Macrostructural Changes of the Acoustic Radiation in Humans with Hearing Loss and Tinnitus Revealed with Fixel-Based Analysis.

Age-related hearing loss is the most prevalent sensory impairment in the older adult population and is related to noise-induced damage or age-related deterioration of the peripheral auditory system. Hearing loss may affect the central auditory pathway in the brain, which is a continuation of the peripheral auditory system located in the ear. A debilitating symptom that frequently co-occurs with hearing loss is tinnitus. Strikingly, investigations into the impact of acquired hearing loss, with and without tinnitus, on the human central auditory pathway are sparse. This study used diffusion-weighted imaging (DWI) to investigate changes in the largest central auditory tract, the acoustic radiation, related to hearing loss and tinnitus. Participants with hearing loss, with and without tinnitus, and a control group were included. Both conventional diffusion tensor analysis and higher-order fixel-based analysis were applied. The fixel-based analysis was used as a novel framework providing insight into the axonal density and macrostructural morphologic changes of the acoustic radiation in hearing loss and tinnitus. The results show tinnitus-related atrophy of the left acoustic radiation near the medial geniculate body. This finding may reflect a decrease in myelination of the auditory pathway, instigated by more profound peripheral deafferentation or reflecting a preexisting marker of tinnitus vulnerability. Furthermore, age was negatively correlated with the axonal density in the bilateral acoustic radiation. This loss of fiber density with age may contribute to poorer speech understanding observed in older adults.SIGNIFICANCE STATEMENT Age-related hearing loss is the most prevalent sensory impairment in the older adult population. Older individuals are subject to the cumulative effects of aging and noise exposure on the auditory system. A debilitating symptom that frequently co-occurs with hearing loss is tinnitus: the perception of a phantom sound. In this large DWI-study, we provide evidence that in hearing loss, the additional presence of tinnitus is related to degradation of the acoustic radiation. Additionally, older age was related to axonal loss in the acoustic radiation. It appears that older adults have the aggravating circumstances of age, hearing loss, and tinnitus on central auditory processing, which may partly be because of the observed deterioration of the acoustic radiation with age.

Auditory prediction errors and auditory white matter microstructure associated with psychotic-like experiences in healthy individuals.

Our sensory systems actively predict sensory information based on previously learnt patterns, which are continuously updated with information from the actual sensory input via prediction errors. Individuals with schizophrenia consistently show reduced auditory prediction errors as well as altered fractional anisotropy (indicative of white matter changes) in the arcuate fasciculus and the auditory interhemispheric pathway, both of which are auditory white matter pathways associated with prediction errors. However, it is not clear if healthy individuals with psychotic-like experiences exhibit similar deficits. Participants underwent electroencephalography (EEG) recordings while listening to a classical two-tone duration deviant oddball paradigm (n = 103) and a stochastic oddball paradigm (n = 89). A subset of participants (n = 89) also underwent diffusion-weighted magnetic resonance imaging (MRI). Fractional anisotropy (FA), was extracted from the arcuate fasciculi and the auditory interhemispheric pathway. While prediction errors evoked by the classical oddball paradigm failed to reveal significant effects, the stochastic oddball paradigm elicited significant clusters at the typical mismatch negativity time window. Furthermore, we observed that FA of the arcuate fasciculi and auditory interhemispheric pathway significantly improved predictive models of psychotic-like experiences in healthy individuals over and above predictions made by auditory prediction error responses alone. Specifically, we observed that decreasing FA in the auditory interhemispheric pathway and reducing ability to learn stochastic irregularities are associated with increasing CAPE + scores. To the extent that these associations have previously been reported in patients with schizophrenia, the findings from this study suggest that both, auditory prediction errors and white matter changes in the auditory interhemispheric pathway, may have the potential to be translated into early screening markers for psychosis.

Manipulation of Auditory Inputs as Rehabilitation Therapy for Maladaptive Auditory Cortical Reorganization.

