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At least 451 records · Page 25Linked to original sources
PubMed1987

The effect of vitamin D deficiency on the cochlear potentials and the perilymphatic ionized calcium concentration of rats.

Sensorineural hearing loss has been frequently reported in patients with renal failure but its etiology has not yet been established. Disturbance of Ca metabolism is present in renal failure and seems to cause hearing loss. The purpose of the present study was to determine whether the disturbance of Ca metabolism has any effect on cochlear function. The cochlear potentials were measured in 19 rats fed with a vitamin D deficient diet. The pathological findings showed prolongation of N1 latency with unchanged N1 amplitude and pseudothreshold, depression of CM amplitude and elevation of the CM pseudothreshold. The latencies of narrow-band APs were prolonged in the entire cochlear partition. Ca2+ concentration in perilymph was 3.2 X 10(-4) M (n = 4) in vitamin D deficient rats and 7.4 X 10(-4) M (n = 4) in the controls. These findings were milder than those obtained in surgically induced renal failure. It was concluded that although vitamin D deficiency is one cause of hearing loss in renal failure, other major factors must be involved. The authors postulate that hearing loss in vitamin D deficiency is mainly attributable to the depression of the Ca2+ concentration in perilymph.

Action Potentials↗
PubMed1995

The action of substance P methyl ester on cochlear potentials in the guinea pig.

The action of the substance P agonist, substance P methyl ester (SPME) on cochlear potentials was examined in the guinea pig. Previous studies have shown that SPME is a selective agonist for neurokinin 1 (NK1) receptor. Perfusion with SPME at a concentration of more than 10(-6)M produced an increase in the amplitudes of the compound action potential and negative summating potential in a dose-dependent manner. N1 latency showed a tendency to be shortened, but this change was not significant. Amplitudes of the cochlear microphonics and endocochlear potential remained unchanged. Substance P fragment 7-11, an inactive analogue, produced no changes in the cochlear potentials. In contrast, the substance P antagonist [D-Pro2, D-Trp7,9]-SP blocked the action of SPME on the cochlear potentials. These results suggest that substance P may modulate neurotransmission through NK1 receptors in the cochlea.

Action Potentials↗
PubMed1997

[Contralateral modification of transitory evoked otoacoustic emissions].

BACKGROUND: In recent publications the influence of contralateral white noise on transient evoked otoacoustic emissions (TEOAE) is discussed with regard on contributions of the efferent auditory system. METHODS: In the present study the effects have been investigated with regards to middle-ear muscles, efferents and cross hearing. TEOAE to monaural 40-80 dB SPL clicks were recorded in normal-hearing adults under simultaneous presentation of 20-60 dB SPL broadband noise to the contralateral ear. Control runs were performed before, during a short break of, and after contralateral stimulation. The control run before contralateral stimulation was used as a reference. RESULTS: Decrease in TEOAE, and increase in accompanying noise floor, were found to follow the contralateral stimulation. In particular a 1-3 dB decrease was found for contralateral noise levels of 40 and 60 dB SPL, even though the readings at 60 dB only were statistically significant (paired-samples t test, p = 0.05). For both TEOAE and noise floor no systematic dependence on click intensity was seen. The control runs during temporary break and after contralateral noise revealed an increase in both TEOAE and noise floor. As a rule, the TEOAE adapted to the reference within 2-3 min following the cessation of contralateral stimulation, whereas the increased noise floor level was still noted after 10 min. CONCLUSIONS: Traditionally, suppressing effects of contralateral stimulation on TEOAE have been attributed to cochlear efferents (CEs). Occasionally, the middle-ear muscle and cross hearing involvement have been considered as well. Substantially, the present results and findings of other workers are inconsistent with the basic knowledge of CE functioning: (I) The decrease in TEOAE under contralateral stimulation is in conflict with an increase in cochlear microphonics and summating potentials observed during activation of CEs: (II) contralateral suppression of TEOAE exhibited no significant dependence on the test-stimulus level while the CEs are known to be efficient in the range of the low signal intensities only, and (III) acoustic activation of the CEs can hardly be expected to reach levels sufficient to influence the TEOAE mechanism. The present findings, i.e. decrease in TEOAE and increase in noise floor level, can more reasonably be explained as being mainly attributable to activation of the middle-ear muscles.

