Auditory Research publications

As diving foragers, sea ducks are vulnerable to underwater anthropogenic activity, including ships, underwater construction, seismic surveys and gillnet fisheries. Bycatch in gillnets is a contributing source of mortality for sea ducks, killing hundreds of thousands of individuals annually. We researched underwater hearing in sea duck species to increase knowledge of underwater avian acoustic sensitivity and to assist with possible development of gillnet bycatch mitigation strategies that include auditory deterrent devices. We used both psychoacoustic and electrophysiological techniques to investigate underwater duck hearing in several species including the long-tailed duck (Clangula hyemalis), surf scoter (Melanitta perspicillata) and common eider (Somateria mollissima). Psychoacoustic results demonstrated that all species tested share a common range of maximum auditory sensitivity of 1.0–3.0 kHz, with the long-tailed ducks and common eiders at the high end of that range (2.96 kHz), and surf scoters at the low end (1.0 kHz). In addition, our electrophysiological results from 4 surf scoters and 2 long-tailed ducks, while only tested at 0.5, 1 and 2 kHz, generally agree with the audiogram shape from our psychoacoustic testing. The results from this study are applicable to the development of effective acoustic deterrent devices or pingers in the 2–3 kHz range to deter sea ducks from anthropogenic threats.

Listening in an acoustically cluttered scene remains a difficult task for both machines and hearing-impaired listeners. Normal-hearing listeners accomplish this task with relative ease by segregating the scene into its constituent sound sources, then selecting and attending to a target source. An assistive listening device that mimics the biological mechanisms underlying this behavior may provide an effective solution for those with difficulty listening in acoustically cluttered environments (e.g., a cocktail party). Here, we present a binaural sound segregation algorithm based on a hierarchical network model of the auditory system. In the algorithm, binaural sound inputs first drive populations of neurons tuned to specific spatial locations and frequencies. The spiking response of neurons in the output layer are then reconstructed into audible waveforms via a novel reconstruction method. We evaluate the performance of the algorithm with a speech-on-speech intelligibility task in normal-hearing listeners. This two-microphone-input algorithm is shown to provide listeners with perceptual benefit similar to that of a 16-microphone acoustic beamformer. These results demonstrate the promise of this biologically inspired algorithm for enhancing selective listening in challenging multi-talker scenes.

Human temporal bone specimens are used in experiments measuring the sound transfer of the middle ear, which is the standard method used in the development of active and passive middle ear implants. Statistical analyses of these experiments usually require that the TB samples are representative of the population of non-pathological middle ears. Specifically, this means that the specimens must be mechanically well-characterized. We present an in-depth statistical analysis of 478 data sets of middle ear transfer functions (METFs) from different laboratories. The data sets are preprocessed and various contributions to the variance of the data are evaluated. We then derive a statistical range as a reference against which individual METF measurements may be validated. The range is calculated as the two-sided 95% tolerance interval at audiological frequencies. In addition, the mean and 95% confidence interval of the mean are given as references for assessing the validity of a sample group. Finally, we provide a suggested procedure for measuring METFs using the methods described herein.

Hearing loss is a chronic health condition that affects millions of people worldwide. In addition to age-related hearing impairment, excessive noise exposure is a leading cause of hearing loss. Beyond the devastating effects of hearing impairment itself, epidemiological studies have identified hearing loss as a major risk factor for age-related cognitive decline, including dementia. At present, we currently lack a full understanding of the brain regions and underlying molecular changes that are responsible for mediating the link between hearing loss and cognitive impairment across aging. In the present study, we exposed 6-month-old rats to an occupational-like noise (100 dB SPL, 4 h/day × 30 days) or sham exposure and investigated both hippocampal-dependent (i.e., spatial learning and memory, assessed using the Morris water maze) and striatal-dependent (i.e., visuomotor associative learning, assessed using an operant-conditioning task) cognitive function across aging at 7, 10, and 13 months of age. We also investigated brain region-specific changes in microglial expression following noise/sham exposure in order to assess the potential contribution of this cell type to noise-induced cognitive impairments. Consistent with human studies, the occupational-like noise exposure resulted in high-frequency hearing loss, evidenced by a significant increase in hearing thresholds at 20 kHz. Ultimately, our results suggest that not all higher-level cognitive tasks or their associated brain regions appear to be equally susceptible to noise-induced deficits during aging, as the occupational-like noise exposure caused an age-dependent deficit in spatial but not visuomotor associative learning, as well as altered microglial expression in the hippocampus but not the striatum. Interestingly, we found no significant relationships between spatial learning ability and the level of hearing loss or altered microglial density in the hippocampus following noise exposure, suggesting that other changes in the brain likely contribute to hippocampal-dependent cognitive dysfunction following noise exposure. Lastly, we found that a subset of younger animals also showed noise-induced deficits in spatial learning; findings which suggest that noise exposure may represent an increased risk for cognitive impairment in vulnerable subjects. Overall, our findings highlight that even a mild occupational-like noise exposure earlier in adulthood can have long lasting implications for cognitive function later in life.