Neurophysiological and neuroimaging data suggest that the brains of not only children but also adults are reorganized based on sensory inputs and behaviors. Plastic changes in the brain are generally beneficial; however, maladaptive cortical reorganization in the auditory cortex may lead to hearing disorders such as tinnitus and hyperacusis. Recent studies attempted to noninvasively visualize pathological neural activity in the living human brain and reverse maladaptive cortical reorganization by the suitable manipulation of auditory inputs in order to alleviate detrimental auditory symptoms. The effects of the manipulation of auditory inputs on maladaptively reorganized brain were reviewed herein. The findings obtained indicate that rehabilitation therapy based on the manipulation of auditory inputs is an effective and safe approach for hearing disorders. The appropriate manipulation of sensory inputs guided by the visualization of pathological brain activities using recent neuroimaging techniques may contribute to the establishment of new clinical applications for affected individuals.

Early asymmetric inter-hemispheric transfer in the auditory network: insights from infants with corpus callosum agenesis.

The left hemisphere specialization for language is a well-established asymmetry in the human brain. Structural and functional asymmetries are observed as early as the prenatal period suggesting genetically determined differences between both hemispheres. The corpus callosum is a large tract connecting mostly homologous areas; some have proposed that it might participate in an enhancement of the left-hemispheric advantage to process speech. To investigate its role in early development, we compared 13 3-4-month-old infants with an agenesis of the corpus callosum ("AgCC") with 18 typical infants using high-density electroencephalography in an auditory task. We recorded event-related potentials for speech stimuli (syllables and babbling noise), presented binaurally (same syllable in both ears), monaurally (babbling noise in one ear) and dichotically (syllable in one ear and babbling noise in the other ear). In response to these stimuli, both groups developed an anterior positivity synchronous with a posterior negativity, yet the topography significantly differed between groups likely due to the atypical gyration of the medial surface in AgCC. In particular, the anterior positivity was lateral in AgCC infants while it covered the midline in typical infants. We then measured the latencies of the main auditory response (P2 at this age) for the different conditions on the symmetrical left and right clusters. The main difference between groups was a ~ 60 ms delay in typical infants relative to AgCC, for the ipsilateral response (i.e. left hemisphere) to babbling noise presented in the left ear, whereas no difference was observed in the case of right-ear stimulation. We suggest that our results highlight an asymmetrical callosal connectivity favoring the right-to-left hemisphere direction in typical infants. This asymmetry, similar to recent descriptions in adults, might contribute to an enhancement of left lateralization for language processing beyond the initial cortical left-hemisphere advantage.

Cortical and thalamic connectivity to the second auditory cortex of the cat is resilient to the onset of deafness.

It has been well established that following sensory loss, cortical areas that would normally be involved in perceiving stimuli in the absent modality are recruited to subserve the remaining senses. Despite this compensatory functional reorganization, there is little evidence to date for any substantial change in the patterns of anatomical connectivity between sensory cortices. However, while many auditory areas are contracted in the deaf, the second auditory cortex (A2) of the cat undergoes a volumetric expansion following hearing loss, suggesting this cortical area may demonstrate a region-specific pattern of structural reorganization. To address this hypothesis, and to complement existing literature on connectivity within auditory cortex, we injected a retrograde neuronal tracer across the breadth and cortical thickness of A2 to provide the first comprehensive quantification of projections from cortical and thalamic auditory and non-auditory regions to the second auditory cortex, and to determine how these patterns are affected by the onset of deafness. Neural projections arising from auditory, visual, somatomotor, and limbic cortices, as well as thalamic nuclei, were compared across normal hearing, early-deaf, and late-deaf animals. The results demonstrate that, despite previously identified changes in A2 volume, the pattern of projections into this cortical region are unaffected by the onset of hearing loss. These results fail to support the idea that crossmodal plasticity reflects changes in the pattern of projections between cortical regions and provides evidence that the pattern of connectivity that supports normal hearing is retained in the deaf brain.

