Auditory Research publications

Objectives: There have been many studies on the relationship between diabetes mellitus and presbycusis. Microangiopathy and neuropathy that's caused by chronic hyperglycemia may lead to damage to the inner ear. Several clinical studies on humans and animal studies have been performed to investigate the association between diabetes and hearing loss, however, this relationship is still a matter of debate. We investigated the association of diabetes and sensorineural hearing loss in an animal model of type-2 diabetes and obesity (the ob/ob mouse [OM]). Methods: The auditory brainstem response (ABR) thresholds were obtained in the OM and the wild type mice (C57BL/6J mice) up to 25 weeks after birth. After the animals were sacrificed, their cochleae were retrieved and then subjected to histopathologic observations. Results: The OM exhibited significantly elevated ABR thresholds at 21 weeks of age, yet the C57BL/6J mice exhibited no significant change until 25 weeks of age. On the histological findings, outer hair cell degeneration and loss of spiral ganglion cells were observed in the middle and basal turns of the OM. On the contrary, no degenerative change was observed until 25 weeks of age in the C57BL/6J mice. Conclusion: This study suggests that chronic hyperglycemia and obesity may lead to early sensorineural hearing loss.

In this study, two experiments were conducted to investigate the specificity of adaptation to real-time formant shifting. During the experiments, talkers were adapted to altered auditory feedback for one vowel (trained vowel) and received unaltered feedback for a different vowel (untrained vowel). In the first experiment, production of the untrained vowel was measured while the talker was in the process of adapting to the altered feedback for the trained vowel. In the second experiment, production of the untrained vowel was measured after talkers had adapted to the altered feedback for the trained vowel. In both experiments, talkers spontaneously modified production of the trained vowel in response to the altered auditory feedback. In the first experiment, talkers slightly altered production of the untrained vowel while the trained vowel was adapting to the altered feedback. In the second experiment, production of the untrained vowel was not altered after talkers had completely adapted to the altered feedback of the trained vowel. These results suggest that the degree of generalization depends on the conditions of adaptation and on the information available about the acoustic environment.

Objectives: Apoptosis of outer hair cell (OHC) can be identified through nuclear staining by specific nuclear changes. The change of filamentous actin (F-actin) is also involved in early cell death process. The study was designed to investigate OHC death along the whole length of the organ of Corti. Methods: BALB/c hybrid mice were used in this study. The noise group was exposed to white noise of 120 dB SPL for 3 hr per day for 3 consecutive days. The tone burst auditory brainstem response (ABR) test was conducted and cochleas from each group were obtained for the immunostaining of FITC phalloidin for F-actin and propidium iodide (PI) for nuclei. Results: ABR threshold of the noise group significantly increased after noise exposure (P<0.001). No threshold shift was found in the control group. Threshold shift of the noise group constantly increased from 4 to 16 kHz, but threshold shifts at 16 kHz and 32 kHz were similar. Patterns of OHC staining were subclassified as FITC+PI- cells, FITC+ PI+ cells, FITC-PI+ cells and missing cells. Proportion of normal live OHCs (FITC+PI-) rapidly decreased from the apex to the base. In the basal turn, FITC-PI+ cells and vacancy OHC (missing cells) were observed easily. Apoptotic and missing cells were most abundant at 60% of the whole length of the Corti organ. Conclusion: We could subclassify morphologic changes in OHC death after noise exposure. Quantitative changes in OHCs along the whole Corti organ showed a plateau pattern similar to that of a frequency-specific threshold shift.

Using field broadcasts of model male calling songs, we tested whether Tibicen pruinosa and T. chloromera (Hemiptera: Cicadidae) are candidate hosts for acoustic parasitoid flies. The model calling song of T. pruinosa attracted 90% of the flies (Sarcophagidae: Emblemasoma sp.; all larvapositing females) when broadcast simultaneously with the model T. chloromera song, a phonotactic bias reconfirmed in single song playbacks. In paired broadcasts of model T. pruinosa songs with different relative amplitudes (3 dB or 6 dB), significantly more flies were attracted to the more powerful song, a result consistent with the responses predicted by a model proposed by Forrest and Raspet [1994]. Using intracellular recordings and dye injections, we characterized the sensitivity of auditory units in sound-trapped flies. Intracellular recordings from six auditory units (5 interneurons, 1 afferent) revealed best sensitivity for frequencies near 3–4 kHz, matching the predominant spectral components of the calling songs of both species of cicada. Interestingly, although flies could be attracted to T. pruinosa broadcasts throughout the day, hourly censuses of singing males revealed that calling occurred exclusively at dusk. Furthermore, the duration of the dusk chorus in T. pruinosa was significantly shorter than the midday chorus of the less attractive song of T. chloromera. We propose that the tight temporal aggregation of the dusk chorus time could function to reduce risk from attracted parasitoids.

