound is moved to more lateral locations. Sensitivity to interaural intensity differences predicts azimuth tuning in the vast majority of neurons. Azimuth receptive field properties are relatively stable across intensity over a moderate range (20–40 dB above threshold) of intensities. This suggests that the maps will be similar across the intensities tested. These results challenge the current view that no systematic representation of azimuth is present in A1 and show that such representations are present locally within individual binaural clusters.

Objective The degeneration of hair cells and spiral ganglion neurons (SGNs) is an important pathologic process in the development of sensorineural hearing loss. In a murine model, predictable and reproducible damage to SGNs occurs through the application of ouabain to the round window. Recent evidence has shown that the chemokine stromal cell–derived factor‐1 (SDF‐1) is a potent chemoattractant of hematopoietic stem cells (HSCs) and provides trophic support to injured tissues during development and maturation. The hypothesis for the current study is that expression of SDF‐1 plays an important role in protecting SGNs and preventing further degeneration in the setting of cochlear injury. Study Design Prospective, controlled. Setting Academic research laboratory. Subject and Methods Auditory brainstem response (ABR) and the expression of SDF‐1 mRNA and protein were examined 1, 3, 7, 14, and 30 days after application of ouabain in 35 adult mice. Results Following ouabain application, real‐time reverse‐transcription polymerase chain reaction for SDF demonstrates increased mRNA expression following ouabain injury in nontransplanted mice. A significant increase in SDF protein expression was also observed using immunolabeling techniques and Western blot analysis. Conclusions SDF‐1 expression is increased in the auditory nerve following cochlear injury. Further knowledge about the cochlear microenvironment, including SDF‐1, is critical to maximizing HSC engraftment in the injured cochlea and providing a therapeutic option for sensorineural hearing loss.

Inhibitory interneurons constitute ∼20% of auditory cortical cells and are essential for shaping sensory processing. Connectivity patterns of interneurons in relation to functional organization principles are not well understood. We contrasted the connection patterns of parvalbumin-immunoreactive cells in two functionally distinct cortical regions: the tonotopic, narrowly frequency-tuned module [central narrow band (cNB)] of cat central primary auditory cortex (AI) and the nontonotopic, broadly tuned second auditory field (AII). Interneuronal connectivity patterns and laminar distribution were identified by combining a retrograde tracer (wheat-germ agglutinin apo-horseradish peroxidase colloidal gold) with labeling of the Ca 2+ binding protein parvalbumin (Pv), a marker for the GABAergic interneurons usually described physiologically as fast-spiking neurons. In AI, parvalbumin-positive (Pv+) cells constituted 13% of the retrograde labeled cells in the immediate vicinity of the injection site, compared to 10% in AII. The retrograde labeling of Pv+ cells along isofrequency countours was confined to the cNB. The spatial spread of labeled excitatory neurons in AI was more than twice that found for Pv+ cells. By contrast, in the AII, the spread of Pv+ cells was nearly equal to that of excitatory neurons. The retrograde labeling of Pv+ cells was anisotropic in AI and isotropic in AII. This demonstration of inhibitory networks in auditory cortex reveals that the connections of cat GABAergic AI and AII cells follow different anatomical plans and thus contribute differently to the shaping of neural response properties. The finding that local connectivity of parvalbumin-immunoreactive neurons in AI is closely aligned with spectral integration properties demonstrates the critical role of inhibition in creating distinct processing modules in AI.

Gamma-band oscillations are a ubiquitous phenomenon in the nervous system and have been implicated in multiple aspects of cognition. In particular, the strength of gamma oscillations at the time a stimulus is encoded predicts its subsequent retrieval, suggesting that gamma may reflect enhanced mnemonic processing. Likewise, activity in the gamma-band can modulate plasticity in vitro . However, it is unclear whether experience-dependent plasticity in vivo is also related to gamma-band activation. The aim of the present study was to determine whether gamma activation in primary auditory cortex modulates both the associative memory for an auditory stimulus during classical conditioning and its accompanying specific receptive field plasticity. Rats received multiple daily sessions of single tone/shock trace and two-tone discrimination conditioning, during which local field potentials and multiunit discharges were recorded from chronically implanted electrodes. We found that the strength of tone-induced gamma predicted the acquisition of associative memory 24 h later and ceased to predict subsequent performance once asymptote was reached. Gamma activation also predicted receptive field plasticity that specifically enhanced representation of the signal tone. This concordance provides a long-sought link between gamma oscillations, cortical plasticity, and the formation of new memories.

