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[A study on the effect of infrasound].

In order to examine the influence of infrasound that is becoming topical in society, human beings and guinea pigs were exposed to infrasound. After exposure, the hearing level, vestibular functions and autonomic nervous functions of human beings were examined, and endocochlear potential (EP) and cochlear microphonics (CM) of guinea pigs were examined. Next, after guinea pigs were exposed to intense audible low frequency sound that was born secondarily from infrasound and/or vibration of whole body concerning about air pressure change of infrasound, their EP and CM were examined. The results obtained were as follows: 1) By exposure of infrasound 10-15Ha 130-135dB LSPL for 30min. to human beings, their hearing level, vestibular functions and autonomic nervous functions were not changed. 2) After exposure of infrasound 15Hz 135-140dB LSPL for 24hrs.-72hrs. to guinea pigs, their EP and CM remained normal. 3) After each exposure of audible low frequency sound 90Hz 120dB SPL for 72hrs., 150Hz 110dB SPL for 72hrs. and 200Hz 100dB SPL for 72hrs. to guinea pigs, their EP became abnormal though their CM remained normal. 4) After exposure of 15Hz 500 mu +/- 30 mu vibration for 72hrs. to guinea pigs, both EP and CM remained normal. 5) After exposure of both audible low frequency sound 150Hz 100dB SPL and vibration 15Hz 500 mu +/- 30 mu for 72hrs. to guinea pigs, their EP became abnormal though their CM remained normal.

Adult↗

[Effects of increasing perilymph calcium levels on various cochlear potentials].

In the present study, we examined the effects of increasing perilymph calcium (12.20 mmol/L) on guinea pig cochlear functions. The results demonstrated that high calcium perilymphs suppressed the magnitude of compound action potential of auditory nerves (CAP) with a prolongation of N1-peak delay at a constant intensity (90 dB SPL), but not of cochlear microphonics (CM). High calcium perilymph didn't change general endocholear potential (G-EP), while reduced the rapid change of EP at on and off set of 115dB SPL white noise exposure. Furthermore the value of negative potential (N-EP) induced by anoxia was decreased because of high calcium perfusions. Machanisms of these effects were discussed.

Action Potentials↗

Cochlear receptor (microphonic and summating potentials, otoacoustic emissions) and auditory pathway (auditory brain stem potentials) activity in auditory neuropathy.

OBJECTIVE: To define both auditory nerve and cochlear receptor functions in subjects with auditory neuropathy (AN). DESIGN: We tested 33 AN subjects (66 ears) and compared them with 21 healthy subjects (28 ears). In AN subjects, the average pure-tone (1, 2, and 4 kHz) threshold loss was 57 dB HL. Click stimuli were used to elicit transient evoked otoacoustic emissions (TEOAEs), cochlear microphonics (CMs), and auditory brain stem responses (ABRs). Both cochlear and ABR potentials were recorded from surface electrodes (vertex-ipsilateral mastoid) using averaging procedures. The amplitudes and latencies of CMs and ABRs and the amplitude of the TEOAEs were analyzed. RESULTS: CM amplitudes recorded from normal ears decreased as a function of subject age. CMs recorded from AN subjects fell within the normal age-adjusted range in 60% of the subjects and were >2 SEEs (standard error of estimate) above the age-adjusted normal regression in 40% of the subjects. TEOAEs were absent in 19 (30%) AN ears (bilaterally in eight, and unilaterally in three subjects) and were present in 44 ears. In AN subjects, correlations among CM amplitude, TEOAE amplitude, and pure-tone average thresholds were not significantly related. CM amplitudes were not significantly different whether TEOAEs or ABRs were present or absent. The ABR was present in 21% of AN subjects and consisted of a low-amplitude Wave V without a preceding Wave I. Measures of CM amplitude and PTA hearing loss were not significantly different in those AN ears with a preserved ABR compared with ears with absent ABRs. Summating potentials to transient click stimuli were of small amplitude (<0.1 microV) and detectable in approximately 50% of the AN and healthy control subjects limiting formal analysis of summating potentials. CONCLUSIONS: In a significant proportion of AN subjects, we found abnormalities of cochlear receptor function, including elevated CM amplitudes and absence of TEOAEs. These two abnormalities occurred independently of each other. A low amplitude Wave V of the ABR was found in approximately one-fifth of AN subjects, evidence that neural synchrony can be partially preserved in some subjects with this disorder.

