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PubMed1982

Effect of substrate-free vascular perfusion upon cochlear potentials and glycogen of the stria vascularis.

The effect of vascular perfusion of the anterior inferior cerebellar artery with synthetic blood containing no metabolic substrates upon the endolymphatic potential (EP) and the cochlear microphonics (CM) was determined in the guinea pig. In substrate-free perfusion the potentials were maintained for an average of 84 min. Subsequently, the EP declined at an average rate of 1.4 mV/min until a new steady-state level was temporarily established when the potential had dropped to about 30 mV. The decline of the CM appeared to be accounted for largely by the decline of the EP. During substrate-free perfusion prior to the onset of the decline of the potentials, the level of strial glycogen remained unchanged; glycogen decreased significantly only after the potentials had started to decline. When substrate-free vascular perfusion was accompanied by simultaneous substrate-free perilymphatic perfusion, the potentials started to decline immediately. On the basis of these data, we conclude that strial glycogen plays no role in the prolonged maintenance of the EP during substrate-free perfusion; rather, the potential seems to be maintained by entry of glucose (and presumably other substrates) from perilymph into the stria vascularis.

Animals↗
PubMed1982

Functional importance of sodium and potassium in the guinea pig cochlea studied with amiloride and tetraethylammonium.

The effects of amiloride on the cochlear responses in the guinea pig were compared with those produced by tetraethylammonium (TEA). Amiloride has been reported to reduce membrane permeability to sodium in a wide variety of ion-transporting epithelia. TEA has been documented to suppress the active potassium permeability increase during the repolarization phase of the action potential in mammalian excitable cells, and to reduce the resting potassium conductance in mammalian smooth muscle cells. Perilymphatic perfusion of 10(-3) M amiloride or intravenous injection at a dose of 20 mg/kg suppressed the whole nerve action potential (AP) of the cochlea but did not significantly affect the cochlear microphonics (CM) or endocochlear potential (EP). Application of amiloride to endolymph by iontophoretic or perfusion techniques also produced no significant changes of CM and EP when compared with appropriate control procedures. Perilymphatic perfusion of 10(-2) M TEA did not suppress CM or EP but the AP was reduced. Iontophoretic application of TEA to the endolymph caused a marked suppression of CM while the EP was significantly increased. The effects of endolymphatic TEA application are consistent with the concept that the normal EP recorded from scala media is the algebraic sum of a positive electrogenic potential and a negative diffusion potential, the latter component being sensitive to potassium permeability changes of the endolymph-perilymph barrier. Maintenance of normal cochlear microphonics also appears dependent upon the maintenance of normal potassium permeability properties of the endolymph-perilymph barrier. The functional importance of normal sodium permeability properties appears less certain.

Action Potentials↗
PubMed1984

Noise and the young mouse: genotype modifies the sensitive period for effects on cochlear physiology and audiogenic seizures.

A sharply defined "critical period" has been described for the young C57BL/6 mouse, during which acoustic trauma will profoundly alter subsequent auditory behavior (audiogenic seizures, acoustic startle reflex). In several genotypes and species, a broader "sensitive period" exists, during which acoustic trauma is most damaging to cochlear functions in the young ear. In order to examine the correspondence of these two events, C57BL/6 and CBA inbred mice, at eight ages ranging from 12 to 54 days, were exposed to 2 min of a 124-dB (SPL) octave band noise (8-16 kHz). A noninvasive electrocochleographic technique was used to assess cochlear microphonic (CM) and action potential (AP) thresholds in exposed mice and their nonexposed littermate controls. This allowed cochlear functional measures and behavioral tests (susceptibility to audiogenic seizures) to be made in the same animals. Noise has no observable effect on the 12-day-old CBA mouse, produced a maximal threshold elevation (47 dB for AP, 28 dB for CM) at 30-36 days, with the effect declining to nearly half of this value in 54-day-old subjects. Susceptibility to audiogenic seizures in the exposed CBA mice was greatest at the peak of this sensitive period for cochlear damage (r = .95). C57BL/6 mice also appeared unaffected when noise exposure occurred at 12 days of age; they had maximal AP (23 dB) and CM (17 dB) threshold elevations at 36 days, and 54-day-old mice had an 18-dB elevation of the AP and their CM was no longer affected. Susceptibility to audiogenic seizures was greatest in C57BL/6 mice exposed to noise at 18 days, and it did not correspond with the sensitive period for cochlear damage (r = .21). Therefore, both genotypes have a sensitive period for the effects of noise trauma on the CM and AP, the CBA has a sensitive period for acoustic priming for audiogenic seizures, and the C57BL/6 has a critical period for acoustic priming. Genetic differences in age-related losses of central nervous system auditory functions are postulated as being responsible for these behavioral differences. These data are compared with known auditory functions of the SJL and BALB/c mouse strains in order to explain genetically determined differences of the sensitive (or critical) period of acoustic priming, and for the length of time the mice subsequently remain susceptible to audiogenic seizures.

