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The purpose of this paper is to show how temporal bone histopathology has been instrumental in adding knowledge about the origin of tinnitus in the cochlea and how it will still be useful for that purpose in the future. The papers published on this subject will be reviewed, and their contributions will be highlighted. The knowledge that is now part of the subject will be pointed out, and future research on this area will be pointed out.

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Background: Short array cochlear implant is indicated as rehabilitation in patients with severe to profound deafness, especially when there is cochlear ossification. In these cases, with reduced intracochlear patency, total insertion becomes more difficult, requiring the use of this type of electrode (15 mm). Few studies have been published to evaluate auditory performance, presenting controversial audiological results.Aims/Objectives: To report the speech perception of users of cochlear implants (CI) with short array. Material and Methods: A retrospective analysis of medical records of patients who underwent surgery for cochlear implantation with a short array, between 2009 and 2020, at the Hospital for Rehabilitation of Craniofacial Anomalies, University of São Paulo (HRAC-USP) was carried out. Results: There was performance evolution in the speech perception tests in the data analysis. Meningitis and congenital hearing loss were the main indications for CI in the sample. Conclusion. CI with a short array is an alternative in the management of patients with a history of cochlear ossification and severe or profound sensorineural hearing loss. Significance: To demonstrate the evolution of speech perception tests with short array cochlear implant in patients with or without ossified cochlea and its characteristics for application in clinical practice.

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Recent studies involving guinea pigs have shown that noise can damage the synapses between the inner hair cells and spiral ganglion neurons, even with normal hearing thresholds-which makes it important to investigate this kind of impairment in humans. The aim was to investigate, with multiple audiological assessments, the auditory function of normal hearing workers exposed to occupational noise. Altogether, 60 workers were assessed (30 in the noise-exposure group [NEG], who were exposed to occupational noise, and 30 in the control group [CG], who were not exposed to occupational noise); the workers were matched according to age. The following procedures were used: complete audiological assessment; speech recognition threshold in noise (SRTN); speech in noise (SN) in an acoustic field; gaps-in-noise (GIN); transient evoked otoacoustic emissions (TEOAE) and inhibitory effect of the efferent auditory pathway; auditory brainstem response (ABR); and long-latency auditory evoked potentials (LLAEP). No significant difference was found between the groups in SRTN. In SN, the NEG performed worse than the CG in signal-to-noise ratio (SNR) 0 (p-value 0.023). In GIN, the NEG had a significantly lower percentage of correct answers (p-value 0.042). In TEOAE, the NEG had smaller amplitude values bilaterally (RE p-value 0.048; LE p-value 0.045) and a smaller inhibitory effect of the efferent pathway (p-value 0.009). In ABR, the NEG had greater latencies of wave V (p-value 0.017) and interpeak intervals III-V and I-V in the LE (respective p-values: 0.005 and 0.04). In LLAEP, the NEG had a smaller P3 amplitude bilaterally (RE p-value 0.001; LE p-value 0.002). The NEG performed worse than the CG in most of the assessments, suggesting that the auditory function in individuals exposed to occupational noise is impaired, even with normal audiometric thresholds.

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Since glutamate is the primary excitatory neurotransmitter in the mammalian cochlea, the mechanisms for the removal of glutamate from the synaptic and extrasynaptic spaces are critical for maintaining normal function of this region. Glial cells of inner ear are crucial for regulation of synaptic transmission throughout since it closely interacts with neurons along the entire auditory pathway, however little is known about the activity and expression of glutamate transporters in the cochlea. In this study, using primary cochlear glial cells cultures obtained from newborn Balb/C mice, we determined the activity of a sodium-dependent and sodium-independent glutamate uptake mechanisms by means of High Performance Liquid Chromatography. The sodium-independent glutamate transport has a prominent contribution in cochlear glial cells which is similar to what has been demonstrated in other sensory organs, but it is not found in tissues less susceptible to continuous glutamate-mediated injuries. Our results showed that xCG- system is expressed in CGCs and is the main responsible for sodium-independent glutamate uptake. The identification and characterization of the xCG- transporter in the cochlea suggests a possible role of this transporter in the control of extracellular glutamate concentrations and regulation of redox state, that may aid in the preservation of auditory function.

