Cochlear microphonic potential in cats. Effects of perilymphatic pressure.
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OBJECTIVE: The purpose of this study was to investigate the kainic acid (KA) toxicity on cochleas. METHOD: One microliter KA in the concentration of 60 mM was applied to the round window membrane of guinea pig. The compound action potential (CAP), cochlear microphonic potential (CM) and distortion product otoacoustic emissions (DPOAE) were measured 12 hours after KA was administrated. RESULT: CAP was suppressed significantly or abolished after the drug administration, however, the CM and DPOAE almost presented no change. CONCLUSION: The targets of KA toxicity are the primary auditory afferent endings.
Inquire into the mechanism of inner ear pathological physiology in autoimmune sensorineural hearing loss (ASHL). With the auditory electric-physiological techniques and enzyme-histochemical method, the change of inner ear hearing function and enzyme activity were observed. These animals, which threshold of auditory nerve compound active potential (CAP) and cochlear microphonic potential(CM) heightening evidently, showed that the amplitude of endolymphatic potential(EP) (include-EP) bring down in various degrees, which was related to the change of the active of Na(+)-K(+)-ATPase and SDH in vascularis stria and endolymphatic sac. The abnormality of enzymes metabolism in inner ear tissues, which following autoimmune inflammation damage, is the pathological foundation of hearing dysfunction.
Using 97 male albino guinea pigs and applying electrophysiological methods, the effects of a 6 kHz tone were investigated at a moderate sound pressure level to the inner ear during a 24-h exposure time. Following exposure to the 6 kHz tone at 90 dB, cochleas showed decreased maximum output voltage of cochlear microphonics (CM) and action potential (AP). In the endolymph, K+ ion and Na+ ion concentrations remained unchanged during 40 min anoxia and 90 dB tone exposure. At 80 dB sound exposure decreases in maximum output voltage of CM and AP and decreases in the absolute value of EP could not be detected. Endolymph K(+)-ion Na(+)-ion concentrations were also unchanged. These findings indicate that diffusion potentials are induced at the same time as decreases of maximum output voltage in CM induced by exposure to sound at 90 dB.
Intracellular receptor potentials were recorded from inner and outer hair cells in response to low-frequency tones, from the basal, high-frequency region of the guinea-pig cochlea. The receptor potentials recorded from inner hair cells are asymmetrical about the resting membrane potential with the depolarizing phase, which corresponds to rarefaction in sound pressure, exceeding the phase of hyperpolarization by a factor of about 3. It was found that the relationship between the peak-to-peak voltage responses and sound pressure level could be described by rectangular hyperbolae. When the frequency of the sound stimulus was progressively increased from 100 Hz to 4 kHz, the 'periodic' (a.c.) component of the receptor potential was attenuated with respect to the 'continuous' (d.c.) component. The characteristics of the inner hair cells could be described by two stages of low-pass filtering, with one of the filters having the same corner frequency as the electrical time constants which varied in different cells between 178 and 840 Hz. Receptor potentials recorded intracellularly from two morphologically identified outer hair cells were symmetrical about the resting membrane potential (about -65-70 mV) and had a maximal amplitude of only 5 mV at frequencies and intensities which yield 20-30 mV voltage responses from inner hair cells. No d.c. component receptor potentials were recorded in response to high-frequency tones. Phase and amplitude measurements were made from receptor potentials from inner hair cells, and from 'cochlear microphonic potentials' which were recorded from the organ of Corti and scala tympani. The phase of depolarization in both potentials was associated with displacement of the basilar membrane towards the scala vestibuli. The phase of the intracellular receptor potentials leads the cochlear microphonic by about 90 degrees and the sound pressure by about 180 degrees at frequencies below 100 Hz. Above this frequency the phase lead progressively declines and at higher frequencies becomes a phase lag. These phase relationships indicate that inner hair cells respond to the velocity of the basilar membrane at frequencies below 200-600 Hz, and to its displacement above this, and that the voltage responses of the inner hair cells are limited by their membrane time constants. It is suggested that outer hair cells respond to basilar membrane displacement throughout their frequency range. It is shown that, with respect to frequency, the different growth rates of the cochlear microphonic potentials and inner hair cell receptor potentials, and the dominance of cochlear microphonic potentials in the organ of Corti, result in an effective electrical interaction between inner hair cells and cochlear microphonic potentials.