The authors examined whether progressively training humans and rats to perform a difficult auditory identification task led to larger improvements than extensive training with highly similar sounds (the easy-to-hard effect). Practice improved humans' ability to distinguish sounds regardless of the training regimen. However, progressively trained subjects were more accurate and showed more generalization, despite significantly less training with the stimuli that were the most difficult to distinguish. Rats showed less capacity to improve with practice but still benefited from progressive training. These findings indicate that transitioning from an easier to a more difficult task during training can facilitate, and in some cases may be essential for, auditory perceptual learning. The results are not predicted by an explanation that assumes interaction of generalized excitation and inhibition but are consistent with a hierarchical account of perceptual learning in which the representational precision required to distinguish stimuli determines the mechanisms engaged during learning.

The neural computations that underlie the processing of auditory-stimulus identity are not well understood, especially how information is transformed across different cortical areas. Here, we compared the capacity of neurons in the superior temporal gyrus (STG) and the ventrolateral prefrontal cortex (vPFC) to code the identity of an auditory stimulus; these two areas are part of a ventral processing stream for auditory-stimulus identity. Whereas the responses of neurons in both areas are reliably modulated by different vocalizations, STG responses code significantly more vocalizations than those in the vPFC. Together, these data indicate that the STG and vPFC differentially code auditory identity, which suggests that substantial information processing takes place between these two areas. These findings are consistent with the hypothesis that the STG and the vPFC are part of a functional circuit for auditory-identity analysis.

Gonadectomized and intact adult C57BL/6J (B6) mice of both sexes were exposed for 12h nightly to an augmented acoustic environment (AAE): repetitive bursts of a 70dB SPL noise band. The high-frequency AAE (HAAE) was a half-octave band centered at 20kHz; the low-frequency AAE (LAAE) was a 2-8kHz band. The effects of sex, gonadectomy, and AAE treatment on genetic progressive hearing loss (a trait of B6 mice) were evaluated by obtaining auditory brainstem response (ABR) thresholds at ages 3-, 6-, and 9-months. At 9-months of age, hair cell counts (cytocochleograms) were obtained, and morphometric measures of the anteroventral cochlear nucleus (AVCN) were obtained. LAAE treatment caused elevation in ABR thresholds (8-24kHz), with the highest thresholds occurring in intact females. LAAE treatment caused some loss of outer hair cells in the basal half of the cochlea (in addition to losses normally occurring in B6 mice), with intact females losing more cells than intact males. The loss of AVCN neurons and shrinkage of tissue volume that typically occur in 9-month-old B6 mice was lessened by LAAE treatment in intact (but not gonadectomized) male mice, whereas the degenerative changes were exacerbated in intact (but not gonadectomized) females. These LAAE effects were prominent in, but not restricted to, the tonotopic low-frequency (ventral) AVCN. HAAE treatment resulted in some loss of neurons in the high-frequency (dorsal) AVCN. In general, LAAE treatment plus male gonadal hormones (intact males) had an ameliorative effect whereas HAAE or LAAE treatment plus ovarian hormones (intact females) had a negative effect on age-related changes in the B6 auditory system.