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Abstract Introduction: Noise-induced hearing loss is one of the most common forms of sensorineural hearing loss. Nevertheless, the mechanisms of noise-induced hearing loss are still not fully understood. Objective: To investigate the dynamics of inflammatory responses in the mammalian cochlea following noise trauma at two different times, once during the light cycle and once during the dark. Methods: We challenged C57BL/6J mice with moderate, continuous noise trauma at either 9 a.m. or 9 p.m. Auditory function, histological changes in hair cells, and modifications in gene expression levels of inflammatory mediators were assessed at specific time points. Shifts in auditory brainstem response thresholds were measured at 1, 3, 7 and 14 days after noise exposure to measure potential noise-induced hearing loss. Cochlear basilar-membrane immunofluorescent staining was performed at 3 and 14 days after noise exposure. The mRNA levels of several inflammatory mediators were measured via quantitative real-time polymerase chain reaction before (pre) and after (0, 3, 12, 24 and 72 h) noise exposure. Results: We found that all noise-exposed mice developed a temporary threshold shift and that there were no significant differences between daytime and nighttime noise exposures in terms of inducing hearing-threshold shifts. Similarly, we did not detect significant histological changes in hair cells between these two groups. However, we discovered an interesting phenomenon in that the peak mRNA levels of IL-1β, IL-6, CCL2 and TNF-α were higher in day noise-exposed mice compared to those in night noise-exposed mice, and these mRNA levels subsided more slowly in day noise-exposed mice. Conclusion: Overall, these observations suggest that the circadian timing of noise exposure has a significant effect on noise-induced inflammatory responses in the mouse cochlea and that a greater inflammatory response might occur after daytime exposure.

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Abstract Introduction Perinatal hypothyroidism has a negative repercussion on the development and maturation of auditory system function. However, its long-term effect on auditory function remains unsettled. Objective To evaluate the effect of prenatal hypothyroidism on the auditory function of adult offspring in rats. Methods Pregnant Wistar rats were given the antithyroid drug methimazole (0.02%-1-methylimidazole-2-thiol- MMI) in drinking water, ad libitum, from gestational day (GD) 9 to postnatal day 15 (PND15). Anesthetized offspring from MMI-treated dams (OMTD) and control rats were evaluated by tympanometry, distortion product otoacoustic emission (DPOAE), and auditory brainstem response (ABR) at PNDs 30, 60, 90, and 120. Results Our data demonstrated no middle ear dysfunction, with the OMTD compliance lower than that of the control group. The DPOAE revealed the absence of outer hair cells function, and the ABR showed normal integrity of neural auditory pathways up to brainstem level in the central nervous system. Furthermore, in the OMTD group, hearing loss was characterized by a higher electrophysiological threshold. Conclusion Our data suggest that perinatal hypothyroidism leads to irreversible damage to cochlear function in offspring.

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Introduction Perinatal hypothyroidism has a negative repercussion on the development and maturation of auditory system function. However, its long-term effect on auditory function remains unsettled. Objective To evaluate the effect of prenatal hypothyroidism on the auditory function of adult offspring in rats. Methods Pregnant Wistar rats were given the antithyroid drug methimazole (0.02% -1-methylimidazole-2-thiol- MMI) in drinking water, ad libitum, from gestational day (GD) 9 to postnatal day 15 (PND15). Anesthetized offspring from MMI-treated dams (OMTD) and control rats were evaluated by tympanometry, distortion product otoacoustic emission (DPOAE), and auditory brainstem response (ABR) at PNDs 30, 60, 90, and 120. Results Our data demonstrated no middle ear dysfunction, with the OMTD compliance lower than that of the control group. The DPOAE revealed the absence of outer hair cells function, and the ABR showed normal integrity of neural auditory pathways up to brainstem level in the central nervous system. Furthermore, in the OMTD group, hearing loss was characterized by a higher electrophysiological threshold. Conclusion Our data suggest that perinatal hypothyroidism leads to irreversible damage to cochlear function in offspring.