The computational role of cortical layers within auditory cortex has proven difficult to establish. One hypothesis is that interlaminar cortical processing might be dedicated to analyzing temporal properties of sounds; if so, then there should be systematic depth-dependent changes in cortical sensitivity to the temporal context in which a stimulus occurs. We recorded neural responses simultaneously across cortical depth in primary auditory cortex and anterior auditory field of CBA/Ca mice, and found systematic depth dependencies in responses to second-and-later noise bursts in slow (1–10 bursts/s) trains of noise bursts. At all depths, responses to noise bursts within a train usually decreased with increasing train rate; however, the rolloff with increasing train rate occurred at faster rates in more superficial layers. Moreover, in some recordings from mid-to-superficial layers, responses to noise bursts within a 3–4 bursts/s train were stronger than responses to noise bursts in slower trains. This non-monotonicity with train rate was especially pronounced in more superficial layers of the anterior auditory field, where responses to noise bursts within the context of a slow train were sometimes even stronger than responses to the noise burst at train onset. These findings may reflect depth dependence in suppression and recovery of cortical activity following a stimulus, which we suggest could arise from laminar differences in synaptic depression at feedforward and recurrent synapses.

Most noise-reduction algorithms used in hearing aids apply a gain to the noisy envelopes to reduce noise interference. The present study assesses the impact of two types of speech distortion introduced by noise-suppressive gain functions: amplification distortion occurring when the amplitude of the target signal is over-estimated, and attenuation distortion occurring when the target amplitude is under-estimated. Sentences corrupted by steady noise and competing talker were processed through a noise-reduction algorithm and synthesized to contain either amplification distortion, attenuation distortion or both. The attenuation distortion was found to have a minimal effect on speech intelligibility. In fact, substantial improvements (> 80 percentage points) in intelligibility, relative to noise-corrupted speech, were obtained when the processed sentences contained only attenuation distortion. When the amplification distortion was limited to be smaller than 6 dB, performance was nearly unaffected in the steady-noise conditions, but was severely degraded in the competing-talker conditions. Overall, the present data suggest that one reason that existing algorithms do not improve speech intelligibility is because they allow amplification distortions in excess of 6 dB. These distortions are shown in this study to be always associated with masker-dominated envelopes and should thus be eliminated.

Objective: The purpose of the present study was to examine the effects of age and visual content on cross-modal enhancement of auditory speech detection. Visual content consisted of three clearly distinct types of visual information: an unaltered video clip of a talker's face, a low-contrast version of the same clip, and a mouth-like Lissajous figure. It was hypothesized that both young and older adults would exhibit reduced enhancement as visual content diverged from the original clip of the talker's face, but that the decrease would be greater for older participants. Design: Nineteen young adults and 19 older adults were asked to detect a single spoken syllable (/ba/) in speech-shaped noise, and the level of the signal was adaptively varied to establish the signal-to-noise ratio (SNR) at threshold. There was an auditory-only baseline condition and three audiovisual conditions in which the syllable was accompanied by one of the three visual signals (the unaltered clip of the talker's face, the low-contrast version of that clip, or the Lissajous figure). For each audiovisual condition, the SNR at threshold was compared with the SNR at threshold for the auditory-only condition to measure the amount of cross-modal enhancement. Results: Young adults exhibited significant cross-modal enhancement with all three types of visual stimuli, with the greatest amount of enhancement observed for the unaltered clip of the talker's face. Older adults, in contrast, exhibited significant cross-modal enhancement only with the unaltered face. Conclusions: Results of this study suggest that visual signal content affects cross-modal enhancement of speech detection in both young and older adults. They also support a hypothesized age-related deficit in processing low-contrast visual speech stimuli, even in older adults with normal contrast sensitivity.

Objectives: The purpose of this study was to examine the effects of degree and configuration of hearing loss on the use of, and benefit from, information in amplified high- and low-frequency speech presented in background noise. Design: Sixty-two adults with a wide range of high- and low-frequency sensorineural hearing loss (5 to 115+ dB HL) participated in the study. To examine the contribution of speech information in different frequency regions, speech understanding in noise was assessed in multiple low- and high-pass filter conditions, as well as a band-pass (713 to 3534 Hz) and wideband (143 to 8976 Hz) condition. To increase audibility over a wide frequency range, speech and noise were amplified based on each individual's hearing loss. A stepwise multiple linear regression approach was used to examine the contribution of several factors to (1) absolute performance in each filter condition and (2) the change in performance with the addition of amplified high- and low-frequency speech components. Results: Results from the regression analysis showed that degree of hearing loss was the strongest predictor of absolute performance for low- and high-pass filtered speech materials. In addition, configuration of hearing loss affected both absolute performance for severely low-pass filtered speech and benefit from extending high-frequency (3534 to 8976 Hz) bandwidth. Specifically, individuals with steeply sloping high-frequency losses made better use of low-pass filtered speech information than individuals with similar low-frequency thresholds but less high-frequency loss. In contrast, given similar high-frequency thresholds, individuals with flat hearing losses received more benefit from extending high-frequency bandwidth than individuals with more sloping losses. Conclusions: Consistent with previous work, benefit from speech information in a given frequency region generally decreases as degree of hearing loss in that frequency region increases. However, given a similar degree of loss, the configuration of hearing loss also affects the ability to use speech information in different frequency regions. Except for individuals with steeply sloping high-frequency losses, providing high-frequency amplification (3534 to 8976 Hz) had either a beneficial effect on, or did not significantly degrade, speech understanding. These findings highlight the importance of extended high-frequency amplification for listeners with a wide range of high-frequency hearing losses, when seeking to maximize intelligibility.