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20 guinea pigs were exposed to a broad band noise (120-140 dB SPL) for short durations. The conditions of stimulation were strictly identical for all animals. Cochlear microphonic responses (CM) were recorded with conventional differential electrodes after each exposure, from the first turn of the cochlea. Variations were observed in the degree of CM depression and also in the alteration of the CM transfer function. The origin of this variability is discussed.

Cochlear microphonic responses (CM) were recorded from the guinea pig cochlea with conventional differential electrodes implanted in the first and second turns. The CM frequency functions were determined by calculating the Fast Fourier Transform of responses to wide-band clicks. These frequency functions appeared to be dependent upon the spectrum of the click. This effect was interpreted as resulting from suppressive interactions between the various components of the click. It is suggested that such CM interactions are related to corresponding effects reported previously concerning cochlear nerve responses.

It is generally assumed that noises have a detrimental effect when the cochlear receptor is overloaded and, more specifically, when the cochlear microphonic (CM) fails to increase linearly with intensity. In order to investigate further the relations between the nonlinearity of CM and damage to the cochlea, a series of experiments was carried out on guinea pigs to relate the short-term CM depression following the presentation of noises or tones with the nonlinearity and the assymmetry. The asymmetrical non-linearity of CM was measured in tracing the input-out functions and also the wave-forms. Two other important tests of the asymmetrical nonlinearity were used: the measure of interference and of summating potential (SP DIF). The results show that the fatigability is greater when there is a large negative asymmetry or a large negative SP. Variations in asymmetry and in SP were observed among individuals. Other changes of symmetry were provoked by asphyxia or by introducing solutions of KCl in the perilymph. These changes were well correlated with the fatigability. These results are interpreted in a model of the cochlear transducer derived from the model of Davis. The assymetry of a flux of potassium ions between endolymph and the hair cells is assumed to be responsible for the alterations associated with cochlear fatigue and trauma.

Various characteristics of cochlear microphonic responses (CM) were measured in the guinea-pig after perfusing scala tympani with KCl solutions. In addition to a decrease of CM magnitude, the nonlinearity and the symmetry of waveform showed typical modifications suggesting, in addition to a depolarization of hair cells, some mechanical alterations.

Cochlear microphonics (CM), action potentials (AP) and endochochlear potential (EP) were recorded on guinea pigs. The introduction of a small quantity of KCl solution (0.1 N) in the perilymph provoked a moderate decrease of CM and AP. During the period of depressed but stable amplitude, the presentation of intense sounds provoked an exaggerated susceptibility to fatigue and a delayed recovery. Similar changes were observed in the evolution of EP. However, the recovery was slower for EP than for CM. The results, as a whole, suggest that the fatigue which is manifested in the depression of cochlear potentials is related to a leakage of potassium ions from endolymph to fluids spaces within the organ of Corti.

Cochlear microphonics (CM) were recorded with differential electrodes from several locations in the guinea pig cochlea. Input-output curves and amplitude-frequency curves were plotted before and after short exposures to intense noise. In addition to amplitude losses, important changes in the intensity functions resulted in a decrease of the nonlinearity and in a modification of the frequency response. The mechanisms producing these alterations are discussed.

Reversible experimental lesions were produced in the central end of the cochlear nerve at the IAM of guinea pigs by various procedures, including the instillation of KCl (0.1 or 0.01 M). As a result the usual diphasic AP waveforms seen in guinea pigs (when click stimuli are used) were transformed into monophasic, widened negative waves. This change, attributed to a neural block, was reversible, e.g. when the instilled KCl was dispersed by irrigation with normal saline. It is suggested that the widened monophasic negative AP's observed at ECochG in cases of acoustic neuroma or similar lesions, are produced in this way.

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.

Cochlear microphonic potential was recorded with differential electrodes implanted in the various turns of the guinea-pig cochlea. Isointensity frequency responses were plotted in normal conditions and after excessive displacements of the cochlear partition. These displacements were provoked by changes of hydrostatic pressure in the perilymph of scala tympani or scala vestibuli. Typical modifications of the frequency response were observed. The most noticeable was a division in two parts of the response zone which suggested the existence of two resonance peaks. Scanning electron microscopy revealed that changes of hydrostatic pressure provoked alterations of the stereocilia in the outer rows of external hair cells, probably in relation with a decoupling of the tectorial membrane from the organ of Corti. These results are discussed in terms of possible alterations of cochlear micromechanics.