Acoustic Stimulation↗
PubMedDate not supplied

Influence of argon laser stapedotomy on cochlear potentials. III. Extracochlear recorded DC potential.

During laser stapedotomy there is an extracochlear recordable DC deflection, which may hamper the recording of the Cochlear Microphonics (CM), or the Compound Action Potential (CAP). The investigation of the nature of this DC potential, its distribution as well as its recovery is the subject of the present paper. In contrast to the laser induced temperature alteration, this DC deflection spreads across the surface of the cochlea. Since the DC deflection only occurs during laser impact and not when perforating the cochlea with steel instruments, the most probable explanation is a heat destruction of the molecular structure of the bone.

Action Potentials↗
PubMed2006

Prestin gene expression in the rat cochlea following intense noise exposure.

Noise-induced permanent loss of cochlear amplification was observed previously with the majority of outer hair cells (OHCs) still surviving in the cochlea and even with a normal OHC receptor potential, indicated by CM (cochlear microphonics) recording [Chen, G.D., Fechter, L.D., 2003. The relationship between noise-induced hearing loss and hair cell loss in rats. Hear. Res. 177(1-2), 81-90; Chen, G.D., Liu, Y., 2005. Mechanisms of noise-induced hearing loss potentiation by hypoxia. Hear. Res. 200, 1-9]. This study focused on effects of an intense noise exposure (10-20 kHz at a level of 110 dB SPL for 4 h) on the OHC motor protein (prestin) and structural proteins in the OHC membrane skeleton. The noise exposure significantly disrupted CM and CAP (cochlear compound action potential). The injured CM recovered after 1-week resting period. The impaired CAP at frequencies lower than the noise band also recovered. However, the CAP recovery at frequencies of the noise band stopped at a linear line one week after the noise exposure, indicating a permanent loss of cochlear amplification. Gene expression of prestin, beta-spectrin, and beta-actin was significantly up-regulated after the noise exposure. The elevated gene expression peaked at the 3rd post-exposure day and returned to baseline 4 weeks after the noise exposure. The up-regulated gene expression may be in response to injury of the proteins, which may be responsible for the loss of cochlear amplification.

Action Potentials↗
PubMed2002

[Protective effect of indirect activator of calcium pump on noise-induced hearing loss].

OBJECTIVE: To investigate the possible protective effect of phorbol-12-myristate-13-acetate (PMA), an activator of protein kinase C (PKC) and indirect activator of Ca2+ pump, on noise-induced hearing loss (NIHL). METHODS: Twenty guinea pigs were divided randomly into two groups, and then perfused with artificial perilymph solutions in one group and with artificial perilymph solutions containing 3 mumol/L PMA in the other one, respectively. All animals were exposed with 100 dB SPL white noise for 2 hours. Cochlear microphonics (CM) and compound action potential (CAP) were recorded from the round window (RW) before noise exposure and 2 hours after noise exposure. RESULTS: There was no significant difference in CAP threshold and CM amplitude between two groups before noise exposure. A significant difference was observed in CAP threshold and CM amplitude between two groups after noise exposure. The amplitude of CM decreased and the threshold of CAP increased in both group after noise exposure, but in the PMA group the decrease of the amplitude of CM was higher while the increase of threshold of CAP lower than that in control (P < 0.05). CONCLUSION: PMA might have partly protective effect on NIHL. These findings indirectly proved that intracellular Ca2+ overload might involve in the mechanism of NIHL.