Adolescent↗

Corresponding effects of hypoxia on the cochlear microphonic and the compound action potential.

Mild hypoxia has an unexpected influence on the compound action potential (CAP) compared to its effect on the cochlear microphonic (CM). While the CM decreases in amplitude near threshold, the low-level CAP increases in amplitude by as much as 400% and decreases in latency and width. The magnitude of latency decrease is dependent on the center frequency of 1/3 octave band-filtered clicks used as stimuli. Below 13 500 Hz the latency is increasingly shortened at a rate of 0.073 ms/octave. At high intensities moderate hypoxia has no effect on either the CM or the CAP. However, with more severe hypoxia the high-level CM also begins to deteriorate. Correspondingly both the high- and low-intensity CAP decrease in magnitude and increase in latency relative to their control values. Assuming that the low-level CM is generated by outer hair cells, these results suggest that one relationship between outer hair cell function and auditory nerve function near function near threshold is that of inhibition. The fact that N1 latency is shortened suggests that this inhibition occurs in the basalward direction.

Acoustic Stimulation↗

Effects of high-frequency sound on the guinea pig cochlea. Electrophysiological study using cochlear microphonics, action and endocochlear potential.

There are only a few studies investigating the effect of high-frequency sound on hearing. Authors investigated experimentally the effect of long exposure to high-frequency sound (19 and 25 kHz) below 100 dB (SPL) on guinea pig inner ear. Changes in cochlear microphonics (decrease of maximum output voltage) and especially in endocochlear potential (decrease of the absolute value of negative potential) were observed. The effects of high-frequency sound (10-30 kHz) on the inner ear were discussed.

Action Potentials↗

Excitotoxic effect of kainic acid on chicken otoacoustic emissions and cochlear potentials.

Kainic acid (KA) is a potent glutamate analog that can temporarily or permanently damage glutamatergic neurons. The purpose of the present study was to determine the short- and long-term effects of KA on chicken otoacoustic emissions and cochlear potentials. A chronic electrode was used to record the compound action potential (CAP), cochlear microphonic (CM), and the slow, positive neural potential (SPNP), a predominantly dc response. The CM, CAP, SPNP, and distortion product otoacoustic emissions (DPOAEs) were recorded before and after infusing 10 microl of a low dose (KA-L, 0.3 mM) or high dose (KA-H, 5 mM) of KA into scala tympani. KA caused a rapid and large reduction in CAP and SPNP amplitude in both the KA-H and KA-L groups; however, the CM and DPOAEs were largely unchanged. The amplitude of the CAP and SPNP in the KA-L group began to recover around 1 week post-KA, but was approximately 50% below normal at 4 weeks post-KA. In contrast, the CAP and SPNP showed no signs of recovery in the KA-H group. The results suggest that KA has no effect on the CM and DPOAEs generated by the hair cells, but selectively damages the CAP generated by the cochlear ganglion neurons. The reduction in the avian SPNP suggests that the response originates in the cochlear afferent neurons, unlike the summating potential (SP) in mammals that is generated in hair cells.

Action Potentials↗

Growth of suppression in the cochlear potentials.

Measurement of two-tone effects in the cochlear microphonic and summating potential indicates that the growth of suppression is different for these two cochlear potentials. Whereas the CM response to the fundamental is reduced 10 dB for each 10 dB increase in suppressor level, the SP decreases at a faster rate; approximately 20 dB per 10 dB increase. Slopes of functions for the CM response to the second harmonic are similar to those for the dc component. Since these results are consistent with the notion that suppression operates by attenuating the input to the CM generator, they are consonant with a mechanical origin of suppression.

Animals↗

The effect of protein kinase C stimulator and inhibitor on cochlear potentials in the guinea pig.

