[Remote masking in cochlear microphonics].
Explore the source record for details and available documents.
Animals↗
SEARCH · Search PubMed
Results for “Cochlear Microphonic Potentials”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Hearing in premature infants. Evoked-cochlear microphones].
This report summarizes our experience in obtaining microphonic potentials in human beings. Special studies were made to obtain microphonic potentials in premature newborns.
Acoustic Stimulation↗
Effects of noise, hypothermia and barbiturate on cochlear electrical activity.
Pentobarbital has been reported as both increasing and decreasing the effects of noise trauma on the inner ear. In the C57BL/6 laboratory mouse, the effects depend upon which electrical events are measured and whether or not the hypothermic effects of pentobarbital are counteracted. Pentobarbital-induced hypothermia per se increased the latency of both the high-intensity-threshold, short-latency (H) and low-intensity-threshold, long-latency (L) waves by approximately 60 mus per degrees C decrease, had no significant effect on H-wave amplitude, but caused a severe reduction of the L-wave amplitude. As little as 1 min of 120 dB SPL high-frequency noise can temporarily reduce the cochlear microphonic (CM) amplitude, abolish the H and reduce the amplitude of the L waves of the click-evoked, volume-conducted gross auditory nerve action potential (AP). 1 week later, CMs were more depressed in subjects which had been anesthetized during 5 min noise exposure, regardless of body temperature during the exposure. The long-term decrement of the L-wave amplitude did not consistently differ as a function of anesthetic state or body temperature at exposure. However, hypothermia protected from, while barbiturate increased the effects of noise stress on the H wave. It was hypothesized that metabolic factors differentially affect the various electrical generators in the inner ear.
Animals↗
Magnitude of the negative summating potential varies with perilymph calcium levels.
Previous results demonstrated that nimodipine, an L-type of Ca2+ channel antagonist, abolished the negative summating potential (SP) recorded from anesthetized guinea pigs (Bobbin et al., 1990), suggesting that Ca2+ is involved in generation of the negative SP. Therefore we examined the effect of changing concentrations of perilymph Ca2+ on this cochlear potential. Perilymph spaces of guinea pig cochleae were perfused with artificial perilymph solutions containing zero mM Ca2+, zero mM Ca2+ with 2 mM EGTA, 30 mM Mg2+ and increasing levels of Ca2+ (2, 4, 8, 16 mM) at a rate of 2.5 microliters/min for 10 min. Immediately after each period of perfusion the compound action potential of the auditory nerve (CAP), cochlear microphonics (CM) and the negative SP evoked by 10 kHz tone bursts of varying intensities were recorded from a wire inserted in the basal turn scala vestibuli. Decreasing the level of Ca2+ decreased the magnitude of the negative SP, whereas increasing the level of Ca2+ progressively increased the magnitude of the negative SP. Mg2+ (30 mM) suppressed the CAP to the same extent as zero mM Ca2+ with 2 mM EGTA, but only slightly increased the magnitude of the negative SP. These results support the hypothesis that Ca2+ and L-type Ca2+ channels are involved in the function of the hair cells and the generation of the negative SP. Mg2+ appears to be a selective antagonist of the Ca2+ channel involved in transmitter release.
Animals↗
Noise-induced cochlear hypoxia is intensity dependent, correlates with hearing loss and precedes reduction of cochlear blood flow.