Action Potentials↗
PubMed2002

Differential ototoxicities induced by lead acetate and tetraethyl lead.

Lead poisoning disrupts many biological structures and functions, including those of the auditory system. This study examined the ototoxic effects of lead acetate (LA) and tetraethyl lead (TEL) of equal lead content on cochlear function and the ability of alpha-phenyl-tert-butyl-nitrone (PBN) to attenuate such effects. Baseline 1.0 microV cochlear microphonic (CM) and compound action potential (CAP) responses were recorded and animals administered either PBN (100 mg/kg, i.p.) or an equal volume of 0.9% saline, followed by an i.p. injection of LA (50 mg/kg) in an ethanol vehicle, TEL (42.7 mg/kg) in a corn oil vehicle, corn oil or ethanol vehicle alone. Two hours after administration, post-exposure CM and CAP responses were recorded. CAP threshold shifts in the saline-LA group were elevated by 5-10 dB at mid to high frequencies relative to controls (20-24 kHz, P<0.05). Mean CAP threshold shifts in the saline-TEL were significantly greater than those of both control groups at all tested frequencies except 2 kHz (P<0.001). However, threshold shifts in the group receiving PBN prior to TEL were significantly smaller than shifts in the group receiving saline prior to TEL (P<0.01). These data suggest that TEL is more ototoxic than is LA and that free radicals partially mediate TEL-induced CAP disruption.

Acoustic Stimulation↗
PubMed1995

Development of cochlear potentials in the neonatal gerbil.

The onset and maturation of hearing was examined in separate groups of sibling and nonsibling neonatal Mongolian gerbils (Meriones unguiculatus). Auditory nerve compound action potentials (CAP) and cochlear microphonics (CM) were measured at the round window, and the endocochlear potential (EP) was recorded at three different locations in pups aged 13 to 30 days after birth (DAB) and in 90 day-old animals. Maturational trends for the three potentials were similar to those previously reported for gerbil neonates. However, CAP thresholds continued to decrease, and CM and CAP input/output functions and EP continued to increase beyond 30 days of age, a time at which many investigators have considered hearing in the gerbil to be mature. The EP developed simultaneously throughout the cochlea and approached 80 mV by 20 DAB. CAP thresholds showed a highly correlated log-linear relationship with EP in groups of nonlittermates and in siblings studied at different ages. In contrast, maximum CAP and CM amplitudes increased with increasing EP, but did not show significant growth until the EP exceeded 70 mV.

Acoustic Stimulation↗
PubMedDate not supplied

Cochlear pathophysiology associated with inner ear immune responses.

The effects of primary and secondary inner ear immune responses were investigated in the guinea pig. Subjects were immunized with keyhole limpet hemocyanin (KLH). Serum and perilymph anti-KLH titers, cochlear microphonic (CM) and VIII nerve N1 compound action potential (AP) thresholds, and cochlear morphology were examined at 2 or 4 weeks post-inner ear KLH inoculation. Primary inner ear immunized subjects developed serum and perilymph anti-KLH titers, exhibited minimal cochlear histopathology and showed only small changes in CM and AP thresholds at 2 or 4 weeks post-inner ear inoculation. Secondary immune response animals, those which were systemically immunized with KLH prior to inner ear challenge, showed significant serum and perilymph anti-KLH titers, and normal CM and AP thresholds at the time of inner ear challenge. At 2 or 4 weeks following inner ear challenge, secondary immunized animals showed very significant increases in CM and AP thresholds, and marked cochlear histopathology. We conclude that secondary inner ear challenge results in significant cochlear pathophysiology, while primary inner ear immunization does not.