Nocturnal moths evolved ultrasound-triggered escape maneuvers for avoiding predatory bats emitting ultrasonic echolocation calls. Using ultrasound for pest control is not a novel concept, but the technique has not been systemized because of the moths’ habituation to sounds and the narrow directionality of conventional ultrasound speakers. Here, we report the use of pulsed ultrasonic white noise, which contributes to achieving ecologically concordant plant protection. An ultrasonic pulse, which is temporal mimicry of the search-phase pulse in the echolocation calls of a sympatric bat, was identified using neuroethological screening of eared moth–repelling ultrasounds; these pulses elicit flight-stopping reactions in moths but have no or little auditory adaptation. Such repellent ultrasounds broadcast from the cylindrical omni-azimuth ultrasound emitters suppressed the intrusion of gravid females of pest moths into cultivation fields. Thus, egg numbers and plant damage by hatched larvae were drastically reduced, enabling farmers to substantially skip applications of chemical insecticides for controlling moth pests.

Animal research focused on chronic tinnitus associated with noise-induced hearing loss can be expensive and time-consuming as a result of the behavioral training required. Although there exist a number of behavioral tests for tinnitus; there have been few formal direct comparisons of these tests. Here, we evaluated animals in two different tinnitus assessment methods. CBA/CaJ mice were trained in an operant conditioning, active avoidance (AA) test, and a reflexive, gap-induced pre-pulse inhibition of acoustic startle (GPIAS) test, or both. Tinnitus was induced in awake mice by unilateral continuous sound exposure using a 2-kHz- or 1 2 octave-wide noise centered at 16 kHz and presented at 113- or 116-dB SPL. Tinnitus was assessed 8 weeks after sound overexposure. Most mice had evidence of tinnitus behavior in at least one of the two behaviors. Of the mice evaluated in AA, over half (55%) had tinnitus positive behavior. In GPIAS, fewer animals (13%) were positive than were identified using the AA test. Few mice were positive in both tests (10%), and only one was positive for tinnitus behavior at the same spectral frequency in both tests. When the association between tinnitus behavior and spontaneous activity recorded in the inferior colliculus was compared, animals with tinnitus behavior in AA exhibited increased spontaneous activity, while those positive in GPIAS did not. Thus, it appears that operant conditioning tests, like AA, maybe more reliable and accurate tests for tinnitus than reflexive tests.

Centrosomal protein dysfunction might cause ciliopathies. However, the role of centrosomal proteins in male infertility remains poorly defined. Here, we identified a pathogenic splicing mutation in CEP78 in male infertile patients with severely reduced sperm number and motility, and the typical multiple morphological abnormalities of the sperm flagella phenotype. We further created Cep78 knockout mice, which showed an extremely low sperm count, completely aberrant sperm morphology, and approximately null sperm motility. The infertility of the patients and knockout mice could not be rescued by an intracytoplasmic sperm injection treatment. Mechanistically, CEP78 might regulate USP16 expression, which further stabilizes Tektin levels via the ubiquitination pathway. Cep78 knockout mice also exhibited impairments in retina and outer hair cells of the cochlea. Collectively, our findings identified nonfunctional CEP78 as an indispensable factor contributing to male infertility and revealed a role for this gene in regulating retinal and outer hair cell function in mice.