Anesthetized and artificially ventilated guinea pigs were exposed to broad-band noise of 95, 101, 106 or 115 dB SPL for 30 min and studied for 180 min after cessation of noise. The partial pressure of oxygen (pO2) in the perilymph, the cochlear blood flow (CoBF) and auditory-evoked potentials were continuously recorded. Arterial blood pressure, electrocardiogram, inspiratory and expiratory gas levels, arterial blood gas levels and acid-base status were kept stable to exclude influences of these parameters on cochlear parameters. Exposure to 95 dB SPL did not affect perilymphatic pO2 or CoBF. Cochlear microphonics (CMs) were reduced, but compound action potentials of the auditory nerve (CAPs) and auditory brainstem potentials (ABRs) increased after exposure to this low-level noise. Perilymphatic pO2 decreased during exposure to 101 dB SPL and then further decreased during the subsequent 60 min after cessation of the noise. CoBF did not change significantly during and 30 min after noise but then paralleled the decline of perilymphatic pO2. However, both parameters showed a clear indication of recovery in the second and third hours after noise. At 101 dB SPL, CMs were again reduced immediately, CAPs were unaltered and ABRs again increased. Exposure to 106 and to 115 dB SPL resulted in a decrease in both perilymphatic pO2 and CoBF; this decrease began during the exposure but became progressively worse after the noise. Hearing loss was observed immediately with exposure and showed no signs of further deterioration after cessation. The observed time courses of changes are important. They reveal that hearing loss and cochlear hypoxia precede reduction in CoBF due to noise exposure. The potential mechanisms underlying these effects are discussed.
Animals↗
Electrocochleography and cochlear pathology.
In experimentally damaged inner ears the structural alterations were correlated to electrocochleographic responses of the ear. Sectioning of the cochlear nerve with degeneration of the type I neurons but intact sensory cells results in normal cochlear microphonics but very weak and atypical nerve responses. By contrast, damage of the organ of Corti with retrograde degeneration abolished primarily the cochlear microphonics, whereas the compound VIII nerve action potential is barely affected when only the outer hair cells are gone and even a small number of surviving inner hair cells is still compatible with a relatively strong compound action potential of the cochlear nerve.
Action Potentials↗
Electrocochleography of ears with mumps deafness.
Electrocochleography was performed on 16 affected ears of 15 deaf patients whose deafness had resulted from the mumps. Although pure-tone audiometry showed no response in each case, the cases of mumps deafness can be classified into the following three types of cochlear impairment according to the cochlear microphonic (CM) response: (1) no action potential (AP) response but a well-developed CM response, with impairment at the neural level and probable functioning of Corti's organ; (2) absence of both the AP CM responses, with severe impairment of both the neural regions and Corti's organ; (3) no AP response but a decreased CM response, with severe impairment of the neural regions and partial impairment of Corti's organ.
Action Potentials↗
Effects of acute lead acetate exposure on adult guinea pigs: electrophysiological study of the inner ear.
The effects on humans of lead acetate exposure may involve the cranial nerves, since vertigo and sensory neuronal deafness have been reported in lead workers; however, there exist only a few reports concerning the dose effects of lead acetate both on the cochlea and the eighth cranial nerve. The effects of lead acetate on the cochlea and the eighth nerve were investigated systematically using cochlear microphonics (CM), whole-nerve action potential (AP), and endocochlear potential (EP) in guinea pigs (male albino Hartley). Guinea pigs were injected with 2 ml of a 1% solution of lead acetate (20 mg) once a week for 1-5 weeks. The threshold of whole-nerve AP (N1) was elevated by injection of lead acetate, even 40 mg, and whole-nerve AP (N1) output voltage decreased after injection of 100 mg of lead acetate. On the other hand, no change was observed in CM after lead acetate injection (100 mg) or in EP after lead acetate exposure (40 mg). The blood concentrations of lead acetate were as follows (mean): control, 4.5 micrograms/dl; Expt 1, 80 micrograms/dl; Expt 2, 126 micrograms/dl; Expt 3, 142 micrograms/dl. We conclude that dysfunction of the eighth nerve is induced by high-dose lead exposure, but that lead exposure does not induce electrophysiological dysfunction of the organ of Corti and the stria vascularis.
Animals↗
Electrocochleographic evaluation of hearing loss in acoustic neuromas.