Adult↗
PubMed1980

A comparison of cochlear microphonics and N1 in audiogenic-seizure-susceptible and control rats.

Although numerous studies have shown that cochlear impairment exists in audiogenic-seizure (AGS)-susceptible mice, there is only one report of cochlear potentials obtained from AGS-susceptible rats. To investigate the hypothesis that cochlear impairment also exists in AGS rats, cochlear microphonics (CM) and the primary afferent activity of the auditory division of the eighth cranial nerve (N1) were studied in AGS rats. AGS rats were obtained from the Veterans Administration Medical Center (Shreveport, La.) colony of Sprague Dawley derived animals, and control rats were obtained from Sprague Dawley, Inc. Two school bells ringing simultaneously were used to produce a sound of approximately 115 dB (AGS test stimulus). Exposure to the AGS test stimulus was once per week for three consecutive weeks. Chloramphenicol was used to treat the frequent otitis media found in the colony of AGS rats. Two categories of AGS-susceptible and control rats were studied: (1) rats exposed to the AGS test stimulus and chloramphenicol regimen; and (2) rats not receiving these treatments. All rats were anesthetized with i.p. Dial-Urethane and prepared for cochlear round window recording. Cochlear microphonics were recorded in response to a click stimulus. A significant decrease in cochlear sensitivity was seen in both groups of AGS rats when compared to appropriate controls as reflected by a 25-35 dB shift in all CM and N1 input-output functions. These results support the hypothesis that a functional cochlear impairment exists in the AGS rat.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1997

Cochlear protection from carbon monoxide exposure by free radical blockers in the guinea pig.

Acute carbon monoxide exposure produces a significant impairment in high-frequency auditory sensitivity that can be prevented using the N-methyl-D-aspartate receptor blocker MK-801. This finding suggests an excitotoxic component to carbon monoxide ototoxicity and establishes the potential for free radical formation. Free radical scavengers and inhibitors are protective in many organs, including the brain and cochlea, during hypoxic events such as ischemia/reperfusion and, in the cochlea, during noise exposure. This study evaluated the protection afforded by two such agents, phenyl-n-tert-butyl-nitrone (PBN), which acts as a general free radical scavenger, and allopurinol, which acts as a free radical inhibitor specific to the xanthine oxidase metabolic pathway. Guinea pigs were pretreated with PBN (100 mg/kg i.p.), allopurinol (100 mg/kg i.p.), or saline 1 hr prior to exposure to carbon monoxide (35 ml/kg i.p.) or to an equal volume of air. They were monitored at 15, 30, and 60 min after carbon monoxide exposure for alterations in compound action potential threshold and cochlear microphonic amplitude. The groups receiving carbon monoxide alone displayed characteristic compound action potential threshold elevations particularly at the higher test frequencies (16-40 kHz), consistent with earlier studies; no loss of cochlear microphonic amplitude was exhibited. Both free radical inhibitors, PBN and allopurinol, blocked loss of auditory threshold sensitivity produced by carbon monoxide. These data suggest that free radical generation may play a significant role in the impairment of high-frequency auditory sensitivity resulting from carbon monoxide.

Allopurinol↗
PubMed2003

Influence of hearing sensitivity on mechano-electric transduction.

This study examined the relation between the extent of permanent hearing loss and the change in a third-order polynomial transducer function (PTF) representing mechano-electric transduction (MET). Mongolian gerbils were exposed to noise for 1 to 128 h. A control group received no exposure. The cochlear microphonic (CM) was recorded from a round-window electrode and stapes velocity was recorded with a laser Doppler vibrometer in response to Gaussian noise. A nonlinear systems identification procedure provided the frequency-domain coefficients of the PTF and their associated coherence functions. In the control group, the PTF in the high frequencies was dominated by linear and cubic terms. In noise-exposed animals, the magnitude of these terms decreased with increasing threshold, suggesting a progressive decrease in the receptor currents through basal hair cells. Moreover, the linear coherence increased and the cubic coherence decreased, indicating that MET in the cochlear base became linear. In the low frequencies, noise exposure altered the group delay of the CM, demonstrating a redistribution of hair-cell currents. The low-frequency PTF was characterized by an increase in the contribution in the quadratic term. With increasing threshold, the slope of the PTF decreased and the saturation for positive CM was eliminated.