Neurocircuitry of impaired affective sound processing: A clinical disorders perspective.

Decoding affective meaning from sensory information is central to accurate and adaptive behavior in many natural and social contexts. Human vocalizations (speech and non-speech), environmental sounds (e.g. thunder, noise, or animal sounds) and human-produced sounds (e.g. technical sounds or music) can carry a wealth of important aversive, threatening, appealing, or pleasurable affective information that sometimes implicitly influences and guides our behavior. A deficit in processing such affective information is detrimental to adaptive environmental behavior, psychological well-being, and social interactive abilities. These deficits can originate from a diversity of psychiatric and neurological disorders, and are associated with neural dysfunctions across largely distributed brain networks. Recent neuroimaging studies in psychiatric and neurological patients outline the cortical and subcortical neurocircuitry of the complimentary and differential functional roles for affective sound processing. This points to and confirms a recently proposed distributed network rather than a single brain region underlying affective sound processing, and highlights the notion of a multi-functional process that can be differentially impaired in clinical disorders.

Important considerations in lesion-symptom mapping: Illustrations from studies of word comprehension.

Lesion-symptom mapping is an important method of identifying networks of brain regions critical for functions. However, results might be influenced substantially by the imaging modality and timing of assessment. We tested the hypothesis that brain regions found to be associated with acute language deficits depend on (1) timing of behavioral measurement, (2) imaging sequences utilized to define the "lesion" (structural abnormality only or structural plus perfusion abnormality), and (3) power of the study. We studied 191 individuals with acute left hemisphere stroke with MRI and language testing to identify areas critical for spoken word comprehension. We use the data from this study to examine the potential impact of these three variables on lesion-symptom mapping. We found that only the combination of structural and perfusion imaging within 48 h of onset identified areas where more abnormal voxels was associated with more severe acute deficits, after controlling for lesion volume and multiple comparisons. The critical area identified with this methodology was the left posterior superior temporal gyrus, consistent with other methods that have identified an important role of this area in spoken word comprehension. Results have implications for interpretation of other lesion-symptom mapping studies, as well as for understanding areas critical for auditory word comprehension in the healthy brain. We propose that lesion-symptom mapping at the acute stage of stroke addresses a different sort of question about brain-behavior relationships than lesion-symptom mapping at the chronic stage, but that timing of behavioral measurement and imaging modalities should be considered in either case. Hum Brain Mapp 38:2990-3000, 2017. © 2017 Wiley Periodicals, Inc.

Limbic-Auditory Interactions of Tinnitus: An Evaluation Using Diffusion Tensor Imaging.

OBJECTIVE: Tinnitus is defined as an imaginary subjective perception in the absence of an external sound. Convergent evidence proposes that tinnitus perception includes auditory, attentional and emotional components. The aim of this study was to investigate the thalamic, auditory and limbic interactions associated with tinnitus-related distress by Diffusion Tensor Imaging (DTI). METHODS: A total of 36 tinnitus patients, 20 healthy controls underwent an audiological examination, as well as a magnetic resonance imaging protocol including structural and DTI sequences. All participants completed the Tinnitus Handicap Inventory (THI) and Visual Analog Scales (VAS) related with tinnitus. The fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values were obtained for the auditory cortex (AC), inferior colliculus (IC), lateral lemniscus (LL), medial geniculate body (MGB), thalamic reticular nucleus (TRN), amygdala (AMG), hippocampus (HIP), parahippocampus (PHIP) and prefrontal cortex (PFC). RESULTS: In tinnitus patients the FA values of IC, MGB, TRN, AMG, HIP decreased and the ADC values of IC, MGB, TRN, AMG, PHIP increased significantly. The contralateral IC-LL and bilateral MGB FA values correlated negatively with hearing loss. A negative relation was found between the AMG-HIP FA values and THI and VAS scores. Bilateral ADC values of PHIP and PFC significantly correlated with the attention deficiency-VAS scores. CONCLUSION: In conclusion, this is the first DTI study to investigate the grey matter structures related to tinnitus perception and the significant correlation of FA and ADC with clinical parameters suggests that DTI can provide helpful information for tinnitus. Magnifying the microstructures in DTI can help evaluate the three faces of tinnitus nature: hearing, emotion and attention.