Action Potentials↗
PubMedDate not supplied

Effect of intracochlear aminooxyacetic acid on cochlear potentials and endolymph composition.

Summary--Aminooxyacetic acid (AOAA; 1 MM) when perfused through the scala tympani of guinea pigs produced a biphasic reduction in the endocochlear potential, together with a shift in the input-output functions of the cochlear microphonics and the compound action potential of the cochlear nerve. Since the ionic (Na+, K+) content of the scala media was not alerted, it appears that such changes did not underlie the reduction recorded in the endocochlear potential. The negative direct current potential recorded in the organ of Corti did not appear to be affected by the drug. Attempts to antagonize the effects of AOAA with pyridoxine failed.

Acetates↗
PubMed1998

The effect of prednisolone and non-steroidal anti-inflammatory agents on the normal and noise-damaged guinea pig inner ear.

The effect of anti-inflammatory agents, such as the synthetic glucocorticoid prednisolone, diclofenac sodium, and histamine H1-receptor antagonist, was studied in unexposed and noise-exposed (broad-band noise, bandwidth 1-12 kHz, 106 dB SPL, 30 min) guinea pigs. The results were compared with the results obtained from no treatment and with isotonic saline (placebo) therapy. The cochlear blood flow (CoBF) and the partial oxygen pressure in the perilymph (PL-pO2) were continuously and simultaneously recorded over a period of 210 min. In addition, cochlear microphonics (CMs), compound action potentials of the auditory nerve (CAPs), and auditory brain stem responses (ABRs) were registered. Noise-induced hearing loss paralleled a decrease of PL-pO2. Both were found to occur before evidence of reduced CoBF. PL-pO2 and CoBF progressively declined post-exposure, while CMs, CAPs, and ABRs did not further deteriorate nor showed signs of recovery up to 180 min after cessation of noise. Treatment started 60 min post-exposure, or after 90 min without manipulation and was then further studied for 120 min. In the unexposed animals, diclofenac sodium and prednisolone induced a significant decline of PL-pO2, while CoBF, CMs, CAPs, and ABRs revealed no change. Isotonic saline did not influence the measured parameters. After infusion of the histamine H1-receptor antagonist, a significant decrease of CoBF together with blood pressure and CMs was observed, while PL-pO2, CAPs, and ABRs showed no change. In the noise-exposed animals, diclofenac sodium induced partial restoration of CM and CAP amplitudes and full restoration of ABRs. Following a high dose of prednisolone (25 mg), partial restoration of CMs and full restoration of CAPs and ABRs were registered. This effect was significantly less pronounced following a low dose of prednisolone (2.5 mg). Restoration of CMs, CAPs, and ABRs was immediate (i.e. 50 min after infusion) and remained stable for another 60 min until the end of the recording period. The histamine H1-receptor antagonist and isotonic saline did not influence CMs, CAPs, and ABRs. None of the applied drugs resulted in relief of progressive noise-induced cochlear hypoxia and post-traumatic ischemia. These findings indicate direct cellular effects of prednisolone and diclofenac sodium in the cochlea taking into account no blood flow and oxygenation. The possible mechanisms involved are discussed.

Acoustic Stimulation↗
PubMed1982

Noise impairment in the guinea pig. I. Changes in electrical evoked activity along the auditory pathway.