The mammalian hearing organ, the organ of Corti, was studied in an in vitro preparation of the guinea pig temporal bone. As in vivo, the hearing organ responded with an electrical potential, the cochlear microphonic potential, when stimulated with a test tone. After exposure to intense sound, the response to the test tone was reduced. The electrical response either recovered within 10-20 min or remained permanently reduced, thus corresponding to a temporary or sustained loss of sensitivity. Using laser scanning confocal microscopy, stimulus-induced changes of the cellular structure of the hearing organ were simultaneously studied. The cells in the organ were labeled with two fluorescent probes, a membrane dye and a cytoplasm dye, showing enzymatic activity in living cells. Confocal microscopy images were collected and compared before and after intense sound exposure. The results were as follows. (1) The organ of Corti could be divided into two different structural entities in terms of their susceptibility to damage: an inner, structurally stable region comprised of the inner hair cell with its supporting cells and the inner and outer pillar cells; and an outer region that exhibited dynamic structural changes and consisted of the outer hair cells and the third Deiters' cell with its attached Hensen's cells. (2) Exposure to intense sound caused the Deiters' cells and Hensen's cells to move in toward the center of the cochlear turn. (3) This event coincided with a reduced sensitivity to the test tone (i.e., reduced cochlear microphonic potential). (4) The displacement and sensitivity loss could be reversible. It is concluded that these observations have relevance for understanding the mechanisms behind hearing loss after noise exposure and that the supporting cells take an active part in protection against trauma during high-intensity sound exposure.
We have used the guinea pig isolated temporal bone preparation to investigate changes in the non-linear properties of the tone-evoked cochlear potentials during reversible step displacements of the basilar membrane towards either the scala tympani or the scala vestibuli. The position shifts were produced by changing the hydrostatic pressure in the scala tympani. The pressures involved were calculated from measurements of the fluid flow through the system, and the cochlear DC impedance calculated (1.5 x 10(11) kg m-4 s-1, n = 10). Confocal microscopic visualization of the organ of Corti showed that pressure increases in the scala tympani caused alterations of the position of the reticular lamina and stereocilia bundles. For low pressures, there was a sigmoidal relation between the DC pressure applied to the scala tympani (and thus the position shift of the organ of Corti) and the amplitude of the summating potential. The cochlear microphonic potential also showed a pronounced dependence on the applied pressure: pressure changes altered the amplitude of the fundamental as well as its harmonics. In addition, the sound pressure level at which the responses began to saturate was increased, implying a transition towards a linear behaviour. An increase of the phase lag of the cochlear microphonic potential was seen when the basilar membrane was shifted towards the scala vestibuli. We have also measured the intracochlear DC pressure using piezoresistive pressure transducers. The results are discussed in terms of changes in the non-linear properties of cochlear transduction. In addition, the implications of these results for the pathophysiology and diagnosis of Meniérè's disease are discussed.
Cochlear microphonics (CM) and compound action potentials (AP) were recorded simultaneously with differential electrodes in the basal turn of the guinea pig cochlea. When CM two-tone suppression (2TS) curves were compared to AP simultaneous masking curves, good correspondence was observed between CM and AP suppression effects. The relationship between the 10 dB bandwidths of CM and AP 2TS curves remained constant for each animal despite differences between animals resulting from natural variations. Under pathological conditions (acute cochlear hypoxia) both CM and AP two-tone suppression effects were greatly reduced or disappeared. These results can be taken as evidence that CM suppression and AP suppression are the products of a common underlying mechanism.