Quantifying and comparing the pattern of thalamic and cortical projections to the posterior auditory field in hearing and deaf cats.

Following sensory loss, compensatory crossmodal reorganization occurs such that the remaining modalities are functionally enhanced. For example, behavioral evidence suggests that peripheral visual localization is better in deaf than in normal hearing animals, and that this enhancement is mediated by recruitment of the posterior auditory field (PAF), an area that is typically involved in localization of sounds in normal hearing animals. To characterize the anatomical changes that underlie this phenomenon, we identified the thalamic and cortical projections to the PAF in hearing cats and those with early- and late-onset deafness. The retrograde tracer biotinylated dextran amine was deposited in the PAF unilaterally, to label cortical and thalamic afferents. Following early deafness, there was a significant decrease in callosal projections from the contralateral PAF. Late-deaf animals showed small-scale changes in projections from one visual cortical area, the posterior ectosylvian field (EPp), and the multisensory zone (MZ). With the exception of these minor differences, connectivity to the PAF was largely similar between groups, with the principle projections arising from the primary auditory cortex (A1) and the ventral division of the medial geniculate body (MGBv). This absence of large-scale connectional change suggests that the functional reorganization that follows sensory loss results from changes in synaptic strength and/or unmasking of subthreshold intermodal connections. J. Comp. Neurol. 524:3042-3063, 2016. © 2016 Wiley Periodicals, Inc.

Noise trauma induced plastic changes in brain regions outside the classical auditory pathway.

The effects of intense noise exposure on the classical auditory pathway have been extensively investigated; however, little is known about the effects of noise-induced hearing loss on non-classical auditory areas in the brain such as the lateral amygdala (LA) and striatum (Str). To address this issue, we compared the noise-induced changes in spontaneous and tone-evoked responses from multiunit clusters (MUC) in the LA and Str with those seen in auditory cortex (AC) in rats. High-frequency octave band noise (10-20 kHz) and narrow band noise (16-20 kHz) induced permanent threshold shifts at high-frequencies within and above the noise band but not at low frequencies. While the noise trauma significantly elevated spontaneous discharge rate (SR) in the AC, SRs in the LA and Str were only slightly increased across all frequencies. The high-frequency noise trauma affected tone-evoked firing rates in frequency and time-dependent manner and the changes appeared to be related to the severity of noise trauma. In the LA, tone-evoked firing rates were reduced at the high-frequencies (trauma area) whereas firing rates were enhanced at the low-frequencies or at the edge-frequency dependent on severity of hearing loss at the high frequencies. The firing rate temporal profile changed from a broad plateau to one sharp, delayed peak. In the AC, tone-evoked firing rates were depressed at high frequencies and enhanced at the low frequencies while the firing rate temporal profiles became substantially broader. In contrast, firing rates in the Str were generally decreased and firing rate temporal profiles become more phasic and less prolonged. The altered firing rate and pattern at low frequencies induced by high-frequency hearing loss could have perceptual consequences. The tone-evoked hyperactivity in low-frequency MUC could manifest as hyperacusis whereas the discharge pattern changes could affect temporal resolution and integration.

Auditory processing and morphological anomalies in medial geniculate nucleus of Cntnap2 mutant mice.