A prospective cross-sectional design was used to characterize congenital bilateral sensorineural hearing loss (SNHL). The underlying material of >30,000 consecutively screened newborns comprised 11 subjects with nonprofound, alleged nonsyndromic, SNHL. Comprehensive audiological testing was performed at ≈11 years of age. Results showed symmetrical sigmoid-like median pure-tone thresholds (PTTs) reaching 50–60 dB HL. The congenital SNHL revealed recruitment, increased upward spread of masking, distortion product otoacoustic emission (DPOAE) dependent on PTT (≤60 dB HL), reduced auditory brainstem response (ABR) amplitude, and normal magnetic resonance imaging. Unaided recognition of speech in spatially separate competing speech (SCS) deteriorated with increasing uncomfortable loudness level (UCL), plausibly linked to reduced afferent signals. Most subjects demonstrated hearing aid (HA) benefit in a demanding laboratory listening situation. Questionnaires revealed HA benefit in real-world listening situations. This functional characterization should be important for the outline of clinical guidelines. The distinct relationship between DPOAE and PTT, up to the theoretical limit of cochlear amplification, and the low ABR amplitude remain to be elucidated. The significant relation between UCL and SCS has implications for HA-fitting. The fitting of HAs based on causes, mechanisms, and functional characterization of the SNHL may be an individualized intervention approach and deserves future research.

Jet lag, shift work, and the extended light hours of modern life disrupt the regular light-dark cycle, affecting the menstrual cycle and decreasing fertility. The circadian pacemaker, the suprachiasmatic nucleus (SCN), is known to modulate ovulation, but the exact mechanism is not understood. Here we explore this connection by imaging neuronal activity in freely-behaving mice following extrinsic (jet lag) and intrinsic circadian circuit perturbations. We show that retina-connected vasoactive intestinal peptide (VIP)-expressing neurons in the SCN directly relay light information to gonadotropin-releasing hormone (GnRH)-expressing neurons to gate ovulation, as measured by recording calcium-sensitive activity of SCNVIP neurons over days in freely behaving mice. We show with machine-learning-based discriminations that the neuronal light-synchronized activity is primarily sex-dependent, and estrous-dependent in the late afternoon. Consistent with such a light-driven switch, we find that a pulse of light in this critical period could rescue estrous cycle regularity and the number of eggs released by animals kept in limited-light conditions. Our in vivo approach thus reveals the dynamic mechanism by which SCNVIP neurons trigger ovulation and demonstrates light-induced rescue of fertility, a finding with potential therapeutic implications for humans struggling with infertility due to shift work or jet lag.

Clinical auditory physiological measures (e.g., auditory brainstem responses, ABRs, and distortion product otoacoustic emissions, DPOAEs) provide diagnostic specificity for differentially diagnosing overt hearing impairments, but they remain limited in their ability to detect specific sites of lesion and subtle levels of cochlear damage. Studies in animal models may hold the key to improve differential diagnosis due to the ability to induce tightly controlled and histologically verifiable subclinical cochlear pathologies. Here, we present a normative set of traditional and clinically novel physiological measures using ABRs and DPOAEs measured in a large cohort of male macaque monkeys. Given the high similarities between macaque and human auditory anatomy, physiology, and susceptibility to hearing damage, this normative data set will serve as a crucial baseline to investigate novel physiological measures to improve diagnostics. DPOAE amplitudes were robust at f2 = 1.22, L1/L2 = 65/55, increased with frequency up to 10 kHz, and exhibited high test re-test reliability. DPOAE thresholds were lowest from 2-10 kHz and highest < 2 kHz. ABRs with a standard clinical electrode montage (vertex-to-mastoid, VM) produced Waves I-IV with a less frequently observed Wave-I, and lower thresholds. ABRs with a vertex-to-tympanic membrane (VT) electrode montage produced a more robust Wave-I, but absent Waves II-IV and higher thresholds. Further study with the VM montage revealed amplitudes that increased with stimulus level and were largest in response to click stimuli, with Wave-II showing the largest ABR amplitude, followed by -IV and -I, with high inter- and intra-subject variability. ABR wave latencies decreased with stimulus level and frequency. When stimulus presentation rate increased or stimuli were presented in close temporal proximity, ABR amplitude decreased, and latency increased. These findings expand upon existing literature of normative clinical physiological data in nonhuman primates and lay the groundwork for future studies investigating the effects of noise-induced pathologies in macaques.

