scholarly journals Electrically evoked auditory nerve responses in the cochlea with normal outer hair cells

2009 ◽  
Vol 4 (2) ◽  
pp. 71-75 ◽  
Author(s):  
Tianying Ren ◽  
Guo Meng–he ◽  
He Wen–xuan ◽  
Josef M. Miller ◽  
Alfred L. Nuttall
2016 ◽  
Vol 15 (1) ◽  
Author(s):  
Solihatul Mardhiah Muhamad Azman ◽  
Sarah Rahmat

Introduction: In Schroeder-phase masking test, different auditory perception ability towards different phases of Schroeder masker is known as ‘phase effect’. Previously, the phase effect mechanism was proposed to be dominantly contributed by peripheral auditory function, mainly by outer hair cells. This study aims to investigate the possible involvement of central auditory function (i.e. auditory nerve) in the phase effect mechanism. Methods: Four normal hearing and four sensorineural hearing loss subjects were recruited. Schroeder-phase masking test was conducted at 500 Hz, 1 kHz, and 2 kHz (75 dB A), and phase effect was recorded. Electrocochleography (ECochG) test via tip-trode recording using 90 dBnHL tone burst at 500 Hz, 1 kHz, and 2 kHz was also conducted on the same subjects. The amplitude of three ECochG components; i) cochlear microphonic (CM) - arises from outer hair cells, ii) summating potential (SP) - arises from inner hair cells, and iii) action potential (AP)- arises from auditory nerve; were recorded. Pearson and Spearman analysis were performed to find correlation between phase effect and individual ECochG components’ amplitude. Results: Result showed no significant correlation between phase effect and all ECochG components’ amplitude at all tested frequencies with exception at 2 kHz. A significant strong correlation (p: 0.02; r: 0.81) between phase effect and action potential’s amplitude at 2 kHz was observed. Conclusions: This finding suggests that central auditory function (i.e. auditory nerve) is possibly involved in the phase effect mechanism. This finding gives new insight towards better understanding of auditory perception.


1991 ◽  
Vol 113 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Sir James Lighthill

This survey lecture on the biomechanics of hearing sensitivity is concerned, not with how the brain in man and other mammals analyzes the data coming to it along auditory nerve fibers, but with the initial capture of that data in the cochlea. The brain, needless to say, can produce all its miracles of interpretation only where it works on good initial data. For frequency selectivity these depend on some remarkable properties of the cochlea as a passive macromechanical system, comprising the basilar membrane with its steeply graded stiffness distribution vibrating within the cochlear fluids. But the biomechanics of hearing sensitivity to low levels of sound (at any particular frequency) calls also into play an active micromechanical system, which during the past few years has progressively been identified as located in the outer hair cells, and which, through a process of positive feedback, amplifies (in healthy ears) that basilar membrane vibration. This in turn offers the inner hair cells an enhanced signal at low sound levels, so that the threshold at which they can generate activity in auditory nerve fibers is, in consequence, very substantially lowered.


2016 ◽  
Vol 115 (3) ◽  
pp. 1644-1653 ◽  
Author(s):  
M. Christian Brown

Medial olivocochlear (MOC) neurons provide an efferent innervation to outer hair cells (OHCs) of the cochlea, but their tonotopic mapping is incompletely known. In the present study of anesthetized guinea pigs, the MOC mapping was investigated using in vivo, extracellular recording, and labeling at a site along the cochlear course of the axons. The MOC axons enter the cochlea at its base and spiral apically, successively turning out to innervate OHCs according to their characteristic frequencies (CFs). Recordings made at a site in the cochlear basal turn yielded a distribution of MOC CFs with an upper limit, or “edge,” due to usually absent higher-CF axons that presumably innervate more basal locations. The CFs at the edge, normalized across preparations, were equal to the CFs of the auditory nerve fibers (ANFs) at the recording sites (near 16 kHz). Corresponding anatomical data from extracellular injections showed spiraling MOC axons giving rise to an edge of labeling at the position of a narrow band of labeled ANFs. Overall, the edges of the MOC CFs and labeling, with their correspondences to ANFs, suggest similar tonotopic mappings of these efferent and afferent fibers, at least in the cochlear basal turn. They also suggest that MOC axons miss much of the position of the more basally located cochlear amplifier appropriate for their CF; instead, the MOC innervation may be optimized for protection from damage by acoustic overstimulation.


2019 ◽  
Vol 121 (6) ◽  
pp. 2163-2180 ◽  
Author(s):  
Andrew K. Pappa ◽  
Kendall A. Hutson ◽  
William C. Scott ◽  
J. David Wilson ◽  
Kevin E. Fox ◽  
...  