Changes in the cochlear microphonics (CM), auditory nerve action potential (AP), and evoked responses from the inferior colliculus (IC-ER) and auditory cortex (AC-ER) of the guinea pig were assessed after exposure to white noise of 115 dB for 30 min. Both continuous and intermittent (200 ms noise and 200 ms pause) exposures were used. In comparison with the pre-exposure level, CM isopotential curves were shifted by 1.1 +/- 0.5 dB (means +/- S.E.) on the average in the range of 0.5-8 kHz (recorded at the round window). The amplitude-intensity function of the click-evoked auditory nerve action potential decreased by 8.4 +/- 1.2 dB, that of the inferior colliculus evoked response by 20.9 +/- 3.7 dB, and the amplitude-intensity function of the auditory cortex evoked potential decreased by 6.2 +/- 4.7 dB. A similar reduction in the amplitude was found after both continuous and intermittent noise exposure. In contrast to the decrease in amplitudes of evoked potentials, the latency-intensity functions of the individual waves of potentials evoked along the auditory pathway did not change when compared at the same click intensity before and after the exposure. The results suggest that individual auditory nuclei are impaired by the noise to different extents and that the impairment does not increase linearly up to the auditory cortex.

Action Potentials↗
PubMedDate not supplied

Remote extracochlear versus intracochlear recordings in the guinea pig.

A comparison was made of the whole-nerve action potential recorded from a wire electrode placed on the tympanic membrane (TM) (remote extracochlear recording) and than recorded from intracochlear electrodes in the first and third turn scala tympani of the guinea pig. Cochlear microphonics and summating potentials were also studied. The expected decreased sensitivity at the TM site was observed in all responses, although the microphonic (CM) was diminished more that the action potential (AP) as compared to the responses monitored via the ST1 electrode. Nevertheless, the TM-recorded cochlear potentials largely mimicked the ST1-recorded potentials in a qualitative manner, i.e., similar configurations of the CM pseudo-threshold functions. It was consistently observed that the N2 of the AP is proportionally larger (relative to N1) in the TM recording than in the ST1 recording. These phenomena were attributed to the complex spread of the bioelectrical potentials in the nonhomogeneous volume conductor formed by the tissues of the temporal bone. It was suggested that the observed change in the N1/N2 ratio at the different sites of recording is due to the different contributions of second-order neuronal discharges to the compound AP. In effect, the TM electrode "sees" proportionally more activity from second-order fibers than does the ST1 electrode, and the ST3 electrode, less.

Action Potentials↗
PubMed1998

Effect of endoplasmic Ca2+-ATPase inhibitors on cochlear potentials in the guinea-pig.

The effect of endoplasmic Ca2+-ATPase inhibitors on cochlear potentials was examined in the guinea-pig. Perilymphatic perfusion with thapsigargin (10[-6] M) produced a significant decrease in the amplitudes of cochlear microphonics, negative summating potential and compound action potential, and a significant prolongation of N1 latency with no change in the endocochlear potential. These changes were all dose dependent. Another endoplasmic Ca2+-ATPase inhibitor, cyclopiazonic acid (10[-5] M), produced the same effects as thapsigargin on cochlear potentials. These results suggest that endoplasmic Ca2+-ATPase inhibitors may have inhibitory functions on cochlear potentials.

Animals↗
PubMedDate not supplied

Experimental hypercholesterolemia and auditory function in the chinchilla.

Possible harmful effects of a high-cholesterol diet on auditory function were suggested by our previous work in rabbits, in which evoked potentials were measured from a chronic electrode inserted into the inferior colliculus. However, serum cholesterol levels in those rabbits tended to be extraordinarily high, i.e., more than 1,500 mg/dL. Chinchillas were used in the present work as an animal model to study the relationship between hypercholesterolemia and auditory dysfunction. One percent cholesterol in standard Chinchow was fed to chinchillas for three months. The experimental groups showed a high mean cholesterol level of 437 +/- 394 mg/dL (N = 9). Isopotential curve of the cochlear microphonics, threshold of action potentials (AP), and endocochlear DC potential did not differ from those in the control group. When moderately intense sound (12 kHz, 95 dB SPL) was given for ten minutes, however, the reduction in AP threshold was significantly greater (P = .036) in the cholesterol group. It is postulated that hypercholesterolemia may be one of the factors involved in differential susceptibility to noise.