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The inner ear is composed by tiny and complex structures that, together with peripheral and central auditory pathways, are responsible for hearing processing. However, not only the anatomy of the cochlea, its compartments and related structures are complex. The mechanisms involved in the regulation of homeostasis in the inner ear fluid, which determines the ionic gradient necessary for hearing and balancing sensory excitability, is an intricate phenomenon that involves several molecules. Among them, Aquaporins (AQP) play a significant role in this process. AQP are part of a family of small, integral membrane proteins that regulate different processes, including bidirectional water and ionic flow in the inner ear. Changes in the expression of these proteins are essential to auditory physiology and several pathophysiological processes in the inner ear. This review focuses on the role of AQP in health and disease of the auditory system.

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Abstract Introduction Diabetes mellitus is a metabolic disease associated with a rise in the level of blood glucose. Individuals with diabetes mellitus are more likely to develop hearing loss, tinnitus, and dizziness due to macro- and microvascular complications. The extent to which auditory and vestibular functions are impaired in individuals with type-2 diabetes mellitus is still under debate. Objective To systematically review studies focusing on auditory and vestibular functions in individuals with type-2 diabetes mellitus. Data Synthesis A search was conducted in the PubMed, MedlinePlus, Ingenta Connect and Google Scholar databases for articles published until June 2019. A total of 15,980 articles were primarily retrieved, 33 of which were shortlisted based on the inclusion criteria set by the investigators for the systematic review. Out of 33 full-length articles, 26 evaluated the functioning of the auditory system, while 7 evaluated the functioning of the vestibular system. Most studies related to auditory functioning reported a significant effect of type-2 diabetes mellitus on the peripheral auditory system, whereas studies on vestibular functioning reported no significant effect of diabetes mellitus on the functioning of the peripheral vestibular end-organ. Conclusion Overall, the results of various audiological and peripheral vestibular tests reveal distinctive peripheral and/or central auditory and vestibular end-organ impairments in individuals with type-2 diabetes mellitus.

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Introduction Diabetes mellitus is a metabolic disease associated with a rise in the level of blood glucose. Individuals with diabetes mellitus are more likely to develop hearing loss, tinnitus, and dizziness due to macro- and microvascular complications. The extent to which auditory and vestibular functions are impaired in individuals with type-2 diabetes mellitus is still under debate. Objective To systematically review studies focusing on auditory and vestibular functions in individuals with type-2 diabetes mellitus. Data Synthesis A search was conducted in the PubMed, MedlinePlus, Ingenta Connect and Google Scholar databases for articles published until June 2019. A total of 15,980 articles were primarily retrieved, 33 of which were shortlisted based on the inclusion criteria set by the investigators for the systematic review. Out of 33 full-length articles, 26 evaluated the functioning of the auditory system, while 7 evaluated the functioning of the vestibular system. Most studies related to auditory functioning reported a significant effect of type-2 diabetes mellitus on the peripheral auditory system, whereas studies on vestibular functioning reported no significant effect of diabetes mellitus on the functioning of the peripheral vestibular end-organ. Conclusion Overall, the results of various audiological and peripheral vestibular tests reveal distinctive peripheral and/or central auditory and vestibular end-organ impairments in individuals with type-2 diabetes mellitus.