Genetic epidemiological studies support a role for CNTNAP2 in developmental language disorders such as autism spectrum disorder, specific language impairment, and dyslexia. Atypical language development and function represent a core symptom of autism spectrum disorder (ASD), with evidence suggesting that aberrant auditory processing-including impaired spectrotemporal processing and enhanced pitch perception-may both contribute to an anomalous language phenotype. Investigation of gene-brain-behavior relationships in social and repetitive ASD symptomatology have benefited from experimentation on the Cntnap2 knockout (KO) mouse. However, auditory-processing behavior and effects on neural structures within the central auditory pathway have not been assessed in this model. Thus, this study examined whether auditory-processing abnormalities were associated with mutation of the Cntnap2 gene in mice. Cntnap2 KO mice were assessed on auditory-processing tasks including silent gap detection, embedded tone detection, and pitch discrimination. Cntnap2 knockout mice showed deficits in silent gap detection but a surprising superiority in pitch-related discrimination as compared with controls. Stereological analysis revealed a reduction in the number and density of neurons, as well as a shift in neuronal size distribution toward smaller neurons, in the medial geniculate nucleus of mutant mice. These findings are consistent with a central role for CNTNAP2 in the ontogeny and function of neural systems subserving auditory processing and suggest that developmental disruption of these neural systems could contribute to the atypical language phenotype seen in autism spectrum disorder.

Auditory dysfunction in schizophrenia: integrating clinical and basic features.

Schizophrenia is a complex neuropsychiatric disorder that is associated with persistent psychosocial disability in affected individuals. Although studies of schizophrenia have traditionally focused on deficits in higher-order processes such as working memory and executive function, there is an increasing realization that, in this disorder, deficits can be found throughout the cortex and are manifest even at the level of early sensory processing. These deficits are highly amenable to translational investigation and represent potential novel targets for clinical intervention. Deficits, moreover, have been linked to specific structural abnormalities in post-mortem auditory cortex tissue from individuals with schizophrenia, providing unique insights into underlying pathophysiological mechanisms.

Cross-modal activation of auditory regions during visuo-spatial working memory in early deafness.

Early deafness can reshape deprived auditory regions to enable the processing of signals from the remaining intact sensory modalities. Cross-modal activation has been observed in auditory regions during non-auditory tasks in early deaf subjects. In hearing subjects, visual working memory can evoke activation of the visual cortex, which further contributes to behavioural performance. In early deaf subjects, however, whether and how auditory regions participate in visual working memory remains unclear. We hypothesized that auditory regions may be involved in visual working memory processing and activation of auditory regions may contribute to the superior behavioural performance of early deaf subjects. In this study, 41 early deaf subjects (22 females and 19 males, age range: 20-26 years, age of onset of deafness < 2 years) and 40 age- and gender-matched hearing controls underwent functional magnetic resonance imaging during a visuo-spatial delayed recognition task that consisted of encoding, maintenance and recognition stages. The early deaf subjects exhibited faster reaction times on the spatial working memory task than did the hearing controls. Compared with hearing controls, deaf subjects exhibited increased activation in the superior temporal gyrus bilaterally during the recognition stage. This increased activation amplitude predicted faster and more accurate working memory performance in deaf subjects. Deaf subjects also had increased activation in the superior temporal gyrus bilaterally during the maintenance stage and in the right superior temporal gyrus during the encoding stage. These increased activation amplitude also predicted faster reaction times on the spatial working memory task in deaf subjects. These findings suggest that cross-modal plasticity occurs in auditory association areas in early deaf subjects. These areas are involved in visuo-spatial working memory. Furthermore, amplitudes of cross-modal activation during the maintenance stage were positively correlated with the age of onset of hearing aid use and were negatively correlated with the percentage of lifetime hearing aid use in deaf subjects. These findings suggest that earlier and longer hearing aid use may inhibit cross-modal reorganization in early deaf subjects. Granger causality analysis revealed that, compared to the hearing controls, the deaf subjects had an enhanced net causal flow from the frontal eye field to the superior temporal gyrus. These findings indicate that a top-down mechanism may better account for the cross-modal activation of auditory regions in early deaf subjects.See MacSweeney and Cardin (doi:10/1093/awv197) for a scientific commentary on this article.