Animals↗
PubMed1997

Effects of local anaesthetics on the gross receptor potentials in the guinea pig cochlea.

Local anaesthetics have been used intravenously and intratympanally to reduce tinnitus. In order to clarify its action in the periphery, we applied 0.5 mM tetracaine in the scala tympani in 18 cochleae and studied the effects on the receptor potentials. We used a temporal bone preparation of the guinea pig ear in vitro exposing the fourth cochlear turn where the cochlear microphonics (CM) and the summating potential (SP) were recorded. The perfusion was kept at a rate of 50 microliters/min. The frequency response of the cochlea was determined at the beginning of each experiment and the responses were recorded at the best frequency of the preparation. In another five cochleae an accumulated dose-response relationship was determined by increasing the tetracaine concentration in steps (50, 100, 300, 500, 1000 and 2000 microM), measuring the difference in amplitude of the receptor potentials. The CM decreased significantly (p < 0.001; mean 0.37 mV; SD 0.29). In 12 cochleae the SP was initially positive and did not increase significantly (p = 0.16; mean 0.07 mV; SD 0.16). In six cochleae the SP was initially negative and all changed polarity to positive and increased significantly (p < 0.05; mean 0.36 mV; SD 0.28). The effects on both the CM and the SP were reversible. Owing to the inter-individual variation between the cochleae the SP/CM ratio was determined and it increased significantly (p < 0.001; mean 0.18; SD 0.11). In the accumulated dose-response experiments the CM decreased significantly (p < 0.05) in a dose-dependent way, whereas the SP did not increase significantly. The SP/CM ratio increased significantly (p < 0.05) at 300 microM and 500 microM. We hypothesize that the peripheral tinnitus-reducing action of local anaesthetics is in part due to a reversal of the SP, but also to a reduction of the CM. The difference in effect of tetracaine on the receptor potentials, the CM and the SP, suggests that the SP is not dependent on the CM.

Anesthetics, Local↗
PubMed1994

Amplitude enhancement is seen in the cochlear nerve but not at, or before, the afferent synapse.

The amplitude of the cochlear nerve compound action potential (CAP) produced by a moderate intensity tonal stimulus (S2) can be enhanced when S2 is preceded by a low intensity S1 of the same frequency. The presence of S1 had no observable influence on the threshold of the CAP to S2. Enhancement was not observed in the cochlear microphonics or summating potentials. Deactivation of the contralateral olivocochlear bundle did not influence enhancement. Tetrodotoxin (TTX) was applied to the round window to block cochlear nerve spike activity, resulting in a residual EPSP-like potential, as described in the guinea pig by Dolan et al. (1989). Kainic acid, in turn, eliminated this EPSP-like response. Even though some differences were found in the responses of the gerbil and their guinea pig preparation to TTX and kainic acid, enhancement was not observed in this residual potential. When enhancement was observed at the level of the CAP, it was observed at brainstem levels. It is suggested that enhancement originates within the cochlear nerve axons.

Acoustic Stimulation↗
PubMed1982

[Electrophysiological study of the ototoxicity of kanamycin via transplacental transmission in the guinea pig (author's transl)].

Pregnant guinea pigs were treated with Kanamycin at three different times during gestation (dating by the post-partum ovulation method) : 11th-20th day, 31st-40th day, 53rd-62nd day of gestation. 29 newborn guinea pigs were studied electrophysiologically by the recording of cochlear microphonics and the action potential obtained at the fenestra cochlear in response to clicks and filtered clicks 8000. Certain animals were tested with filtered clicks 2000 and 4000. 6 tested animals showed electrophysiological results identical to those usually seen in adult guinea pigs intoxicated with Kanamycin. The results obtained suggest the existence of a relationship between the ototoxicity of Kanamycin and the time of installation of auditory function. Microphonic potentials and auditory nerve action potentials were found to be more affected when intoxication took place during the last 15 days of gestation.

Animals↗