The multichannel design of contemporary cochlear implants (CIs) is predicated on the assumption that each channel activates a relatively restricted and independent sector of the deaf auditory nerve array, just as a sound within a restricted frequency band activates a restricted region of the normal cochlea The independence of CI channels, however, is limited; and the factors that determine their independence, the relative overlap of the activity patterns that they evoke, are poorly understood. In this study, we evaluate the spread of activity evoked by cochlear implant channels by monitoring activity at 16 sites along the tonotopic axis of the guinea pig inferior colliculus (IC). "Spatial tuning curves" (STCs) measured in this way serve as an estimate of activation spread within the cochlea and the ascending auditory pathways. We contrast natural stimulation using acoustic tones with two kinds of electrical stimulation either (1) a loose fitting banded array consisting of a cylindrical silicone elastomer carrier with a linear series of ring contacts; or (2) a space-filling array consisting of a tapered silicone elastomer carrier that is designed to fit snugly into the guinea pig scala tympani with a linear series of ball contacts positioned along it Spatial tuning curves evoked by individual acoustic tones, and by activation of each contact of each array as a monopole, bipole or tripole were recorded. Several channel configurations and a wide range of electrode separations were tested for each array, and their thresholds and selectivity were estimated. The results indicate that the tapered space-filling arrays evoked more restricted activity patterns at lower thresholds than did the banded arrays. Monopolar stimulation (one intracochlear contact activated with an extracochlear return) using either array evoked broad activation patterns that involved the entire recording array at current levels <6dBSL, but at relatively low thresholds. Bi- and tri-polar configurations of both array types evoked more restricted activity patterns, but their thresholds were higher than those of monopolar configurations. Bipolar and tripolar configurations with closely spaced contacts evoked activity patterns that were comparable to those evoked by pure tones. As the spacing of bipolar electrodes was increased (separations >1mm), the activity patterns became broader and evoked patterns with two distinct threshold minima, one associated with each contact.

The basic helix-loop-helix (bHLH) transcription factor Math5 (Atoh7) is required for retinal ganglion cell (RGC) and optic nerve development. Using Math5-lacZ knockout mice, we have identified an additional expression domain for Math5 outside the eye, in functionally connected structures of the central auditory system. In the adult hindbrain, the cytoplasmic Math5-lacZ reporter is expressed within the ventral cochlear nucleus (VCN), in a subpopulation of neurons that project to medial nucleus of the trapezoid body (MNTB), lateral superior olive (LSO), and lateral lemniscus (LL). These cells were identified as globular and small spherical bushy cells based on their morphology, abundance, distribution within the cochlear nucleus (CN), co-expression of Kv1.1, Kv3.1b and Kcnq4 potassium channels, and projection patterns within the auditory brainstem. Math5-lacZ is also expressed by cochlear root neurons in the auditory nerve. During embryonic development, Math5-lacZ was detected in precursor cells emerging from the caudal rhombic lip from embryonic day (E)12 onwards, consistent with the time course of CN neurogenesis. These cells co-express MafB and are post-mitotic. Math5 expression in the CN was verified by mRNA in situ hybridization, and the identity of positive neurons was confirmed morphologically using a Math5-Cre BAC transgene with an alkaline phosphatase reporter. The hindbrains of Math5 mutants appear grossly normal, with the exception of the CN. Although overall CN dimensions are unchanged, the lacZ-positive cells are significantly smaller in Math5 -/- mice compared to Math5 +/- mice, suggesting these neurons may function abnormally. The auditory brainstem response (ABR) of Math5 mutants was evaluated in a BALB/cJ congenic background. ABR thresholds of Math5 -/- mice were similar to those of wild-type and heterozygous mice, but the interpeak latencies for Peaks II-IV were significantly altered. These temporal changes are consistent with a higher-level auditory processing disorder involving the CN, potentially affecting the integration of binaural sensory information.

Cochlear implant surgery is currently the therapy of choice for profoundly deaf patients. However, the functionality of cochlear implants depends on the integrity of the auditory spiral ganglion neurons. This study assesses the combined efficacy of two classes of agents found effective in preventing degeneration of the auditory nerve following deafness, neurotrophic factors, and antioxidants. Guinea pigs were deafened and treated for 4 weeks with either local administration of GDNF or a combination of GDNF and systemic injections of the antioxidants ascorbic acid and Trolox. The density of surviving spiral ganglion cells was significantly enhanced and the thresholds for eliciting an electrically evoked brain stem response were significantly reduced in GDNF treated animals compared to deafened-untreated. The addition of antioxidants significantly enhanced the evoked responsiveness over that observed with GDNF alone. The results suggest multiple sites of intervention in the rescue of these cells from deafferentation-induced cell death.