The cochlear summating potential (SP) to a tone is a baseline shift that persists for the duration of the burst. It is often considered the most enigmatic of cochlear potentials because its magnitude and polarity vary across frequency and level and its origins are uncertain. In this study, we used pharmacology to isolate sources of the SP originating from the gerbil cochlea. Animals either had the full complement of outer and inner hair cells (OHCs and IHCs) and an intact auditory nerve or had systemic treatment with furosemide and kanamycin (FK) to remove the outer hair cells. Responses to tone bursts were recorded from the round window before and after the neurotoxin kainic acid (KA) was applied. IHC responses were then isolated from the post-KA responses in FK animals, neural responses were isolated from the subtraction of post-KA from pre-KA responses in NH animals, and OHC responses were isolated by subtraction of post-KA responses in FK animals from post-KA responses in normal hearing (NH) animals. All three sources contributed to the SP; OHCs with a negative polarity and IHCs and the auditory nerve with positive polarity. Thus the recorded SP in NH animals is a sum of contributions from different sources, contributing to the variety of magnitudes and polarities seen across frequency and intensity. When this information was applied to observations of the SP recorded from the round window in human cochlear implant subjects, a strong neural contribution to the SP was confirmed in humans as well as gerbils. NEW & NOTEWORTHY Of the various potentials produced by the cochlea, the summating potential (SP) is typically described as the most enigmatic. Using combinations of ototoxins and neurotoxins, we show contributions to the SP from the auditory nerve and from inner and outer hair cells, which differ in polarity and vary in size across frequency and level. This complexity of sources helps to explain the enigmatic nature of the SP.


1978 ◽  
Vol 41 (2) ◽  
pp. 365-383 ◽  
Author(s):  
P. Dallos ◽  
D. Harris

1. Recordings were made from chinchilla auditory nerve fibers after portions of the cochlear outer hair cell (OHC) population were destroyed with the antibiotic kanamycin. In most cases the inner hair cell (IHC) population was completely preserved as determined by phase-contrast microscopy. We presume that the remaining IHCs are functionally normal, and thus that recordings obtained from fibers originating from the lesioned cochlear segment reflect IHC behavior. 2. Behavioral thresholds were measured for all animals both before and after the production of the cochlear lesion. The audiograms and the histological evaluation of the ears were the basis for assessing whether a particular fiber originated in a normal, pathological (shifted threshold; IHC only), or border region. These criteria also identified the animals that sustained IHC damage together with the destruction of part of the OHC population. Only the data obtained from those fibers which probably originated from the OHC-free segment of the cochlea are considered in detail. 3. Fibers whose characteristic frequency (CF) identified them as belonging to the normal (audiometrically and histologically) region, were found to be normal in all respects. 4. Fibers from the border region (where the audiogram has a steep slope between normal and hearing-loss regions probably corresponding to the segment where OHC loss progresses from less than 10% to more than 90%) had very complex response patterns. Their frequency threshold curves (FTC) showed great variability. In general, the closer the fiber was to the fully developed lesion, the more abnormal its FTC became. 5. Those units that were concluded to have originated from the OHC-free part of the cochlea could be divided into three categories on the basis of the shape of their FTCs. A small fraction had very broad tuning (9%). The majority (53%) had approximately normal tail segment, normal bandwidth of the tip segment, and highly elevated threshold at CF. A group of fibers (38%) could not be assigned a CF. Probably the FTC of most of these latter fibers are similar to those of the previous group, but the sharply tuned short tip segment was either missed or was not reachable on account of its extremely high threshold level. 6. Such indexes of fiber response as latency, spontaneous rate, and time pattern (PST histograms) were not affected by the loss of OHCs. 7. On the basis of the data and of the assumptions made it was suggested that outer hair cells provide a frequency-dependent sensitizing influence to the inner hair cells. The frequency dependence could best be expressed as a flat-topped band pass characteristic.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Ken Hashimoto ◽  
Tyler T. Hickman ◽  
Jun Suzuki ◽  
Lingchao Ji ◽  
David C. Kohrman ◽  
...  

Abstract Noise exposures causing only transient threshold shifts can destroy auditory-nerve synapses without damaging hair cells. Here, we asked whether virally mediated neurotrophin3 (NT3) overexpression can repair this damage. CBA/CaJ mice at 6 wks were injected unilaterally with adeno-associated virus (AAV) containing either NT3 or GFP genes, via the posterior semicircular canal, 3 wks prior to, or 5 hrs after, noise exposure. Controls included exposed animals receiving vehicle only, and unexposed animals receiving virus. Thresholds were measured 2 wks post-exposure, just before cochleas were harvested for histological analysis. In separate virus-injected animals, unexposed cochleas were extracted for qRT-PCR. The GFP reporter showed that inner hair cells (IHCs) were transfected throughout the cochlea, and outer hair cells mainly in the apex. qRT-PCR showed 4- to 10-fold overexpression of NT3 from 1–21 days post-injection, and 1.7-fold overexpression at 40 days. AAV-NT3 delivered prior to noise exposure produced a dose-dependent reduction of synaptopathy, with nearly complete rescue at some cochlear locations. In unexposed ears, NT3 overexpression did not affect thresholds, however GFP overexpression caused IHC loss. In exposed ears, NT3 overexpression increased permanent threshold shifts. Thus, although NT3 overexpression can minimize noise-induced synaptic damage, the forced overexpression may be harmful to hair cells themselves during cochlear overstimulation.