OBJECTIVE: This study aimed to clarify the pathophysiology involved in the cause of hearing impairment due to acoustic neuromas (AN) with electrocochleograph (ECoG). STUDY DESIGN: The study design was a retrospective case study. SETTING: This study was conducted in a tertiary referral center. PATIENT: Thirty-four patients diagnosed as having AN by magnetic resonance imaging between 1988 and 1995. INTERVENTION: Diagnostic. MAIN OUTCOME MEASURES: The authors made a comparison between the patients' ECoG findings and the size of their tumors as determined by magnetic resonance imaging and a pure-tone audiometry (PTA). The disparity between the threshold of PTA and the detective threshold of compound action potential (CAP) or that of the cochlear microphonics (CM) was calculated. When the threshold of the PTA was worse than the detective threshold of the CAP or the CM, the disparity was regarded as indicating a hearing loss of retrocochlear origin. RESULTS: There was no correlation found between tumor size and the detective threshold of CAP or CM. Disparity was found to correlate with tumor size. CONCLUSIONS: These findings seem to indicate that retrocochlear damage in AN increases parallel to the growth of the tumor and that retrocochlear damage can be detected by the ECoG before surgery.
Adult↗
[Protective effect of nitric oxide against hydrogen peroxide-induced hearing loss].
Previous research showed that reactive oxygen species (ROS) play an important role in ototoxity. The present research was to investigate whether nitric oxide, an important neurotransmitter in the inner ear, could prevent hydrogen peroxide-induced hearing loss through the nitric oxide/cyclic GMP pathway in guinea pig cochlea. Fifty adult pigmented guinea pigs (250~350 g) of either sex with positive prier reflex were randomly divided into five groups. All of the animals underwent whole cochlear perfusion for two hours. The solution that was perfused into the cochlear of different group was artificial perilymph (AP) for group 1200 micromol/L H2O2 for group 2100 micromol/L L-Arg for group 3, H2O2+L-Arg for group 4 and H2O2+L-Arg+L-NNA for group 5 respectively. Compound action potential (CAP, evoked by click) and cochlear microphonic (CM, evoked by tone burst) were recorded every thirty minutes to show the effects of different reagents on cochlear function. In order to assess cell viability after perfusion, the fluorescent dyes Hoechst that stains all cell nuclei and propidium iodide (PI) that specifically stains nuclei of dead cells, were used. The CAP threshold shifts and CM amplitude decreased after perfusion with H2O2+L-Arg. They were significantly lower than those of H2O2 group. No obvious cell death was noticed after H2O2+L-Arg perfusion, while only 54% of hair cells were alive after H2O2 perfusion. There were no significant differences between the group of H2O2 and that of H2O2+L-Arg+L-NNA group. Our results suggest that nitric oxide may partly be able to protect guinea pigs from hydrogen peroxide-induced hearing loss.
Animals↗
Tympanic and transtympanic electrocochleography in acoustic neuroma and vestibular nerve section surgery.
Eighth nerve action potential (AP) amplitudes and latencies and cochlear microphonic (CM) amplitudes were compared using tympanic and transtympanic electrocochleography (ECOG) in two patient groups. Tympanic ECOG was performed with a wick electrode placed on the tympanic membrane (TM). Transtympanic ECOG was performed with a needle electrode placed on the promontory of the anesthetized patient. Eighteen subjects were tested by tympanic ECOG as part of a preoperative assessment for either acoustic neuroma removal or transection of the vestibular portion of the eighth cranial nerve. Surgery occurred within 1 week of the preoperative evaluation. Intraoperative auditory monitoring was performed using transtympanic ECOG. Baseline recordings were compared to the preoperative tympanic ECOG data. Stimuli were condensation and rarefaction clicks and tone bursts, presented by an insert earphone. As expected, the two methods resulted in essentially identical response latencies and large amplitude differences, although the response amplitudes were extremely variable. The AP amplitude and the CM amplitude did not increase by the same factor with the transtympanic (TT) electrode compared to the tympanic electrode. On comparison of preoperative and intraoperative response amplitudes with regard to stimulus polarity, tympanic electrocochleography appears to be a useful method of gathering preliminary information on the status of the patient's auditory system. In this study, tympanic ECOG was found to have some predictive value when trying to ascertain the best intraoperative monitoring situation.