Multisensory neurons in the dorsal cochlear nucleus (DCN) achieve their bimodal response properties [Shore (2005) Eur. J. Neurosci. , 21 , 3334–3348] by integrating auditory input via VIIIth nerve fibers with somatosensory input via the axons of cochlear nucleus granule cells [Shore et al. (2000) J. Comp. Neurol. , 419 , 271–285; Zhou & Shore (2004) J. Neurosci. Res. , 78 , 901–907]. A unique feature of multisensory neurons is their propensity for receiving cross‐modal compensation following sensory deprivation. Thus, we investigated the possibility that reduction of VIIIth nerve input to the cochlear nucleus results in trigeminal system compensation for the loss of auditory inputs. Responses of DCN neurons to trigeminal and bimodal (trigeminal plus acoustic) stimulation were compared in normal and noise‐damaged guinea pigs. The guinea pigs with noise‐induced hearing loss had significantly lower thresholds, shorter latencies and durations, and increased amplitudes of response to trigeminal stimulation than normal animals. Noise‐damaged animals also showed a greater proportion of inhibitory and a smaller proportion of excitatory responses compared with normal. The number of cells exhibiting bimodal integration, as well as the degree of integration, was enhanced after noise damage. In accordance with the greater proportion of inhibitory responses, bimodal integration was entirely suppressive in the noise‐damaged animals with no indication of the bimodal enhancement observed in a sub‐set of normal DCN neurons. These results suggest that projections from the trigeminal system to the cochlear nucleus are increased and/or redistributed after hearing loss. Furthermore, the finding that only neurons activated by trigeminal stimulation showed increased spontaneous rates after cochlear damage suggests that somatosensory neurons may play a role in the pathogenesis of tinnitus.

The intervals between acoustic elements are important in audition. Although neurons have been recorded that show interval tuning, the underlying mechanisms are unclear. The anuran auditory system is well suited for addressing this problem. One class of midbrain neurons in anurans responds selectively over a narrow range of pulse-repetition rates (PRRs) and only after several sound pulses have occurred with the “correct” timing. This “interval-counting” process can be reset by a single incorrect interval. Here we show, from whole-cell patch recordings of midbrain neurons in vivo , that these computations result from interplay between inhibition and rate-dependent excitation. An individual pulse or slowly repeated pulses elicited inhibition and subthreshold excitation. Excitation was markedly enhanced, however, when PRR was increased over a neuron-specific range. Spikes were produced when the enhanced excitation overcame the inhibition. Interval-number thresholds were positively correlated with the strength of inhibition and number of intervals required to augment the excitation. Accordingly, interval-number thresholds decreased when inhibition was attenuated by loading cells with cesium fluoride. The selectivity of these neurons for the interpulse interval, and therefore PRR, was related to the time course of excitatory events and the rate dependence of enhancement; for cells that were tuned to longer intervals, EPSPs were broader, and enhancement occurred at slower PRRs. The frequency tuning of the inhibition generally spanned that of the excitation, consistent with its role in temporal computation. These findings provide the first mechanistic understanding of interval selectivity and counting in the nervous system.

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 within-channel (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. Within-channel 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 Neuroscan electroencephalogram system using within-channel and across-channel 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 right-frontal spatial locations. Conclusions: 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 response is relatively larger and the P2 latency is relatively shorter than for nonsalient 2nd marker onsets, providing noninvasive, nonbehavioral indicators of the neural coding of this important temporal cue in the thalamic-cortical region of the central auditory system. Gap duration appears to be most clearly indicated by P1 and T-complex amplitude.

