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There are three times as many outer hair cells (OHC) as inner hair cells (IHC), yet IHC transmit virtually all acoustic information to the brain as they synapse with 90-95% of type I auditory nerve fibers. Here we review a comprehensive series of experiments aimed at determining how loss of the IHC/type I system affects hearing by selectively destroying these cells in chinchillas using the ototoxic anti-cancer agent carboplatin. Eliminating IHC/type I neurons has no effect on distortion product otoacoustic emission or the cochlear microphonic potential generated by OHC; however, it greatly reduces the summating potential produced by IHC and the compound action potential (CAP) generated by type I neurons. Remarkably, responses from remaining auditory nerve fibers maintain sharp tuning and low thresholds despite innervating regions of the cochlea with ~80% IHC loss. Moreover, chinchillas with large IHC lesions have surprisingly normal thresholds in quiet until IHC losses exceeded 80%, suggesting that only a few IHC are needed to detect sounds in quiet. However, behavioral thresholds in broadband noise are elevated significantly and tone-in-narrow band noise masking patterns exhibit greater remote masking. These results suggest the auditory system is able to compensate for considerable loss of IHC/type I neurons in quiet but not in difficult listening conditions. How does the auditory brain deal with the drastic loss of cochlear input? Recordings from the inferior colliculus found a relatively small decline in sound-evoked activity despite a large decrease in CAP amplitude after IHC lesion. Paradoxically, sound-evoked responses are generally larger than normal in the auditory cortex, indicative of increased central gain. This gain enhancement in the auditory cortex is associated with decreased GABA-mediated inhibition. These results suggest that when the neural output of the cochlea is reduced, the central auditory system compensates by turning up its gain so that weak signals once again become comfortably loud. While this gain enhancement is able to restore normal hearing under quiet conditions, it may not adequately compensate for peripheral dysfunction in more complex sound environments. In addition, excessive gain increases may convert recruitment into the debilitating condition known as hyperacusis.

Children with perinatally acquired HIV (CPHIV) are at increased risk of neurodevelopmental difficulties, including hearing-related impairments, despite early initiation of antiretroviral therapy (ART). Previous studies have reported a higher prevalence of hearing loss in CPHIV compared with uninfected children; however, the contribution of the central auditory system to these auditory differences remains unclear. Understanding central auditory processing in CPHIV is important, as even subtle auditory difficulties during childhood can negatively affect speech and language development, academic performance, and quality of life. Functional MRI was used to examine neural responses to auditory stimulation in 108 11-year-old children (60 CPHIV and 48 children without HIV). During scanning, participants listened to pure tones at low (500 Hz), middle (1,500 Hz), and high (4,000 Hz) frequencies. CPHIV demonstrated modestly elevated hearing thresholds (reflecting poorer hearing sensitivity) at several frequencies; however, the prevalence of clinically defined hearing loss did not differ between groups. Across all children, pure-tone stimulation elicited robust bilateral activation of the auditory cortices, with both the spatial extent and magnitude of activation decreasing as tone frequency increased. Relative to controls, CPHIV exhibited significantly reduced bilateral auditory cortex responses across frequencies. These group differences persisted after accounting for sex and handedness and after excluding children with hearing loss. Associations between hearing thresholds and auditory cortex activation were generally weak, except at 4,000 Hz in CPHIV, where poorer hearing was associated with stronger auditory cortex activation, consistent with a compensatory neural response. Despite largely normal peripheral hearing, CPHIV receiving ART exhibited reduced bilateral auditory cortex responses during pure-tone processing. These findings suggest that alterations within the central auditory system may contribute to auditory vulnerability in CPHIV.

The age-appropriate morphofunctional formation of the central parts of the auditory system determines the normal trajectory of a child’s auditory and speech development. Impairments can lead to the emergence of central auditory processing disorders (CAPD) and associated problems of psychoverbal and general development. Psychoacoustic testing is quite informative and is the most accessible diagnostic tool for detecting signs of CAPD, including in pediatric practice; it can be performed from age four years as long as normative data for the relevant age groups are available. The aim of the present work was to carry out audiological assessments of the functional state of the central components of the auditory system using psychoacoustic methods in healthy children of different ages. Materials and methods. A total of 125 healthy full-term children aged 4–17 years with normal peripheral auditory function without hearing, speech, language, cognitive, or academic problems were examined. The children were divided into five age groups(years:months): 4:00–5:11; 6:00–7:11; 8:00–9:11; 10:00–11:11; 12:00 years and older. Along with traditional audiological examination, all children were given tests to assess the functional state of the central parts of the auditory analyzer: assessment of the perception of rhythmic stimulus sequences; the Random Gap Detection Test (RGDT); a monaural low-redundancy speech test in silence and on the background of noise interference; a binaural interaction test using alternating binaural speech; dichotic testing; testing using a simplified version of the Russian matrix sentence test in noise (RUMatrix). Results. Data on the sensitivity of the tests used in these studies assessing the functional state of different structures of the central part of the auditory system indicated that signs of maturation developed in the bottom-up direction as children aged. The pace of ontogenetic processes, assessed from the results of the corresponding tests, depended on subjects’ age groups. The morphofunctional development of the central part of the auditory system was found not to be complete by adolescence. Conclusions. The results obtained here can be used for differential diagnosis between immaturity of the central auditory system, CAPD, and hearing disorders and language disabilities of different types in children of different age groups.