Differential Modification of Cortical and Thalamic Projections to Cat Primary Auditory Cortex Following Early- and Late-Onset Deafness.

Following sensory deprivation, primary somatosensory and visual cortices undergo crossmodal plasticity, which subserves the remaining modalities. However, controversy remains regarding the neuroplastic potential of primary auditory cortex (A1). To examine this, we identified cortical and thalamic projections to A1 in hearing cats and those with early- and late-onset deafness. Following early deafness, inputs from second auditory cortex (A2) are amplified, whereas the number originating in the dorsal zone (DZ) decreases. In addition, inputs from the dorsal medial geniculate nucleus (dMGN) increase, whereas those from the ventral division (vMGN) are reduced. In late-deaf cats, projections from the anterior auditory field (AAF) are amplified, whereas those from the DZ decrease. Additionally, in a subset of early- and late-deaf cats, area 17 and the lateral posterior nucleus (LP) of the visual thalamus project concurrently to A1. These results demonstrate that patterns of projections to A1 are modified following deafness, with statistically significant changes occurring within the auditory thalamus and some cortical areas. Moreover, we provide anatomical evidence for small-scale crossmodal changes in projections to A1 that differ between early- and late-onset deaf animals, suggesting that potential crossmodal activation of primary auditory cortex differs depending on the age of deafness onset.

Sources of pathology underlying listening disorders in children.

Some children referred to audiology and developmental disability services have listening difficulties, despite normal audiograms. These children may be tested for 'auditory processing disorder' (APD), a controversial construct suggesting that neural dysfunction in the central auditory system leads to impaired auditory perception. An important question, not currently tested in clinical evaluation, is whether listening difficulties result from problems with bottom-up auditory sensory processing or top-down modulating cognition. Perceptual variability and poor performance on standardized tests suggest that listening difficulties are primarily cognitive in origin. However, evidence for impaired olivocochlear function and temporal processing deficits may implicate peripheral or central auditory dysfunction in some cases. Wide-spread, top-down modulation of auditory cortical, brainstem and ear function suggests that afferent and efferent control systems may not be simple to segregate. During normal maturation, hearing appears to develop in proportion to the complexity of both stimuli and tasks. But some younger individuals have mature hearing, highlighting individual differences that suggest APD may be due to a generalized developmental delay. Recent studies have investigated specific hypotheses showing, for example, that spatial hearing and executive function are compromised in some children with listening difficulties. Using speech stimuli (e.g. consonant-vowel syllables) to examine auditory brainstem responses, and psychophysiological relations between dichotic hearing and cortical physiology, various effects of auditory experience and development point the way to promising approaches for further studies of APD. Newer technology, from genetic sequencing to MRI, may have the sensitivity to test whether and how frequently APD is associated with impaired processing in the auditory system.

Frequency discrimination in ears with and without contralateral cochlear dead regions.

OBJECTIVE: The purpose of this study was to test the ability to discriminate low-frequency pure-tone stimuli for ears with and without contralateral dead regions, in subjects with bilateral high-frequency hearing loss; we examined associations between hearing loss characteristics and frequency discrimination of low-frequency stimuli in subjects with high-frequency hearing loss. DESIGN: Cochlear dead regions were diagnosed using the TEN-HL test. A frequency discrimination test utilizing an adaptive three-alternative forced choice method provided difference limens for reference frequencies 0.25 kHz and 0.5 kHz. STUDY SAMPLE: Among 105 subjects with bilateral high-frequency hearing loss, unilateral dead regions were found in 15 subjects. These, and an additional 15 matched control subjects without dead regions, were included in the study. RESULTS: Ears with dead regions performed best at the frequency discrimination test. Ears with a contralateral dead region performed significantly better than ears without a contralateral dead region at 0.5 kHz, the reference frequency closest to the mean audiogram cut-off, while the opposite result was obtained at 0.25 kHz. CONCLUSIONS: Results may be seen as sign of a contralateral effect of unilateral dead regions on the discrimination of stimuli with frequencies well below the audiogram cut-off in adult subjects with bilateral high-frequency hearing loss.