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Some mutations in gap junction protein Connexin 26 (Cx26) lead to syndromic deafness, where hearing impairment is associated with skin disease, like in Keratitis Ichthyosis Deafness (KID) syndrome. This condition has been linked to hyperactivity of connexin hemichannels but this has never been demonstrated in cochlear tissue. Moreover, some KID mutants, like Cx26S17F, form hyperactive HCs only when co-expressed with other wild-type connexins. In this work, we evaluated the functional consequences of expressing a KID syndromic mutation, Cx26S17F, in the transgenic mouse cochlea and whether co-expression of Cx26S17F and Cx30 leads to the formation of hyperactive HCs. Indeed, we found that cochlear explants from a constitutive knock-in Cx26S17F mouse or conditional in vitro cochlear expression of Cx26S17F produces hyperactive HCs in supporting cells of the organ of Corti. These conditions also produce loss of hair cells stereocilia. In supporting cells, we found high co-localization between Cx26S17F and Cx30. The functional properties of HCs formed in cells co-expressing Cx26S17F and Cx30 were also studied in oocytes and HeLa cells. Under the recording conditions used in this study Cx26S17F did not form functional HCs and GJCs, but cells co-expressing Cx26S17F and Cx30 present hyperactive HCs insensitive to HCs blockers, Ca2+ and La3+, resulting in more Ca2+ influx and cellular damage. Molecular dynamic analysis of putative heteromeric HC formed by Cx26S17F and Cx30 presents alterations in extracellular Ca2+ binding sites. These results support that in KID syndrome, hyperactive HCs are formed by the interaction between Cx26S17F and Cx30 in supporting cells probably causing damage to hair cells associated to deafness.

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INTRODUCTION: Noise-induced hearing loss is one of the most common forms of sensorineural hearing loss. Nevertheless, the mechanisms of noise-induced hearing loss are still not fully understood. OBJECTIVE: To investigate the dynamics of inflammatory responses in the mammalian cochlea following noise trauma at two different times, once during the light cycle and once during the dark. METHODS: We challenged C57BL/6J mice with moderate, continuous noise trauma at either 9 a.m. or 9 p.m. Auditory function, histological changes in hair cells, and modifications in gene expression levels of inflammatory mediators were assessed at specific time points. Shifts in auditory brainstem response thresholds were measured at 1, 3, 7 and 14 days after noise exposure to measure potential noise-induced hearing loss. Cochlear basilar-membrane immunofluorescent staining was performed at 3 and 14 days after noise exposure. The mRNA levels of several inflammatory mediators were measured via quantitative real-time polymerase chain reaction before (pre) and after (0, 3, 12, 24 and 72 h) noise exposure. RESULTS: We found that all noise-exposed mice developed a temporary threshold shift and that there were no significant differences between daytime and nighttime noise exposures in terms of inducing hearing-threshold shifts. Similarly, we did not detect significant histological changes in hair cells between these two groups. However, we discovered an interesting phenomenon in that the peak mRNA levels of IL-1ß, IL-6, CCL2 and TNF-α were higher in day noise-exposed mice compared to those in night noise-exposed mice, and these mRNA levels subsided more slowly in day noise-exposed mice. CONCLUSION: Overall, these observations suggest that the circadian timing of noise exposure has a significant effect on noise-induced inflammatory responses in the mouse cochlea and that a greater inflammatory response might occur after daytime exposure.

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OBJECTIVE: This study describes the cochlear morphometry of a mexican population analysed by laterality and sex. The objective is to compare Cochlear Length (CL) evaluation between Alexiades et al. formula and manual method described by Würfel et al. PATIENTS: Hispanic patients from Mexico, with an age of 18 years or older, were included. Morphometric examination was performed retrospectively on 200 subjects who underwent previously temporal bone imaging for clinical purposes. MATERIALS AND METHODS: Horos for Mac program was used to measure CL, cochlear height, distance A, and distance B. WorkStation AW Volume Share 2 was used to obtain volume. CL was measured in 400 temporal bones (228 females, 172 males). RESULTS: The mean CL was 34.02mm±2.15mm. A significant difference was found in all variables between sex (P=≤0.05) and laterality (P=≤0.05). The Alexiades equation was used for determining CL and compared with the manual formula, with no significant differences (κ=0.71). However, the time consumption was 5 times faster with the calculated method. The Alexiades formula was demonstrated to be a reliable method measurement. CONCLUSION: Preoperative Computed Tomography evaluation of the internal ear helps to plan the Cochlear Implants (CI) surgical approach and allows to choose an appropriate electrode length for each necessity. Our findings may be useful to facilitate and adapt preoperative management of CI surgery by considering the characteristics of cochlear morphology of Latin-American populations.