Author(s):  
Zhixian Wang ◽  
Pinjin Zhu ◽  
Jianhe Sun ◽  
Xuezheng Song

Hearing research is important not only for clinical, professional and military medicine, but also for toxicology, gerontology and genetics. Ultrastructure of the cochlea attracts much attention of electron microscopists, (1―3) but the research lags far behind that of the other parts of the organnism. On the basis of careful microdissection, technical improvment and accurate observation, we have got some new findings which have not been reported in the literature.We collected four cochleas from human corpses. Temporal bones dissected 1 h after death and cochleas perfused with fixatives 4 h after death were good enough in terms of preservation of fine structures. SEM:The apical surface of OHCs (Outer hair cells) and DTs (Deiters cells) is narrower than that of IPs (Inner pillar cells). The mosaic configuration of the reticular membrane is not typical. The stereocilia of IHCs (Inner hair cells) are not uniform and some kinocilia could be seen on the OHCs in adults. The epithelial surface of RM (Reissner’s membrane) is not smooth and no mesh could be seen on the mesothelial surface of RM. TEM.


2013 ◽  
Vol 40 (2) ◽  
Author(s):  
Asti Kristianti ◽  
Teti Madiadipoera ◽  
Bogi Soeseno

Background: Chemotherapy is worldwide used nowadays, and its toxicity still remain a problemespecially toxicity to the ear (ototoxicity). Cisplatin (cis-diamminedichloroplatinum) is one of themost commonly used chemotherapy and highly potent in treating epithelial malignancies. Ototoxicitycaused by cisplatin is irreversible, progressive, bilateral, sensorineural hearing loss especially on highfrequency (4-8 KHz) accompanied by tinnitus. Purpose: To observe the cochlear outer hair cells damagein malignancies patients treated with cisplatin. Methods: This study is an observational analytic studywith prospective design to determine the influence of high dose cisplatin on cochlear outer hair cellsfunction. The research was carried out at the ENT-HNS Department, Hasan Sadikin General HospitalBandung, from November 2007 until June 2008. Audiometry, tympanometry, and distortion productotoacoustic emission (DPOAE) examinations were conducted before chemotherapy and DPOAE, andtimpanometry was again measured three days after first and second cycles of cisplatin administration. McNemar test was performed to calculate the effects of high-dose cisplatin to the cochlear outer haircells function. To compare pre and post-cisplatin on alteration of cochlear hair cells function, Wilcoxontest was used. Results: In this study 60 ears from 30 subjects that meet the inclusion criteria, consistedof 25 man (83.3%) and 5 women (16.7%). The prevalence of damaged cochlear outer hair cells were63% at first cycle and 70% at second cycle of cisplatin administration. The decline of cochlear outerhair cells function was significant (p<0.001). Conclusion: High-dose cisplatin decreases cochlear outerhair cells function in patients with malignant neoplasm. Abstrak : Latar belakang: Kemoterapi sekarang rutin digunakan secara klinis di seluruh dunia. Sejalan denganhal tersebut toksisitas kemoterapi, khususnya terhadap telinga saat ini menjadi perhatian. Sisplatin(cis-diamminedichloroplatinum) adalah salah satu obat kemoterapi yang paling banyak digunakandan paling manjur untuk terapi keganasan epitelial. Efek ototoksik sisplatin yaitu terjadi gangguandengar sensorineural yang irreversible, progresif, bilateral pada frekuensi tinggi (4-8 kHz), dan disertaidengan tinitus. Tujuan: Untuk menilai penurunan fungsi sel rambut luar koklea pada penderita tumorganas sesudah pemberian sisplatin dosis tinggi dengan menggunakan DPOAE. Metode: Studi analitikobservasional dengan rancangan prospektif di Bagian IK. THT-KL RS. Hasan Sadikin Bandung mulaibulan November 2007 sampai dengan Juni 2008. Pada penelitian ini dilakukan pemeriksaan audiometrinada murni, timpanometri, dan distortion product otoacoustic emission (DPOAE) prakemoterapi, kemudianDPOAE dan timpanometri diulang tiga hari sesudah siklus pertama dan kedua kemoterapi sisplatin. Datayang diperoleh diuji dengan uji McNemar dan uji Wilcoxon. Hasil: Dari penelitian didapat 60 telingadari 30 subjek penelitian yang memenuhi kriteria inklusi yang terdiri dari 25 laki-laki (83,3%) dan 5perempuan (16,7%). Insidens penurunan fungsi sel rambut luar koklea sebesar 63% (38 kasus) sesudahsiklus pertama dan 70% (42 kasus) sesudah siklus kedua. Hubungan penurunan fungsi sel rambut luarkoklea memberikan nilai yang sangat bermakna sejak pemberian siklus pertama (p<0,001). Kesimpulan:Pemberian sisplatin dosis tinggi pada penderita tumor ganas menyebabkan penurunan fungsi sel rambutluar koklea.Kata kunci: kemoterapi, sisplatin dosis tinggi, sel rambut luar koklea.


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