We have identified a novel nucleus of the mammalian brain and termed it the tectal longitudinal column (TLC). Basic histologic stains, tract-tracing techniques and three-dimensional reconstructions reveal that the rat TLC is a narrow, elongated structure spanning the midbrain tectum longitudinally. This paired nucleus is located close to the midline, immediately dorsal to the periaqueductal gray matter. It occupies what has traditionally been considered the most medial region of the deep superior colliculus and the most medial region of the inferior colliculus. The TLC differs from the neighboring nuclei of the superior and inferior colliculi and the periaqueductal gray by its distinct connections and cytoarchitecture. Extracellular electrophysiological recordings show that TLC neurons respond to auditory stimuli with physiologic properties that differ from those of neurons in the inferior or superior colliculi. We have identified the TLC in rodents, lagomorphs, carnivores, nonhuman primates, and humans, which indicates that the nucleus is conserved across mammals. The discovery of the TLC reveals an unexpected level of longitudinal organization in the mammalian tectum and raises questions as to the participation of this mesencephalic region in essential, yet completely unexplored, aspects of multisensory and/or sensorimotor integration.

We studied the effects of electrically microstimulating a gaze-control area in the owl's forebrain, the arcopallial gaze fields (AGFs), on the responsiveness of neurons in the optic tectum (OT) to visual and auditory stimuli. Microstimulation of the AGF enhanced the visual and auditory responsiveness and stimulus discriminability of OT neurons representing the same location in space as that represented at the microstimulation site in the AGF. At such OT sites, AGF microstimulation also sharpened auditory receptive fields and shifted them toward the location represented at the AGF stimulation site. At the same time, AGF microstimulation suppressed the responsiveness of OT neurons that represented visual or auditory stimuli at other locations in space. The top-down influences of this forebrain gaze-control area on sensory responsiveness in the owl OT are strikingly similar to the space-specific regulation of visual responsiveness in the monkey visual cortex produced by voluntary attention as well as by microstimulation of the frontal eye fields. This experimental approach provides a means for discovering mechanisms that underlie the top-down regulation of sensory responses.

Perception of complex sounds depends on the encoding of the dynamic and static structures within the ongoing stimulus by the auditory system. Aging has been associated with deficits in both areas, thus, the difficulty that the elderly have in speech comprehension could due to hearing loss, or to a loss of temporal sensitivity, or some combination of both. We investigated the effects of sensorineural hearing loss (SNHL) on neural correlates of temporal resolution by recording the responses of inferior colliculus neurons to a gap detection paradigm. We used C57BL/6 (C57) strain of laboratory mouse, which carries the Ahl deafness gene that initiates a progressive high frequency SNHL beginning at about 2 months of age and rapidly progresses to total deafness by 18 months. We compared gap encoding from inferior collicular neurons from young, normal-hearing C57 mice and middle-aged, hearing-impaired, C57 mice, quantifying minimal gap threshold, and recovery functions. The proportion of unit types, spontaneous rates and degree of monotonicity were comparable between young and middle-aged C57 mice. As expected, single unit thresholds were elevated by 30-40 dB in middle-aged C57 mice. However, no significant differences in mean minimal gap thresholds or in the slopes of the gap recovery functions were found between the two age groups. Thus, the results suggest that moderate high frequency SNHL does not affect temporal processing as measured by the gap detection paradigm.

The clawed frog Xenopus laevis produces vocalizations consisting of distinct patterns of clicks. This study provides the first description of spontaneous, pure-tone and communication-signal evoked discharge properties of auditory nerve (n.VIII) fibers and dorsal medullary nucleus (DMN) cells in an obligatorily aquatic anuran. Responses of 297 n.VIII and 253 DMN units are analyzed for spontaneous rates (SR), frequency tuning, rate-intensity functions, and firing rate adaptation, with a view to how these basic characteristics shape responses to recorded call stimuli. Response properties generally resemble those in partially terrestrial anurans. Broad tuning exists across characteristic frequencies (CFs). Threshold minima are -101 dB re 1 mm/s at 675 Hz; -87 dB at 1,600 Hz; and -61 dB at 3,000 Hz (-90, -77, and -44 dB re 1 Pa, respectively), paralleling the peak frequency of vocalizations at 1.2-1.6 kHz with approximately 500 Hz in 3 dB bandwidth. SRs range from 0 to 80 (n.VIII) and 0 to 73 spikes/s (DMN). Nerve and DMN units of all CFs follow click rates in natural calls, < or =67 clicks/s and faster. Units encode clicks with a single spike, double spikes, or bursts. Spike times correlate closely with click envelopes. No temporal filtering for communicative click rates occurs in either n.VIII or the DMN.