Acoustic Stimulation↗
Sensorial substitution using sound-vibratory stimuli on the teeth: a new approach to the rehabilitation of the profoundly deaf.
In 20 normal-hearing subjects, hypoacusics and anacusics ranging from 4 to 44 years of age, we have developed a study related to the analysis of brain evoked potential: B E R, E R P 40 Hz, cochlear microphonic responses and P 300 stimulating sound in the ear, and vibration to the teeth. With vibratory stimuli to the teeth, the brainstem potential didn't appear in anacusics; however, it appeared in subjects with perception deafness and transmission deafness. The potential type E R P 40 Hz (Galambos et al, 1981) appeared in hypoacusics, but not in anacusics; however, the subjective sensation of the vibration remained with them in absence of all the auditory registrable responses; nevertheless, we were able to record the P 300. We recorded perfectly cochlear responses in anacusics using vibratory stimuli of 500 Hz and higher applied to their teeth, even though they didn't have any other type of normal auditory response. The potential P 300 was obtained in normal hearing, hypocusics and anacusics, with the proper latencies according to their ages.
Acoustic Stimulation↗
Electrochemical profile for potassium ions across the cochlear hair cell membranes of normal and noise-exposed guinea pigs.
The electrochemical driving force for movement of potassium ions across the hair cell membranes was determined in normal and noise-exposed guinea pigs. The measurement of the electrical potential and the potentiometric determination of K+ activity difference across the cell membranes were accomplished with double-barreled K+-selective liquid membrane microelectrodes. Identification of hair cells was based on the sudden increase of the a.c. component of the receptor potential associated with the appearance of the membrane potential and an increase in K+ activity. The results suggest that K+ ions in the hair cell interior and the extracellular space of the organ of Corti are near electrochemical equilibrium. However, the electrochemical gradient for K+ between the hair cell interior and the subtectorial endolymph was very high. These findings imply that the resting potential of hair cells is mainly generated by the diffusion of K+ across the basolateral hair cell membrane and is not affected by contact of the apical cell membrane with K+-rich endolymph. Although cochlear microphonics recorded extracellularly were severely suppressed in guinea pigs exposed to broadband noise at 115 dBA for 7 days, the electrochemical profile for K+ across cell membranes of surviving hair cells did not show marked changes. The ratio of intracellular a.c. receptor potential to extracellular cochlear microphonics was much greater in surviving hair cells of noise-exposed guinea pigs.
Animals↗
Rupture of Reissner's membrane during acute endolymphatic hydrops in the guinea pig: a model for Ménière's disease?
CONCLUSION: The changes in cochlear function during a destructive acute endolymphatic hydrops were relatively small. This might be consistent with the hypothesis that an endolymphatic hydrops is a marker of disordered inner ear homeostasis rather than the cause of the clinical symptoms of Ménière's disease. OBJECTIVE: Assessment of cochlear function during induction of a destructive acute endolymphatic hydrops. MATERIALS AND METHODS: During repetitive microinjections of 0.5 microl of artificial endolymph at a rate of 50 nl/s the 2f1-f2 and f2-f1 cochlear microphonics distortion products (CMDP) and 2f1-f2 distortion products otoacoustic emissions (DPOAE) were recorded in the guinea pig. RESULTS: A 'catastrophe' occurred in the inner ear when 2.5-3.5 microl of artificial endolymph was injected. A rupture of Reissner's membrane was then found, most often in the apical turn of the cochlea. This rupture had only minor effects on the endocochlear potential, whereas it caused a marked decrease in 2f1-f2 DPOAE amplitude. The 2f1-f2 and f2-f1 CMDP amplitude increased during each injection prior to the rupture. After the rupture the f2-f1 CMDP amplitude decreased during each injection, possibly due to a shift of the cochlear transducer operating point position.