To determine a possible role of protein kinase C (PKC) in the cochlear, the effects of a PKC stimulator (phorbol-12-myristate-13-acetate; PMA), an inactive analogue of PKC stimulator (4 alpha-phorbol-12,13-didecanoate; 4 alpha-PDD) and a PKC inhibitor (D-sphingosine) on cochlear potentials were examined in the guinea pig. The perilymphatic perfusion with PMA (3 x 10(-6) M) produced an increase in compound action potential (CAP) amplitude and no change in N1 latency, the amplitudes of negative summating potential (-SP), cochlear microphonics (CM) and endocochlear potential (EP). The perfusion with 4 alpha-PDD (3 x 10(-6) M) did not change the sound-evoked cochlear potentials and the EP. The perfusion with D-sphingosine (10(-5) M) produced a decrease in CAP amplitude and no change in N1 latency and the amplitudes of -SP, CM and EP. The results suggest that PKC may be involved in the mechanism underlying the CAP generation.

Acoustic Stimulation↗

Comparative ototoxicity of chloramphenicol and kanamycin with ethacrynic acid.

Chloramphenicol is not ototoxic if administered for systemic effect, but topical applications of it to the middle ear produce severe cochlear toxic effects. Ethacrynic acid potentiates the ototoxicity of aminoglycosides. Guinea pigs were administered chloramphenicol or kanamycin sulfate with ethacrynic acid to compare the ototoxicity of chloramphenicol and ethacrynic acid with the ototoxicity of kanamycin and ethacrynic acid. Preyer's reflex audiometry and measurement of the endocochlear dc potential, the cochlear microphonics, and the negative potential of the organ of Corti indicate that ethacrynic acid does not potentiate the ototoxicity of chloramphenicol. There is not even indirect evidence that the blood-cochlear barrier for chloramphenicol is altered by ethacrynic acid. Assuming that the ototoxicity of chloramphenicol and ethacrynic acid are similar for man and guinea pig, the combination of the administration of chloramphenicol and ethacrynic acid of systemic effect in dosages commonly used clinically should not produce greater ototoxicity than either agent administered alone.

Animals↗

The rat cochlea in the absence of circulating adrenal hormones: an electrophysiological and morphological study.

Circulating adrenal hormones affect strial function. Removal of endogenous levels of adrenal steroids by bilateral adrenalectomy (ADX) in rats causes a decrease of Na(+)/K(+)-ATPase activity in the cochlear lateral wall [Rarey et al., 1989. Arch. Otolaryngol. Head Neck Surg. 115, 817-821] and a decrease of the volume of the marginal cells in the stria vascularis [Lohuis et al., 1990. Acta Otolaryngol. (Stockh.) 110, 348-356]. To study further the effect of absence of circulating adrenocorticosteroids on cochlear function, 18 male Long Evans rats underwent either an ADX or a SHAM operation. Electrocochleography was performed 1 week after surgery for tone bursts in a frequency range of 1-16 kHz. Thereafter, the cochleas were harvested and examined histologically. No significant changes in the amplitude growth curves of the summating potential (SP), the compound action potential (CAP) and the cochlear microphonics (CM) were detected after ADX. However, visually, there appeared to be a decrease of endolymphatic volume (tentatively called imdrops). Reissner's membrane (RM) extended less into scala vestibuli in ADX animals than in SHAM-operated animals. The ratio between the length of RM and the straight distance between the medial and lateral attachment points of RM were used as an objective measure to quantify this effect in each sub-apical half turn of the cochlea. The decrease in length of RM was statistically significant. Thus, circulating adrenal hormones appear to be necessary for normal cochlear fluid homeostasis. Absence of one or more of these hormones leads to shrinkage of the scala media (imdrops). However, the absence of adrenal hormones does not affect the gross cochlear potentials. Apparently, the cochlea is capable of compensating for the absence of circulating adrenal hormones to sustain the conditions necessary for proper cochlear transduction.

Action Potentials↗

Evidence that inner hair cells are the major source of cochlear summating potentials.