Pretraining lesions of rat perirhinal cortex (PR) severely impair pavlovian fear conditioning to a 22 kHz ultrasonic vocalization (USV) cue. However, PR lesions are without significant effect when the cue is a continuous tone at the same or a lower frequency. Here we examined fear-conditioning-produced changes in single-unit firing elicited in rat PR by a 22 kHz tone cue or a 22 kHz USV cue. Chronic recording electrodes were introduced from the lateral surface of the skull. Altogether, 200 well isolated units were studied in 28 rats. Overall, 73% of the recorded single units (145 of 200 units) evidenced statistically significant firing changes in response to the tone or USV conditional stimulus (CS) after it had been paired several times with an aversive unconditional stimulus (US). Interestingly, 33% of units (66 of 200 units) that were initially CS-unresponsive became CS-responsive after conditioning. After conditioning, there were two notable differences between single-unit responses elicited by the USV cue and those elicited by the tone cue. First, 11% of the units (14 of 123 units) recorded from the USV-conditioned group displayed a precisely timed increase in firing rate during the 260 ms interval in which the US had previously occurred. This US-timed response was unique to the USV-conditioned group. Second, the mean latency of cue-elicited firing was ∼30 ms longer in the USV-conditioned group than in the tone-conditioned group. These cue-specific differences in acquired firing latencies and acquired firing patterns suggest that spectrotemporal properties of a CS can control the essential circuitry or neurophysiological mechanisms underlying fear conditioning.

Auditory brainstem-evoked response (ABR) thresholds were obtained in a longitudinal study of C57BL/6J mice between 10 and 53 weeks old, with repeated testing every 2 weeks. On alternate weeks, acoustic startle reflex (ASR) amplitudes were measured, elicited by tone pips with stimulus frequencies of 3, 6, 12, and 24 kHz, and intensities from subthreshold up to 110 dB sound pressure level. The increase in ABR thresholds for 3 and 6 kHz test stimuli followed a linear time course with increasing age from 10 to 53 weeks, with a slope of about 0.7 dB/week, and for 48 kHz a second linear time course, but beginning at 10 weeks with a slope of about 2.3 dB/week. ABR thresholds for 12, 24, and 32 kHz increased after one linear segment with a 0.7 dB slope, then after a variable delay related to the test frequency, shifted to a second segment having slopes of 3-5 dB/week. Hearing loss initially reduced the ASR for all eliciting stimuli, but at about 6 months of age, the response elicited by intense 3 and 6 kHz stimuli began to increase to reach values about three times above normal, and previously subthreshold stimuli came to elicit vigorous responses seen at first only for the intense stimuli. This hyperacusis-like effect appeared in all mice but was especially pronounced in mice with more serious hearing loss. These ABR data, together with a review of histopathological data in the C57BL/6 literature, suggest that the non-frequency-specific slow time course of hearing loss results from pathology in the lateral wall of the cochlea, whereas the stimulus-specific hearing loss with a rapid time course results from hair cell loss. Delayed exaggeration of the ASR with hearing loss reveals a deficit in centrifugal inhibitory control over the afferent reflex pathways after central neural reorganization, suggesting that this mouse may provide a useful model of age-related tinnitus and associated hyperacusis.

The ascending and descending projections of the central auditory system form multiple tonotopic loops. This study specifically examines the tonotopic pathway from the auditory thalamus to the auditory cortex and then to the auditory midbrain in mice. We observed the changes of receptive fields in the central nucleus of the inferior colliculus of the midbrain evoked by focal electrical stimulation of the ventral division of the medial geniculate body of the thalamus. The receptive field of an auditory neuron was characterized by five parameters: the best frequency, minimum threshold, bandwidth, size of receptive field, and average spike number. We found that focal thalamic stimulation changed the parametric values characterizing the recorded collicular receptive fields toward those characterizing the stimulated thalamic receptive fields. Cortical inactivation with muscimol prevented the development of the collicular plasticity induced by focal thalamic stimulation. Our data suggest that the intact colliculo-thalamo-cortico-collicular loops are important for the coordination of sound-guided plasticity in the central auditory system.