Action Potentials↗
PubMed1992

[Investigations of the ototoxicity of dicortinef (ear drops)].

The authors investigated the ototoxic influence of Dicortinef in laboratory animals. Their examinations were performed on 15 guinea pigs (weighing 210-380 g.) after application of this medicine to the fenestra rotunda. The harmful effect of Dicortinef was expressed by the characteristic fall in the microphonic potential (PM) and potential of the acoustic nerve (AP).

Animals↗
PubMed2005

Unraveling the electrically evoked compound action potential.

With the advent of eCAP recording tools such as NRT and NRI for cochlear implants, neural monitoring has become widely used to ascertain the integrity of the neural/electrode interface as well as for assisting in the setting of program levels. The basic concepts of eCAP recordings are deduced from the acoustical equivalent of the electrocochleogram. There are, however, indications that under electrical stimulation some of these do not hold, like the unitary response concept (i.e., the principle that every fiber produces the same contribution to the eCAP). Computer modeling has proven to be a valuable tool for gaining insight into the functioning of electrical stimulation. In this study the extension of a three-dimensional human cochlea, incorporating back-measuring capabilities, is described. Using this new model, the contribution of single fiber action potentials (SFAPs) to the measured eCAP is investigated. The model predicts that contrary to common belief--the compound action potential as measured by the cochlear implant system does not necessarily reflect the propagated action potential along the auditory nerve.

Action Potentials↗
PubMed1994

Effects of mutations at the W locus (c-kit) on inner ear pigmentation and function in the mouse.

The W locus encodes a tyrosine kinase receptor, c-kit, which affects survival of melanoblasts from the neural crest. The primary cochlear defect in Viable Dominant Spotting (Wv/Wv) mutants is a lack of melanocytes within the stria vascularis (SV) associated with an endocochlear potential (EP) close to zero and hearing impairment. In this study, we compare inner ear pigmentation with cochlear potentials in three other W alleles (Wx, Wsh, and W41) and reveal an unequivocal correlation between presence of strial melanocytes and presence of an EP. Asymmetry was common, and 8.3% of Wsh/Wx, 25% of Wsh/Wsh, 60% of W41/Wx, and 69.2% of W41/W41 ears had a pigmented stria and an EP, while the remainder had no strial melanocytes and no EP. In those mutants that partially escaped the effects of the mutation, strial melanocytes rarely extended the entire length of the stria, but were confined to the middle and/or basal turns of the cochlea. The extent of strial pigmentation was unrelated to the EP value, which was measured from the basal turn only. Compound action potential (CAP) responses recorded from ears with an EP were variable and they showed greatly raised thresholds or were absent in all ears where the EP was close to zero. In controls, melanocytes in the vestibular part of the ear were found in the utricle, crus commune, and ampullae, whereas in many mutants only one or two of these regions were pigmented. There was a broad correlation between pigmentation of the stria and pigmentation of the vestibular region but this was not absolute. All W41/Wx, Wsh/Wsh, and W41/W41 mutants had some pigment on the pinna but, in contrast to controls where melanocytes were found in the epidermis and dermis of the pinna, pigment cells were reduced in number and generally restricted to the dermis. Injection of normal neural crest cells into 9.5-day-old mutant embryos increased the extent of skin pigmentation on the head and coat of adult chimeras and was associated with a small increase in the proportion of pigmented strias.

Action Potentials↗
PubMed1983

A comparison between basilar membrane and inner hair cell receptor potential input-output functions in the guinea pig cochlea.