Animals↗
Temperature effects on the peripheral auditory apparatus.
Cooling with a thermoelectric cold probe, well localized in the region of the cochlea, produces a rapid, reversible decrease in the amplitude and increase in the latency of the action potential induced by clicks. These changes closely resemble those produced by reducing click intensity. Temperature also affects the amplitude of the cochlear microphonic, but the amount of change is considerably less than, and is poorly correlated with, the amplitlude change of the action potential. It is speculated that temperature may act on a hypothetical " excitatory process" in the cochlea, which comes after the cochlear microphonic in the sequence leading to production of the action potential of the auditory nerve.
Animals↗
Smooth muscle in the annulus fibrosus of the tympanic membrane: physiological effects on sound transmission in the gerbil.
In a wide variety of mammals, the rim of the tympanic membrane (annulus fibrosus) has an array of contractile elements, either smooth muscle [Henson and Henson, J. Assoc. Res. Otolaryngol. 1 (2000) 25-32] or myofibroblasts [Kuijpers et al., Hear. Res. 128 (1999) 80-88]. These elements are anchored peripherally to the bony tympanic ring and centrally to incoming fibers of the pars tensa. Their arrangement suggests that they are involved in the control of tympanic membrane tension. In this study, cochlear microphonic (CM) threshold changes were recorded in gerbils to study the physiological effects of these contractile elements. It was demonstrated that the application of substances known to make smooth muscle contract (vanadate and norepinephrine) caused concentration-dependent elevations in CM thresholds. Maximum changes of 8-9 dB occurred with the lowest frequency tested (2.16 kHz). The application of muscle-relaxing drugs reversed these effects. Controls showed that the threshold changes were not induced by effects on middle or inner ear structures. These results add to emerging evidence that the tympanic membrane has intrinsic control of tension and is potentially able to have some control over energy levels reaching the cochlea.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
Sensory evoked potentials in neurotoxicology.
This paper provides a summary of routine evoked potential tests used with rats, with elaboration on the cochlear microphonic portion of the auditory brainstem response, the effects of chemicals on high frequency (above 40 Hz) components of the somatosensory evoked potential, on cerebellar recording of sensory evoked potentials, and on central conduction time. An alternative to peak-valley amplitude and latency measurements is discussed, wherein a computer analyzes evoked potentials for differences from control in waveform shape, latency, and power. Since multiple use of statistics is common, resulting in an inflated false positive rate, an alpha criterion of less than 0.05 is recommended. Instead of dividing alpha by the number of statistical tests (Bonferroni), a less severe correction of dividing alpha by the square root of the number of tests is proposed.
Animals↗
Low-frequency modulation of inner hair cell and organ of Corti responses in the guinea pig cochlea.
Low-frequency tones are used to study changes in responsiveness as a function of phase in inner hair cell (IHC) and organ of Corti (OC) responses recorded from second turn of the guinea pig cochlea. In these experiments a 40 Hz stimulus is combined with a variable frequency probe to determine the degree to which tones at and below best frequency (BF) are modulated. Changes in responsiveness produced by the low-frequency input are quantified and related to position of the basilar membrane which is estimated using the phase of the cochlear microphonic measured in the OC fluid space. Results obtained when 40 Hz is presented at its lowest effective level demonstrate that ac responses to low-level BF probes are reduced for basilar membrane displacements to scala tympani while probe tones well below BF are modulated in the opposite direction. The transition between these two response patterns occurs when the overall DC produced in the OC by the two-tone input changes from positive to negative. Because of this association, the frequency dependence exhibited in the bias results may be linked to mechanisms responsible for generating the two polarities of the summating potential and the DC receptor potentials that it reflects. An attempt is also made to relate bias-induced changes in hair cell receptor potentials to modulations in single-unit rate responses. In other words, to address variations in the temporal relationships between excitation and suppression measured in the auditory nerve.
Acoustic Stimulation↗