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RESUMO Objetivo avaliar o perfil audiológico e a funcionalidade coclear em indivíduos com SW. Método estudo com 39 indivíduos, sendo 22 indivíduos com SW com idade entre 7 e 17 anos, sendo 15 do sexo masculino e 7 do sexo feminino e 17 indivíduos com desenvolvimento típico e normo-ouvintes. Todos os indivíduos foram avaliados por meio da audiometria tonal limiar, medidas de imitância acústica e análise das Emissões Otoacústicas Transientes (EOAT). Foi avaliado o perfil audiológico dos indivíduos com SW, e também foram comparadas as respostas das EOAT entre os indivíduos com SW sem perda auditiva e indivíduos controles. Resultados perda auditiva foi observada em 50% dos pacientes, sendo 78,95% neurossensorial e 21,05% mista. Esta perda foi predominantemente de grau leve a moderado, acometendo principalmente as frequências a partir de 3 kHz. Quanto às EOAT, observou-se maior incidência de ausência e de respostas de menor amplitude em indivíduos com SW. Conclusão indivíduos com SW apresentam disfunção das células ciliadas, principalmente da região basal da cóclea. Assim, a análise das EOAT é um recurso clínico importante a ser considerada na avaliação audiológica de rotina.

ABSTRACT Purpose to evaluate cochlear functionality in Williams syndrome (WS) individuals. Methods a study with 39 individuals, being 22 with WS aged between 7 and 17 years, 15 male and 7 female, and 17 individuals with typical development and normal hearing. All individuals were evaluated using pure tone audiometry, acoustic immittance measurements, and Transient Evoked Otoacoustic Emissions (TEOAE). The audiological profile in individuals with WS was analyzed, and TEOAE responses were compared between WS individuals without hearing loss and typical developmental individuals. Results The hearing loss was observed in 50% of patients, being 78.95% sensorineural and 21.05% mixed. This hearing loss was predominantly mild to moderate, affecting mainly frequencies above 3 kHz. As for TEOAE, there was a higher incidence of absence and lower amplitude responses in individuals with WS. Conclusion WS individuals have hair cell dysfunction, mainly in the basal region of the cochlea. Thus, TEOAE analysis is an important clinical resource to be considered in the routine audiological evaluation.

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Introducción. Las sorderas o hipoacusias prelinguales son de etiología genética entre el 60 y el 68% de los casos; de estos, del 20 al 40% son malformaciones del oído interno. De los casos de hipoacusia no sindrómica ligada al X se han descrito siete tipos. De las malformaciones de oído interno, la partición coclear incompleta tipo III es la menos frecuente.Objetivo. Presentar el reporte clínico-genético de una familia mexicana, con indi-viduos varones afectados por sordera neurosensorial congénita con malformación de oído interno. Material y Métodos. Se realizó estudio de una familia en la que nueve miembros presentaban sordera. Se estudiaron cuatro de ellos y una madre sin manifestaciones, a través del estudio clínico general por médico genetista, el estudio audiológico (otos-copía y audiometría) por médico audiólogo y el estudio de tomografía computada (TC) por médico radiólogo.Resultados. Los pacientes estudiados presentaron sordera neurosensorial congéni-ta, de severa a profunda bilateral. A través de la TC, se evidenció malformación de oído interno. Tres pacientes presentaron partición coclear incompleta tipo III y un paciente partición incompleta tipo I. Debido al estudio clínico y al árbol genealógico, se definió diagnóstico de hipoacusia neurosensorial no sindrómica ligada al X. La TC de la madre sin manifestaciones no presentó evidencia de malformaciones en oído interno (MOI).Conclusión. El estudio de imagen es fundamental para definir presencia o no de MOI en todos los pacientes con hipoacusia y así poder guiar la terapéutica y el aseso-ramiento genético, así como realizar los estudios moleculares más adecuados

