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Histochemical methods were employed to determine the course of the olivocochlear bundle (OCB) within the vestibular nerve of guinea pigs. Following transection of the inferior vestibular nerve, cholinesterase staining in the cochlea was greatly reduced. Transaction of the superior vestibular nerve, however, yielded no detectable change in staining. It is concluded that the cochlear efferent innervation in guinea pigs is carried in the inferior vestibular nerve, at the point of entry into the medial bulla.

Nimodipine, an L-type Ca2+ channel antagonist, was tested using sound-evoked cochlear potentials in guinea pigs to investigate whether these channels are involved in cochlear function. Perilymph spaces of guinea pig cochleae were perfused with artificial perilymph solutions containing 0.1-10 microM nimodipine at a rate of 2.5 microliters/min for 10 min. The cochlear potentials evoked by 10 kHz tone bursts of varying intensities were recorded from the basal turn of the scala vestibuli. Cochlear perfusion of nimodipine resulted in reversible, dose-related suppression of the compound action potential of the auditory nerve (CAP; N1-P1), a prolongation of N1 latency at suprathreshold levels, an elevated CAP threshold, a decrease in N1 latency at a constant amplitude measured at CAP threshold, a reduction in cochlear microphonics (CM), and a reduction of the negative summating potential (SP) to a point where it became positive (i.e., a reversal of SP). The endocochlear potential (EP) was not affected. These results support the hypothesis that L-type Ca2+ channels are directly involved in the operation of the organ of Corti. We speculate that L-type Ca2+ channels are integrally involved in generation of a negative summating potential and the dc motion of the cochlear partition described by others.

Fitting hearing aids on young infants presents a unique set of problems, and to some extent, requires a unique set of skills. First, a complete, frequency-specific evoked potential assessment is needed to define the loss and establish hearing aid fitting targets. The selected hearing aids must be flexible and must be adjusted to account for the acoustic characteristics of a small ear canal. Automatic volume control, wide dynamic range compression, directional microphones, and direct audio input are among the optional features to consider. In general, advanced technology, such as digital, programmable hearing aids offer the greatest flexibility in meeting the instrument-related challenges of the infant hearing-aid fitting. Finally, hearing aids are only one component of the management sequence. An early interventionist must be involved from the start to coordinate rehabilitation and ensure that the needs of the entire family are being met in the process.

Iron deficiency anemia is a frequently occurring clinical disorder. Despite the suggested association with hearing loss in the literature, cochlear sequelae of iron deficiency have yielded conflicting results in experimental studies. Auditory function was tested in iron-deficient and normal male Wistar albino rats using distortion product otoacoustic emissions and auditory brainstem response audiometry for the clarification of the opposing results in the literature. Hemoglobin, hematocrit, serum iron and albumin levels were monitored to verify iron deficiency. Although dramatic differences in weight gain and blood test parameters were noted, no significant change in auditory function due to iron deficiency was detected.

The reliability of the device implantation has greatly improved since 1994, when the device was officially approved as a medical device. We compared audiological data for the two groups of patients; one group has used the device for more than 10 years and the other for less than 10 years. There were no marked differences in any of the parameters examined. In both groups, a hearing level improvement of 36 dB was obtained 3 months postoperatively and at the most recent examination the improvement decreased to 21 dB. However, the device affords socially adequate hearing. In none of the patient deterioration was bone conduction caused by use of the device noted.

Educational objectives: To develop an awareness of the effectiveness of behavioral audiologic testing in children under 3 years of age and to develop an understanding of advances in ABR and otoacoustic emissions and their role in testing of young children.

A growing body of research suggests that the efferent innervation to the cochlea, the olivocochlear bundle (OCB), may modulate the mechanical function of the cochlea. However, the role of tonic OCB input in cochlear function remains poorly understood. The purpose of this study was to determine the influence of tonic efferent input on cochlear mechanics, by transecting the entire OCB in guinea pigs, and observing changes in tuning curves and acoustic distortion products. The OCB was transected by avulsing the inferior vestibular nerve as it enters the internal auditory canal of the right bulla. Auditory brainstem response (ABR) thresholds, ABR tuning curves, and acoustic distortion products were measured before and after surgery. Successful transection of the OCB was verified histochemically. Results revealed no consistent changes in tuning curves or in the growth functions of the distortion products. To the extent that these measures reflect cochlear mechanical nonlinearities, it is concluded that tonic OCB input is not necessary for grossly normal cochlear mechanical function in the 10‐kHz region of the guinea pig cochlea. It thus seems unlikely that the efferents are involved in establishing a ‘‘set point’’ for cochlear operation.

We tested 6,7-dinitroquinoxaline-2,3-dione (DNQX); 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX); 6,7-dichloro-3-hydroxy-2-quinoxalinecarboxylic acid (DHQC); and 3-hydroxy-2-quinoxalinecarboxylic acid (3HQC), new kainate and quisqualate receptor antagonists, upon cochlear potentials in guinea pig. Perilymph spaces of guinea pig cochleae were perfused with artificial perilymph solutions containing up to 1000 microM concentrations of DHQC and 3HQC, and 500 microM concentrations of DNQX and CNQX, at a rate of 2.5 microliters/min for 10 min. Cochlear potentials evoked by 10 kHz tone bursts of varying intensity were recorded from the basal turn scala vestibuli. Cochlear perfusion of the four drugs resulted in a dose-related suppression of the compound action potential of the auditory nerve (CAP; N1-P1), a prolongation of N1 latency at suprathreshold levels, an elevated CAP threshold, and a decreased N1 latency at CAP threshold. None of the drugs had significant effects on cochlear microphonics (CM) or the summating potential (SP). EC50 values (concentrations causing a 50% reduction in CAP amplitude at 68 dB SPL) were 8 microM for DNQX, 30 microM for DHQC, 35 microM for CNQX, and 1 mM for 3HQC. Results support the hypothesis that kainate and quisqualate receptors are involved in neurotransmission between the hair cell and afferent nerve.