During development, the organization of the auditory system into distinct functional subcircuits depends on the spatially and temporally ordered sequence of neuronal specification, differentiation, migration and connectivity. Regional patterning along the antero-posterior axis and neuronal subtype specification along the dorso-ventral axis intersect to determine proper neuronal fate and assembly of rhombomere-specific auditory subcircuits. By taking advantage of the increasing number of transgenic mouse lines, recent studies have expanded the knowledge of developmental mechanisms involved in the formation and refinement of the auditory system. Here, we summarize several findings dealing with the molecular and cellular mechanisms that underlie the assembly of central auditory subcircuits during mouse development, focusing primarily on the rhombomeric and dorso-ventral origin of auditory nuclei and their associated molecular genetic pathways.

Hearing loss is associated with decreased speech perception as well as with changes in the auditory pathway. The effects of those changes on binaural speech perception with hearing aids are not yet fully understood. To provide further evidence on the functional changes of the auditory pathway, several speech perception tests (unilateral and bilateral, aided and unaided, in quiet and in noise) were conducted in a population of 370 bilateral hearing aid users covering the entire range of the World Health Organisation’s most recent classification of hearing loss. To characterise the effects of asymmetric hearing thresholds, a generalised linear model was used for regression analysis. The model revealed a detrimental effect of the poorer ears’ thresholds on both the unaided and the aided unilateral word recognition scores that were attained by the better ear. Moreover, aided binaural word recognition (in quiet and in noise) was affected to a degree that cannot be explained on the sole basis of bilateral summation. Thus, this study provides evidence that there is a reorganisation and altered functioning of the afferent and efferent auditory pathways due to asymmetric hearing loss. Consequently, more attention should be paid to provision with a hearing aid as early as possible, and separately for each ear.

Aging negatively influences the structure of the human brain including the white matter. The objective of our study was to identify, using fixel-based morphometry, the age induced changes in the pathways connecting several regions of the central auditory system (inferior colliculus, Heschl's gyrus, planum temporale) and the pathways connecting these structures with parts of the limbic system (anterior insula, hippocampus and amygdala). In addition, we were interested in the extent to which the integrity of these pathways is influenced by hearing loss and tinnitus. Tractographic data were acquired using a 3 T MRI in 79 volunteers. The participants were categorized into multiple groups in accordance with their age, auditory thresholds and tinnitus status. Fixel-based analysis was utilized to identify alterations in the subsequent three parameters: logarithm of fiber cross-section, fiber density, fiber density and cross-section. Two modes of analysis were used: whole brain analysis and targeted analysis using fixel mask, corresponding to the pathways connecting the aforementioned structures. A significantly negative effect of aging was present for all fixel-based metrics, namely the logarithm of the fiber cross-section, (7 % fixels in whole-brain, 14% fixels in fixel mask), fiber density (5 % fixels in whole-brain, 15% fixels in fixel mask), fiber density and cross section (7 % fixels in whole-brain, 19% fixels in fixel mask). Expressed age-related losses, exceeding 30% fixels, were particularly present in pathways connecting the auditory structures with limbic structures. The effect of hearing loss and/or tinnitus did not reach significance. Our results show that although an age-related reduction of fibers is present in pathways connecting several auditory regions, the connections of these structures with limbic structures are even more reduced. To what extent this fact influences the symptoms of presbycusis, such as decreased speech comprehension, especially in noise conditions, remains to be elucidated.