Introduction. The pre-lingual deafness or hearing loss are of genetic cause in be-tween 60% and 68% of cases, among these, between 20% and 40% are malforma-tion of the inner ear. From the non-syndromic hearing loss cases that are linked to the X chromosome, seven types have been described. Among these inner ear malforma-tions, incomplete cochlear partition type III is the less frequent.Objective. Present the clinical genetical report of a Mexican family, with male in-dividuals affected by congenital neurosensory deafness with inner ear malformation.Materials and methodology. A study on a family in which nine members were affected by deafness was done. Four of them, plus a mother without manifestation, were studied through a general clinical study by a geneticist, an audiological study (otoscopy and audiometry) by an audiologist, and a computed tomography (CT) scan by a radiologist.Results. The studied patients presented congenital neurosensory deafness, from se-vere to deep bilateral. Via the CT, the inner ear malformation was made clear. Three of the patients presented incomplete cochlear partition type III and one patient in-complete cochlear partition type I. Due to the clinical study and the family tree, it was diagnosed non-syndromic neurosensory deafness linked to X. The CT of the mother without manifestation did not show evidence of inner ear malformations.Conclusion. The study by image is fundamental to define whether there is or not a presence of inner ear malformations in any patient with heading loss to be able to guide the therapeutics and the genetic counseling, as well as to make more accurate molecular studies

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RESUMO Objetivo Verificar se o tratamento com os antivirais de ação direta para a hepatite C provocam efeitos adversos na audição. Métodos A casuística foi composta por 16 indivíduos portadores do vírus da hepatite C, de ambos os gêneros, com média de idade de 51 anos. Foram excluídos do grupo indivíduos com perda auditiva do tipo condutiva ou mista e que apresentassem fatores de risco para perda auditiva. A avaliação foi realizada em dois momentos: antes do uso dos antivirais de ação direta e após o término do tratamento de três meses. Incluiu os seguintes procedimentos: anamnese, inspeção do meato acústico externo, audiometria tonal liminar, limiar de recepção de fala, índice de reconhecimento de fala, medidas de imitância acústica e emissões otoacústicas evocadas por estímulo transiente e produto de distorção. Resultados: Houve baixa ocorrência de zumbido e vertigem. Não houve diferença estatisticamente significativa entre os resultados da avaliação pré-tratamento e pós-tratamento. Conclusão O tratamento com antivirais de ação direta contra o vírus da hepatite C não provocou efeitos adversos na função auditiva.

ABSTRACT Purpose To verify whether treatment with hepatitis C direct-acting antivirals has adverse effects on hearing. Methods The sample consisted of 16 individuals with hepatitis C virus, of both sexes, with an average age of 51 years. Individuals with conductive or mixed hearing loss who presented risk factors for hearing loss were excluded from the group. The evaluation was carried out in two moments: before the use of direct-acting antivirals and after the three-month treatment. It included the following procedures: anamnesis, external auditory canal inspection, pure tone audiometry, speech reception threshold, speech recognition index, acoustic immittance measures and transient and distortion product otoacoustic emissions. Results There was a low incidence of tinnitus and vertigo. There was no statistically significant difference between the results of the pre- and post-treatment assessment. Conclusion The treatment with direct-acting antivirals against the hepatitis C virus did not cause any adverse effects on hearing function.