Dysfunction of the peripheral auditory nerve (AN) contributes to dynamic changes throughout the central auditory system, resulting in abnormal auditory processing, including hypersensitivity. Altered sound sensitivity is frequently observed in autism spectrum disorder (ASD), suggesting that AN deficits and changes in auditory information processing may contribute to ASD-associated symptoms, including social communication deficits and hyperacusis. The MEF2C transcription factor is associated with risk for several neurodevelopmental disorders, and mutations or deletions of MEF2C produce a haploinsufficiency syndrome characterized by ASD, language, and cognitive deficits. A mouse model of this syndromic ASD ( Mef2c -Het) recapitulates many of the MEF2C haploinsufficiency syndrome-linked behaviors, including communication deficits. We show here that Mef2c -Het mice of both sexes exhibit functional impairment of the peripheral AN and a modest reduction in hearing sensitivity. We find that MEF2C is expressed during development in multiple AN and cochlear cell types; and in Mef2c -Het mice, we observe multiple cellular and molecular alterations associated with the AN, including abnormal myelination, neuronal degeneration, neuronal mitochondria dysfunction, and increased macrophage activation and cochlear inflammation. These results reveal the importance of MEF2C function in inner ear development and function and the engagement of immune cells and other non-neuronal cells, which suggests that microglia/macrophages and other non-neuronal cells might contribute, directly or indirectly, to AN dysfunction and ASD-related phenotypes. Finally, our study establishes a comprehensive approach for characterizing AN function at the physiological, cellular, and molecular levels in mice, which can be applied to animal models with a wide range of human auditory processing impairments. SIGNIFICANCE STATEMENT This is the first report of peripheral auditory nerve (AN) impairment in a mouse model of human MEF2C haploinsufficiency syndrome that has well-characterized ASD-related behaviors, including communication deficits, hyperactivity, repetitive behavior, and social deficits. We identify multiple underlying cellular, subcellular, and molecular abnormalities that may contribute to peripheral AN impairment. Our findings also highlight the important roles of immune cells (e.g., cochlear macrophages) and other non-neuronal elements (e.g., glial cells and cells in the stria vascularis) in auditory impairment in ASD. The methodological significance of the study is the establishment of a comprehensive approach for evaluating peripheral AN function and impact of peripheral AN deficits with minimal hearing loss.

The “cocktail party” problem—how a listener perceives speech in noisy environments—is typically studied using speech (multi-talker babble) or noise maskers. However, realistic cocktail party scenarios often include background music (e.g., coffee shops, concerts). Studies investigating music’s effects on concurrent speech perception have predominantly used highly controlled synthetic music or shaped noise, which do not reflect naturalistic listening environments. Behaviorally, familiar background music and songs with vocals/lyrics inhibit concurrent speech recognition. Here, we investigated the neural bases of these effects. While recording multichannel EEG, participants listened to an audiobook while popular songs (or silence) played in the background at a 0 dB signal-to-noise ratio. Songs were either familiar or unfamiliar to listeners and featured either vocals or isolated instrumentals from the original audio recordings. Comprehension questions probed task engagement. We used temporal response functions (TRFs) to isolate cortical tracking to the target speech envelope and analyzed neural responses around 100 ms (i.e., auditory N1 wave). We found that speech comprehension was, expectedly, impaired during background music compared to silence. Target speech tracking was further hindered by the presence of vocals. When masked by familiar music, response latencies to speech were less susceptible to informational masking, suggesting concurrent neural tracking of speech was easier during music known to the listener. These differential effects of music familiarity were further exacerbated in listeners with less musical ability. Our neuroimaging results and their dependence on listening skills are consistent with early attentional-gain mechanisms where familiar music is easier to tune out (listeners already know the song’s expectancies) and thus can allocate fewer attentional resources to the background music to better monitor concurrent speech material.

Early predator detection is a key component of the predator-prey arms race and has driven the evolution of multiple animal hearing systems. Katydids (Insecta) have sophisticated ears, each consisting of paired tympana on each foreleg that receive sound both externally, through the air, and internally via a narrowing ear canal running through the leg from an acoustic spiracle on the thorax. These ears are pressure-time difference receivers capable of sensitive and accurate directional hearing across a wide frequency range. Many katydid species have cuticular pinnae which form cavities around the outer tympanal surfaces, but their function is unknown. We investigated pinnal function in the katydid Copiphora gorgonensis by combining experimental biophysics and numerical modelling using 3D ear geometries. We found that the pinnae in C. gorgonensis do not assist in directional hearing for conspecific call frequencies, but instead act as ultrasound detectors. Pinnae induced large sound pressure gains (20–30 dB) that enhanced sound detection at high ultrasonic frequencies (>60 kHz), matching the echolocation range of co-occurring insectivorous gleaning bats. These findings were supported by behavioural and neural audiograms and pinnal cavity resonances from live specimens, and comparisons with the pinnal mechanics of sympatric katydid species, which together suggest that katydid pinnae primarily evolved for the enhanced detection of predatory bats.