Simulating psychophysical tuning curves in listeners with dead regions.

OBJECTIVE: This study investigates the relation between diagnosis of dead regions based on the off-frequency psychophysical tuning curve (PTC) tip and the frequency and level of the probe tone. DESIGN: A previously developed functional model of auditory processing was used to simulate the complete loss of inner hair cells (IHC), dysfunction of outer hair cells (OHC), complete loss of IHCs in combination with OHC dysfunction, and IHC insensitivity. The model predictions were verified through comparison with experimental data. STUDY SAMPLE: This study compares PTC data of five normal-hearing listeners and six hearing-impaired listeners with model-simulated PTC data. RESULTS: It was shown that OHC activity and IHC insensitivity may significantly alter the shift of PTC tips with increasing probe level. CONCLUSIONS: Model results suggest that OHC activity and IHC insensitivity can change the outcome of dead region diagnosis using PTCs. Supplementary to PTC dead region diagnostic information, model results may provide additional information regarding the edge frequency of a dead region and OHC function.

Noise-induced hearing loss (NIHL) as a target of oxidative stress-mediated damage: cochlear and cortical responses after an increase in antioxidant defense.

This study addresses the relationship between cochlear oxidative damage and auditory cortical injury in a rat model of repeated noise exposure. To test the effect of increased antioxidant defenses, a water-soluble coenzyme Q10 analog (Qter) was used. We analyzed auditory function, cochlear oxidative stress, morphological alterations in auditory cortices and cochlear structures, and levels of coenzymes Q9 and Q10 (CoQ9 and CoQ10, respectively) as indicators of endogenous antioxidant capability. We report three main results. First, hearing loss and damage in hair cells and spiral ganglion was determined by noise-induced oxidative stress. Second, the acoustic trauma altered dendritic morphology and decreased spine number of II-III and V-VI layer pyramidal neurons of auditory cortices. Third, the systemic administration of the water-soluble CoQ10 analog reduced oxidative-induced cochlear damage, hearing loss, and cortical dendritic injury. Furthermore, cochlear levels of CoQ9 and CoQ10 content increased. These findings indicate that antioxidant treatment restores auditory cortical neuronal morphology and hearing function by reducing the noise-induced redox imbalance in the cochlea and the deafferentation effects upstream the acoustic pathway.

Behavioral consequences of unilateral inferior colliculus lesions in the rat.

This study was carried out to determine the behavioral sensitivity to sound of rats with unilateral lesions of inferior colliculus (IC) located ipsilateral or contralateral to the projection pathway from one ear. Absolute thresholds for the detection of a broad-band noise burst were compared for rats with a profound conductive hearing loss in one ear and a lesion placed either ipsilateral or contralateral to the normally functioning ear. The rats were trained to make withdrawal responses to avoid a shock when they detected the presence of a noise burst. Sound pressure level was systematically lowered to obtain psychophysical curves from which absolute thresholds could be determined. Complete lesions of the contralateral IC resulted in substantial elevations in absolute threshold relative to normal whereas equivalent lesions of the ipsilateral IC produced relatively little elevation. In neither case did unilateral destruction of the IC produce a total inability to respond to sound. Contralateral IC lesions that included the dorsal nucleus of the lateral lemniscus (DNLL) produced a significantly greater elevation in behavioral thresholds than complete lesions limited to the IC. The results indicate a predominance of the contralateral over the ipsilateral pathway to IC for maintaining normal thresholds. They also indicate that other pathways that bypass the IC are likely involved in detecting the presence of a sound.