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RESUMO Objetivo avaliar o efeito da variação da intensidade de estimulação sobre as respostas das emissões otoacústicas produto de distorção em indivíduos com perda auditiva neurossensorial, utilizando um protocolo de gradiente de fase das emissões. Métodos estudo observacional transversal. Participaram 38 indivíduos com diagnóstico de perda auditiva neurossensorial de grau leve, moderado ou severo. Foram realizadas anamnese, meatoscopia, audiometria tonal liminar, logoaudiometria, imitanciometria, emissões otoacústicas produto de distorção e emissões otoacústicas residuais. As emissões otoacústicas residuais foram coletadas com o equipamento Echodia, modelo Elios®. O protocolo utilizado permite a variação dos parâmetros frequência e intensidade e as respostas são analisadas por meio do teste do Gradiente de Fase. As respostas registradas nas emissões residuais foram consideradas como "presente", "ausente" e "artefato", considerando a variação da fase em função de f1. Resultados Foram incluídas 72 orelhas. Houve diferença estatisticamente significativa nas frequências de 1300 Hz e 2000 Hz, ao comparar os resultados das emissões residuais. Ao correlacionar o resultado da audiometria e a intensidade de estimulação que evocou a emissão residual, houve correlação positiva para as frequências de 1000 Hz e 4000Hz. O "artefato" foi registrado, principalmente, nas frequências mais agudas: 56,2% em 3000 Hz e 58,2% em 4000 Hz. A emissão otoacústica residual presente foi registrada em 18,6% em 1000 Hz, 13,4% em 2000 Hz, 6,3% em 3000 Hz e 7,5% em 4000 Hz. Conclusão o aumento da intensidade de estimulação no exame de emissões pode auxiliar no estudo das células ciliadas residuais, desde que seja utilizado um protocolo capaz de diferenciar respostas fisiológicas de artefatos.

ABSTRACT Purpose To study the effect of stimulation intensity variation on the responses of distortion products in subjects with sensorineural hearing loss using a new protocol to register the otoacoustic emissions. Methods This is a cross-sectional observational study. The following procedures were performed: anamnesis, otoscopy, pure tone audiometry, speech audiometry, tympanometry, distortion product and residual otoacoustic emissions. The residual DPOAE were collected with the Echodia equipment, Elios®. The protocol that was developed allows the variation of frequency and intensity parameters and the responses are analyzed by phase gradient test. Responses recorded in residual otoacoustic emissions were considered "present", "absent" or "artifact". Results The total included ears was 72. On residual otoacoustic emissions test, at a frequency of 1300Hz and 2000Hz, there was statistically significant difference. By analyzing the average found in the audiometry and the results of residual emissions, only the frequency of 1300Hz showed a statistically significant association in all groups. By correlating the results of the audiometry and the stimulation intensity used to evoke the residual emission, there was positive correlation for the frequencies of 1000Hz and 4000Hz. The "artifact" was mostly recorded in the higher frequencies: 56.2% in 3000Hz and 58.2% in 4000 Hz. Residual EOAPD present was recorded as 18.6% at 1000Hz, 13.4% at 2000Hz, 6.3% at 3000Hz and 7.5% at 4000Hz. Conclusion The increased stimulation intensity in the otoacoustic emissions test can aid in the study of residual outer hair cells, as long as a protocol is used to check the correctness of the responses.

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Vertebrate hair cell (HC) systems are innervated by efferent fibers that modulate their response to external stimuli. In mammals, the best studied efferent-HC synapse, the cholinergic medial olivocochlear (MOC) efferent system, makes direct synaptic contacts with HCs. The net effect of MOC activity is to hyperpolarize HCs through the activation of α9α10 nicotinic cholinergic receptors (nAChRs) and the subsequent activation of Ca2+-dependent SK2 potassium channels. A serious obstacle in research on many mammalian sensory systems in their native context is that their constituent neurons are difficult to access even in newborn animals, hampering circuit observation, mapping, or controlled manipulation. By contrast, fishes and amphibians have a superficial and accessible mechanosensory system, the lateral line (LL), which circumvents many of these problems. LL responsiveness is modulated by efferent neurons which aid to distinguish between external and self-generated stimuli. One component of the LL efferent system is cholinergic and its activation inhibits LL afferent activity, similar to what has been described for MOC efferents. The zebrafish (Danio rerio) has emerged as a powerful model system for studying human hearing and balance disorders, since LL HC are structurally and functionally analogous to cochlear HCs, but are optically and pharmacologically accessible within an intact specimen. Complementing mammalian studies, zebrafish have been used to gain significant insights into many facets of HC biology, including mechanotransduction and synaptic physiology as well as mechanisms of both hereditary and acquired HC dysfunction. With the rise of the zebrafish LL as a model in which to study auditory system function and disease, there has been an increased interest in studying its efferent system and evaluate the similarity between mammalian and piscine efferent synapses. Advances derived from studies in zebrafish include understanding the effect of the LL efferent system on HC and afferent activity, and revealing that an α9-containing nAChR, functionally coupled to SK channels, operates at the LL efferent synapse. In this review, we discuss the tools and findings of these recent investigations into zebrafish efferent-HC synapse, their commonalities with the mammalian counterpart and discuss several emerging areas for future studies.