Neural activity in the sensory cortex combines stimulus responses and ongoing activity, but it remains unclear whether these reflect the same underlying dynamics or separate processes. In the present study, we show in mice that, during wakefulness, the neuronal assemblies evoked by sounds in the auditory cortex and thalamus are specific to the stimulus and distinct from the assemblies observed in ongoing activity. By contrast, under three different anesthetics, evoked assemblies are indistinguishable from ongoing assemblies in the cortex. However, they remain distinct in the thalamus. A strong remapping of sensory responses accompanies this dynamic state change produced by anesthesia. Together, these results show that the awake cortex engages dedicated neuronal assemblies in response to sensory inputs, which we suggest is a network correlate of sensory perception.

In the post-natal mouse cochlea, type II spiral ganglion neurons (SGNs) innervating the electromotile outer hair cells (OHCs) of the ‘cochlear amplifier' selectively express the type III intermediate filament peripherin gene ( Prph) . Immunolabeling showed that Prph knockout (KO) mice exhibited disruption of this (outer spiral bundle) afferent innervation, while the radial fiber (type I SGN) innervation of the inner hair cells (~95% of the SGN population) was retained. Functionality of the medial olivocochlear (MOC) efferent innervation of the OHCs was confirmed in the Prph KO, based on suppression of distortion product otoacoustic emissions (DPOAEs) via direct electrical stimulation. However, “contralateral suppression” of the MOC reflex neural circuit, evident as a rapid reduction in cubic DPOAE when noise is presented to the opposite ear in wildtype mice, was substantially disrupted in the Prph KO. Auditory brainstem response (ABR) measurements demonstrated that hearing sensitivity (thresholds and growth-functions) were indistinguishable between wildtype and Prph KO mice. Despite this comparability in sound transduction and strength of the afferent signal to the central auditory pathways, high-intensity, broadband noise exposure (108 dB SPL, 1 h) produced permanent high frequency hearing loss (24–32 kHz) in Prph KO mice but not the wildtype mice, consistent with the attenuated contralateral suppression of the Prph KO. These data support the postulate that auditory neurons expressing Prph contribute to the sensory arm of the otoprotective MOC feedback circuit.

Severe hearing loss or deafness is often caused by cochlear hair cell loss and can be mitigated by a cochlear implant (CI). CIs target the auditory nerve, consisting of spiral ganglion cells (SGCs), which degenerate gradually, following hair cell loss. In animal models, it has been established that treatment with the neurotrophins brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) reduce SGC degeneration. In this study, we aimed to investigate whether treatment with both BDNF and NT-3 (Cocktail) is superior to treatment with each neurotrophin separately regarding cell preservation and neural responsiveness to electrical stimulation. To this end, deafened guinea pigs received neurotrophic treatment in their right ear via a gelatin sponge on the perforated round window membrane, followed by cochlear implantation 4 weeks later in the same ear for electrophysiological recordings to various stimulation paradigms. Normal-hearing and deafened untreated guinea pigs were included as positive and negative controls, respectively. Substantial SGC loss occurred in all deafened animals. Each of the neurotrophic treatments led to enhanced SGC survival mainly in the basal turn of the cochlea, gradually decreasing toward the apex. The Cocktail treatment resulted in the highest SGC survival in the treated ear, followed by BDNF, with the least protection of SGCs following NT-3 treatment. Survival of the SGC’s peripheral processes (PPs) followed the same trend in response to the treatment. However, survival of SGCs and PPs in the contralateral untreated ears was also highest in the Cocktail group. Consequently, analysis of the ratio between the treated and untreated ears showed that the BDNF group, which showed low SGC survival in the untreated ear, had the highest relative SGC survival of the three neurotrophin-treated groups. Neurotrophic treatment had positive effects in part of the electrically evoked compound action-potential recording paradigms. These effects were only observed for the BDNF or Cocktail treatment. We conclude that treatment with either BDNF or a cocktail of BDNF and NT-3 is preferred to NT-3 alone. Furthermore, since the Cocktail treatment resulted in better electrophysiological responsiveness and overall higher SGC survival than BDNF alone, we are inclined to recommend the Cocktail treatment rather than BDNF alone.