The role of the inner hair cells (IHCs) in generating the cochlear summating potentials (SP) was assessed by measuring SP, cochlear nerve action potentials (CAP), cochlear microphonics (CM) and 2f1-f2 distortion product otoacoustic emissions (DPOAEs) in 15 chinchillas with either acute chemical de-afferentation, accomplished by applying kainic acid to the round window, or surgical de-afferentation and basal IHC loss, which developed within two months after sectioning the auditory nerve. In the auditory nerve sectioned ears, type I ganglion cells disappeared whereas most, if not all, type II ganglion cells were still present. Histological analysis of surface preparations and sections through the modiolus verified the de-afferentation in both models and showed a large IHC loss at the base of the cochlea in the ears with the auditory nerve sectioned while other structures of the cochlea remained intact. Unoperated (left) ears of 9 animals served as controls. CM and DPOAEs were normal in all ears whereas the CAP was substantially depressed in de-afferented ears. Comparisons among the SP input-output functions suggest that (1) the IHCs are the major generator of SP recorded from the round window in chinchilla, in particular at low to moderate stimulus levels, (2) the SP recorded from the round window largely reflects the responses from hair cells at the base of the cochlea, and (3) kainic acid results in an increase of SP amplitude to high-level stimuli whereas the SP to low- to moderate-level stimuli remains in the normal range.

Acoustic Stimulation↗

Ethacrynic acid. Effects on the cochlear potentials in normal and high blood oxygen.

The effect of ethacrynic acid (EA) at different blood O(2) saturations on cochlear potentials of guinea pigs was investigated. All 18 young healthy guinea pigs received 50 mg/kg/h of EA intravenously and were divided into three groups: first group, normal (90.00+/-6.30-86.17+/-4.83 mm Hg); second group, lower Po(2) (78.00+/-4.74-70.00+/-4.42 mm Hg); and third group, high Po(2) (174.40+/-13.41-179.00+/-26.15 mm Hg). The partial pressure of oxygen (Po(2)), the partial pressure of carbon dioxide (Pco(2)), and the pH of the blood were measured before EA administration and at the end of the experiment (3 h later) by drawing blood samples from the contralateral carotid artery. Cochlear potentials-endocochlear potential (EP), cochlear microphonics (CM), and action potentials (AP)-were recorded by standard methods from the first turn of the cochlea. Experimental data seem to indicate that elevation of the Po(2) to 174-179 mm Hg during relatively high doses of EA treatment prevents the declines in cochlear potentials which were observed in the first and second groups (normal and lower Po(2)), and preserves active ion transport which is responsible for the generation of cochlear potentials. These data suggest a means by which to reduce the ototoxic effect of EA and possibly indicates a method of treatment for hearing loss which developed after the administration of EA.

Action Potentials↗

Postnatal development of the brainstem auditory evoked potential and far-field cochlear microphonic in non-sedated rat pups.

Normal postnatal development of the scalp-recorded cochlear microphonic (CM) response and brainstem auditory evoked potential (BAEP) were studied in rat pups. BAEP latencies decreased and amplitudes increased as a function of maturation. These changes occurred rapidly between 14 and 23 days of age with gradual change occurring thereafter. The observed latency changes indicated that the auditory pathway matures in a sequential manner from the most peripheral to the most rostral structures. For example, CM latency stabilized (matured) by day 17 while BAEP wave I and II latencies stabilized by days 23 and 35, respectively. BAEP waves III and IV still showed significant latency decreases between days 42 and 70. The between-litter variability for CM and BAEP wave latencies also decreased with age. In contrast to peak latency measures, CM and BAEP amplitudes followed an independent time course of postnatal development. CM amplitude did not increase significantly after day 14. Amplitudes of all 4 BAEP components increased steadily from day 14 to 29, then stabilized. Unlike latency variability, amplitude variability was independent of age. There were no significant gender-dependent differences in amplitudes or latencies between the ages of 14 and 70 days.

Age Factors↗

Evidence for intracochlear impedance changes following ethacrynic acid administration.

The effects of intra-arterial 30-, 40-, and 50-mg/kg doses of ethacrynic acid upon cochlear function in guinea pigs were studied for periods of three to five hours. Cochlear potentials recorded in the first turn included the endocochlear potential, whole nerve response, cochlear microphonics, and summating potentials in scala media, scala tympani, and scala vestibuli. Evidence of organ of Corti damage at 50 mg/kg was found in addition to electrical impedance changes in the cochlear membranes at all dose levels.