Cochlear outer hair cells (OHC) receive direct efferent feedback from the caudal auditory brainstem via the medial olivocochlear (MOC) bundle. This circuit provides the neural substrate for the MOC reflex, which inhibits cochlear amplifier gain and is believed to play a role in listening in noise and protection from acoustic overexposure. The human MOC reflex has been studied extensively using otoacoustic emissions (OAE) paradigms; however, these measurements are insensitive to subsequent \"downstream\" efferent effects on the neural ensembles that mediate hearing. In this experiment, click- and chirp-evoked auditory nerve compound action potential (CAP) amplitudes were measured electrocochleographically from the human eardrum without and with MOC reflex activation elicited by contralateral broadband noise. We hypothesized that the chirp would be a more optimal stimulus for measuring neural MOC effects because it synchronizes excitation along the entire length of the basilar membrane and thus evokes a more robust CAP than a click at low to moderate stimulus levels. Chirps produced larger CAPs than clicks at all stimulus intensities (50-80 dB ppeSPL). MOC reflex inhibition of CAPs was larger for chirps than clicks at low stimulus levels when quantified both in terms of amplitude reduction and effective attenuation. Effective attenuation was larger for chirp- and click-evoked CAPs than for click-evoked OAEs measured from the same subjects. Our results suggest that the chirp is an optimal stimulus for evoking CAPs at low stimulus intensities and for assessing MOC reflex effects on the auditory nerve. Further, our work supports previous findings that MOC reflex effects at the level of the auditory nerve are underestimated by measures of OAE inhibition.

The phonological deficit in dyslexia is associated with altered low-gamma oscillatory function in left auditory cortex, but a causal relationship between oscillatory function and phonemic processing has never been established. After confirming a deficit at 30 Hz with electroencephalography (EEG), we applied 20 minutes of transcranial alternating current stimulation (tACS) to transiently restore this activity in adults with dyslexia. The intervention significantly improved phonological processing and reading accuracy as measured immediately after tACS. The effect occurred selectively for a 30-Hz stimulation in the dyslexia group. Importantly, we observed that the focal intervention over the left auditory cortex also decreased 30-Hz activity in the right superior temporal cortex, resulting in reinstating a left dominance for the oscillatory response. These findings establish a causal role of neural oscillations in phonological processing and offer solid neurophysiological grounds for a potential correction of low-gamma anomalies and for alleviating the phonological deficit in dyslexia.

Noise that is capable of inducing the hearing loss (NIHL) has a strong impact on the inner ear structures and causes early and most obvious pathophysiological changes in the auditory periphery. Several studies indicated that intrinsic apoptotic cell death mechanisms are the key factors inducing cellular degeneration immediately after noise exposure and are maintained for days or even weeks. In addition, studies demonstrated several changes in the central auditory system following noise exposure, consistent with early apoptosis-related pathologies. To clarify the underlying mechanisms, the present study focused on the noise-induced gene and protein expression of the pro-apoptotic protease activating factor-1 (APAF1) and the anti-apoptotic B-cell lymphoma 2 related protein a1a (BCL2A1A) in the cochlear nucleus (CN), inferior colliculus (IC) and auditory cortex (AC) of the murine central auditory pathway. The expression of mRNA was upregulated immediately after trauma in all tissues investigated, whereas the protein levels were significantly reduced at least in the auditory brainstem. Conversely, acute noise has decreased the expression of gene along the auditory pathway. The changes in APAF1 protein level were not statistically significant. It is tempting to speculate that the acoustic overstimulation leads to mitochondrial dysfunction and induction of apoptosis by regulation of proapoptotic and antiapoptotic proteins. The inverse expression pattern on the mRNA level of both genes might reflect a protective response to decrease cellular damage. Our results indicate the immediate presence of intrinsic apoptosis following noise trauma. This, in turn, may significantly contribute to the development of central structural deficits. Auditory pathway-specific inhibition of intrinsic apoptosis could be a therapeutic approach for the treatment of acute (noise-induced) hearing loss to prevent irreversible neuronal injury in auditory brain structures and to avoid profound deficits in complex auditory processing.

This work presents a memristive device based on a composite of Scindapsus aureus (SA) and gold nanoparticles (Au NPs), which exhibits excellent resistive switching characteristics and supports multiple forms of synaptic plasticity such as paired-pulse facilitation (PPF), spike-rate-dependent plasticity (SRDP), and spike-timing-dependent plasticity (STDP). The device demonstrates reliable retention, reproducibility, and switching stability. The SA:Au NP composite originates from a natural plant source and possesses green, biodegradable, and biocompatible features, highlighting its potential as a sustainable bio-memristive material for neuromorphic systems. Furthermore, the device exhibits sensitivity to the time interval between paired input pulses, simulating the neural response to interaural time differences (ITDs) in the auditory system. Although not a conventional acoustic sensor, its Δt-responsiveness based on synaptic behavior reveals promising potential in neuromorphic auditory perception and perceptual computing applications. This study provides a foundational synaptic unit for future artificial hearing systems capable of spatial sound localization.