Nuclear positioning is important for the functionality of many cell types and is mediated by interactions of cytoskeletal elements and nucleoskeleton proteins. Nesprin proteins, part of the linker of nucleoskeleton and cytoskeleton (LINC) complex, have been shown to participate in nuclear positioning in multiple cell types. Outer hair cells (OHCs) in the inner ear are specialized sensory epithelial cells that utilize somatic electromotility to amplify auditory signals in the cochlea. Recently, Nesprin-4 (encoded by Syne4 ) was shown to play a crucial role in nuclear positioning in OHCs. Syne4 deficiency in humans and mice leads to mislocalization of the OHC nuclei and cell death resulting in deafness. However, it is unknown how Nesprin-4 mediates the position of the nucleus, and which other molecular components are involved in this process. Here, we show that the interaction of Nesprin-4 and the microtubule motor kinesin-1 is mediated by a conserved 4 amino-acid motif. Using in vivo AAV gene delivery, we show that this interaction is critical for nuclear positioning and hearing in mice. Nuclear mislocalization and cell death of OHCs coincide with the onset of hearing and electromotility and are solely restricted to outer, but not inner, hair cells. Likewise, the C. elegans functional homolog of Nesprin-4, UNC-83, uses a similar motif to mediate interactions between migrating nuclei and kinesin-1. Overall, our results suggest that OHCs require unique cellular machinery for proper nuclear positioning at the onset of electromotility. This machinery relies on the interaction between Nesprin-4 and kinesin-1 motors supporting a microtubule cargo model for nuclear positioning.

Fear and anxiety are brain states that evolved to mediate defensive responses to threat. While it is clear that the defense reaction includes multiple interacting behavioural, autonomic and endocrine adjustments, their integrative nature is poorly understood. In particular, threat has been associated with various cardiac changes, yet a clear consensus on their relevance for the integrated defense reaction is missing. We here define rapid microstates associated with specific behaviours and heart rate dynamics, both affected by long-lasting macrostates and reflecting context-dependent threat levels. In addition, we demonstrate that one of the most commonly used defensive behavioural responses, freezing measured by immobility, is part of an integrated cardio-behavioural microstate mediated by specific midbrain circuit elements. Our work puts forth a framework for systematic integration of cardiac and behavioural readouts that presents the basis for a better understanding of complex neural defensive states and their associated systemic functions.

Repressor element 1-silencing transcription factor (REST) is a transcriptional repressor that recognizes neuron-restrictive silencer elements in the mammalian genomes in a tissue- and cell-specific manner. The identity of REST target genes and molecular details of how REST regulates them are emerging. We performed conditional null deletion of Rest (cKO), mainly restricted to murine hair cells (HCs) and auditory neurons (aka spiral ganglion neurons [SGNs]). Null inactivation of full-length REST did not affect the development of normal HCs and SGNs but manifested as progressive hearing loss in adult mice. We found that the inactivation of REST resulted in an increased abundance of K v 7.4 channels at the transcript, protein, and functional levels. Specifically, we found that SGNs and HCs from Rest cKO mice displayed increased K v 7.4 expression and augmented K v 7 currents; SGN’s excitability was also significantly reduced. Administration of a compound with K v 7.4 channel activator activity, fasudil, recapitulated progressive hearing loss in mice. In contrast, inhibition of the K v 7 channels by XE991 rescued the auditory phenotype of Rest cKO mice. Previous studies identified some loss-of-function mutations within the K v 7.4-coding gene, Kcnq4 , as a causative factor for progressive hearing loss in mice and humans. Thus, the findings reveal that a critical homeostatic K v 7.4 channel level is required for proper auditory functions.

Peripheral sensory organ damage leads to compensatory cortical plasticity that supports a remarkable recovery of perceptual capabilities. A major knowledge gap is the lack of precise mechanisms that explain how this plasticity is implemented and distributed over a diverse collection of excitatory and inhibitory cortical neurons. Here, we explored these mechanisms in mouse A1. After peripheral damage, we found recovered sound-evoked activity of excitatory principal neurons (PNs) and parvalbumin (PVs) interneurons (INs), reduced activity in somatostatin-INs (SOMs), and recovered activity in vasoactive intestinal peptide-INs (VIPs). Given the sequentially organized cortical network where VIPs inhibit INs, SOMs inhibit PVs and PNs, and PVs inhibit PNs, our results suggest that PVs contribute to PN stability, SOMs allow for increased PN and PV activity, and VIPs enable the PN and PV recovery by inhibiting SOMs. These results highlight a strategic, cooperative, and cell-type-specific plasticity program that restores cortical sound processing after peripheral damage.