Intracellular recordings were made from inner hair cells and basilar membrane motion was measured at a similar place, but in different preparations, in the first turn of the guinea pig cochlea. Potential recordings were made using glass microelectrodes and mechanical measurements were made using the Mössbauer technique. Intensity functions of DC receptor potential and basilar membrane velocity in animals with good and poor thresholds are presented. In animals with good thresholds, stimuli at and above the characteristic frequency produce similarly compressive input-output functions for both inner hair cell receptor potentials and basilar membrane motion. However, for frequencies lower than the characteristic frequency, receptor potential input-output functions obtained from animals in good and poor condition show saturation at high stimulus intensities at which basilar membrane motion is linear. This discrepancy is believed to be due to a nonlinear inner hair cell transduction mechanism. We propose that nonlinearity observed in receptor potential input-output functions is a consequence of the simple cascading of a frequency-dependent nonlinear mechanical input and a frequency-independent nonlinear transduction process.

Action Potentials↗
PubMed1986

Wever and Lawrence revisited: effects of nulling basilar membrane movement on concomitant whole-nerve action potential.

It has been assumed for decades that mechanically stimulating hair cells, both inner and outer (IHC, OHC), leads to CM and subsequent neural activity. A test of that assumption was attempted in this experiment. Tone-pips of 300 msec duration at 4 or 5 kc/s with fast rise times were simultaneously presented to the cochleae of 10 chinchillas, through the external meatus and a hole drilled into the scala tympani. A round-window electrode allowed the recording of CM and computer-averaged whole-nerve action potentials (CAP). Stimulus levels and relative phase could be adjusted to yield CAPs of similar amplitude and shape to either stimulus alone. When the two stimuli were combined, the vectorial CM could be changed by about 30 db between maximum and minimum levels when delta phi was changed by 180 degrees. However, the combined CAP was relatively insensitive to delta phi. If basilar membrane motion was minimized at CM minimum, the data mean that some other principle than basilar membrane motion must underlie or generate neural activity. These data are not consistent with the traditional view that basilar membrane motion underlies sensitivity and frequency discrimination, and are congruent with theories of sensitivity of hair cells or their stereocilia to direct acoustic or electric stimulation, with basilar membrane mechanical stimulation assigned some secondary role. The author offers an electromodel comprising one system of basilar membrane motion of supramolecular dimensions leading to mechanical stimulation of OHCs and their large CM, and a second parallel system excited by the same stapes displacements but of submolecular dimensions leading to a propagated acoustic wave through the cochlear partition and to acoustic----electric transduction by the tectorial membrane; the output of that membrane is picked up in the fluids of the subtectorial space by the electro-sensitive IHCs and analyzed by them in some unknown manner for frequency. These IHCs are then the sole direct precursors of neural activity. A seeming anomaly was found in that at delta phi = CM minimum, when the traditional model would predict reduced basilar membrane movement, a reduced CM, consequent reduction in neural activity, and an increase in the latency of the N1 component of the CAP, latency was in fact slightly but uniformly decreased. It was suggested that in this phase condition the larger CM may have been correlated with the suppressive action of the OHCs upon the IHCs.

Action Potentials↗
PubMed1996

Different effects of noise and salicylate and their interactions on the guinea pig cochlea.

We investigated the effects of noise and salicylate on the guinea pig cochlea by monitoring the acoustic nerve compound action potential (CAP) as well as the 2f1-f2 distortion product in the cochlear microphonics (DP-CM). The alterations of DP-CMs by noise and salicylate revealed an apparent difference, even when the noise-induced and salicylate-induced CAP threshold shifts were equal. This result indicated that noise and salicylate might have an effect on different sites in the cochlea. Combined effects were altered by changing the order in which the two agents were applied. The existing noise-induced damage attenuated the additional ototoxicity of salicylate. In contrast, attenuation did not occur when salicylate administration preceded noise exposure. Considering known effects of noise and/or salicylate altering mechano-electrical transduction (MET) and electro-mechanical transduction of the cochlear outer hair cells, our results seem to suggest that the MET plays a key role in the transduction mechanism in the cochlea.

Animals↗