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Top-down modulation of sensory responses to distracting stimuli by selective attention has been proposed as an important mechanism by which our brain can maintain relevant information during working memory tasks. Previous works in visual working memory (VWM) have reported modulation of neural responses to distracting sounds at different levels of the central auditory pathways. Whether these modulations occur also at the level of the auditory receptor is unknown. Here, we hypothesize that cochlear responses to irrelevant auditory stimuli can be modulated by the medial olivocochlear system during VWM. Twenty-one subjects (13 males, mean age 25.3 yr) with normal hearing performed a visual change detection task with different VWM load conditions (high load = 4 visual objects; low load = 2 visual objects). Auditory stimuli were presented as distractors and allowed the measurement of distortion product otoacoustic emissions (DPOAEs) and scalp auditory evoked potentials. In addition, the medial olivocochlear reflex strength was evaluated by adding contralateral acoustic stimulation. We found larger contralateral acoustic suppression of DPOAEs during the visual working memory period (n = 21) compared with control experiments (n = 10), in which individuals were passively exposed to the same experimental conditions. These results show that during the visual working memory period there is a modulation of the medial olivocochlear reflex strength, suggesting a possible common mechanism for top-down filtering of auditory responses during cognitive processes.NEW & NOTEWORTHY The auditory efferent system has been proposed to function as a biological filter of cochlear responses during selective attention. Here, we recorded electroencephalographic activity and otoacoustic emissions in response to auditory distractors during a visual working memory task in humans. We found that the olivocochlear efferent activity is modulated during the visual working memory period suggesting a common mechanism for suppressing cochlear responses during selective attention and working memory.

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The α9α10 nicotinic acetylcholine receptor (nAChR) plays a fundamental role in inner ear physiology. It mediates synaptic transmission between efferent olivocochlear fibers that descend from the brainstem and hair cells of the auditory sensory epithelium. The α9 and α10 subunits have undergone a distinct evolutionary history within the family of nAChRs. Predominantly in mammalian vertebrates, the α9α10 receptor has accumulated changes at the protein level that may ultimately relate to the evolutionary history of the mammalian hearing organ. In the present work, we investigated the responses of α9α10 nAChRs to choline, the metabolite of acetylcholine degradation at the synaptic cleft. Whereas choline is a full agonist of chicken α9α10 receptors it is a partial agonist of the rat receptor. Making use of the expression of α9α10 heterologous receptors, encompassing wild-type, heteromeric, homomeric, mutant, chimeric, and hybrid receptors, and in silico molecular docking, we establish that the mammalian (rat) α10 nAChR subunit underscores the reduced efficacy of choline. Moreover, we show that whereas the complementary face of the α10 subunit does not play an important role in the activation of the receptor by ACh, it is strictly required for choline responses. Thus, we propose that the evolutionary changes acquired in the mammalian α9α10 nAChR resulted in the loss of choline acting as a full agonist at the efferent synapse, without affecting the triggering of ACh responses. This may have accompanied the fine-tuning of hair cell post-synaptic responses to the high-frequency activity of efferent medial olivocochlear fibers that modulate the cochlear amplifier.