Animals↗

Cerebellar actions on cochlear microphonics and on auditory nerve action potential.

The influence exerted by cerebellar stimulation upon cochlear microphonics (CM) and auditory nerve action potential (AP) has been analyzed in curarized guinea pigs. Round window recordings demonstrated that conditioning electrical stimulus trains delivered to the cerebellar cortex diminished the CM and AP amplitude at the same time and in a parallel fashion. On the other hand, cooling of the cerebellar cortex showed the opposite results of increased amplitudes. All pre-receptorial mechanisms were avoided. A PDP-12 computer performed parametric and non-parametric statistical analysis showing the differences to be significant for the shifts. Evidence of simultaneous inhibitory cerebellar action on both potentials has been demonstrated and a cerebello-olivo-cochlear pathway is proposed for such action upon the receptor cells and/or incoming fibers.

Acoustic Stimulation↗

Augmented gentamicin ototoxicity induced by vancomycin in guinea pigs.

Vancomycin has been reported to be an ototoxic drug in the clinical literature. At best, this literature is confusing. There are no reports of ototoxicity of vancomycin in experimental animals, even when it is administered concurrently with ethacrynic acid, a drug known to augment the ototoxic effect of most other ototoxic drugs. In most of the cases of permanent ototoxicity that have been reported, the patient was treated with an aminoglycoside antibiotic as well as vancomycin. This study found no evidence of vancomycin ototoxicity in guinea pigs, but found that vancomycin greatly enhanced the ototoxicity of gentamicin.

Acoustic Stimulation↗

Effect on cochlear potentials of lateral semicircular canal destruction.

Recording of the cochlear potentials was successfully performed during experimental labyrinthectomy in the guinea pig and in three patients with acoustic neuromas during translabyrinthine removal of the tumors. In the guinea pig, complete interruption of the duct of the lateral semicircular canal including the endolymphatic canal caused little change in the endocochlear DC potential of the first cochlear turn and input-output function curve of the N1 component of the compound action potential elicited by 8-kHz tone bursts. Further drilling of the vestibular labyrinth in the guinea pig caused decline of these potentials when the vestibular was opened. In patients with acoustic neuromas, the interruption of the duct of the lateral semicircular canal hardly altered the N1 input-output function curve and N1 input-latency function curve during the 1-hour observation period. Consistent preservation of cochlear function even after interruption of lateral semicircular canals suggests the possibility of partial surgical labryrinthectomy with preservation of hearing for lesions involving semicircular canals.

Acoustic Stimulation↗

Tympanic electrocochleography for diagnosis of Menière's disease.

OBJECTIVE: Tympanic electrocochleography (ECOG) is a noninvasive technique for recording cochlear potentials with an electrode placed on the tympanic membrane. Electrocochleography is used clinically in the evaluation of patients for endolymphatic hydrops. This study was undertaken to obtain normative data for ECOG responses to clicks and tone bursts and to determine clinical indicators that result in high test specificities. DESIGN: Three cochlear potentials were measured; the eighth nerve compound action potential, the cochlear microphonic, and the summating potential. The subjects were 53 normal hearing adults with negative histories for symptoms of Menière's disease. The ECOG responses were measured with a silver wire-rayon wick electrode that was placed on the tympanic membrane under direct microscopic visualization. Stimuli were condensation, rarefaction, and alternating polarity clicks and 1- and 2-kHz tone bursts. RESULTS: Measures that appear to be useful in the evaluation of endolymphatic hydrops include the summating potential to action potential ratio, action potential latency difference to condensation and rarefaction clicks, and the tone-burst-evoked summating potential. Relationships among these measures were investigated, and abnormal criteria were determined that result in test specificities of 95%. CONCLUSIONS: Menière's disease is viewed as a progressive disease in which ECOG characteristics vary with the disease state. Cases are presented to illustrate ECOG responses in various stages of the disease. The normative data presented in this article are useful for the detection of Menière's disease in its early stages.

Adult↗