Biomedical subjects
Publications and source records attributed to N C Rich.
Intense (up to 59 dB SPL) spontaneous otoacoustic emissions are produced by both ears of a young dog. The right ear produces a single, very narrow-band (less than 4 Hz) emission at about 9100 Hz. Brainstem evoked-response audiometry suggests that this emission is generated near the transition between normal and abnormal regions of the cochlea.
The first author's right ear produces a spontaneous otoacoustic emission (SOAE) at 7529 Hz and 16 dB SPL. An external continuous tone is able to suppress the SOAE. The 3 dB iso-suppression curve is broadly tuned and displaced, relative to the SOAE, toward higher frequencies. An audiogram notch exists at frequencies just below that of the SOAE. We explain the occurrence of both spontaneous and impulsively evoked OAEs in terms of disruption of active feedback mechanisms of the OHCs upon basilar membrane vibration. According to this hypothesis, each segment of the organ of Corti feeds back positively upon its segment of basilar membrane and negatively upon adjacent segments. If a patch of OHC loss exists, adjacent segments of the basilar membrane are released from the negative feedback and respond to an impulsive stimulus with exaggerated oscillations at their resonance frequencies, thus producing OAEs. At particularly sharp transitions between normal and abnormal regions of the organ of Corti SOAEs may be generated.
Single unit activity was recorded in the auditory nerves of chinchillas. Period histograms were constructed for responses to tones with frequencies 30-1000 Hz. For low-frequency tones at near-threshold levels, peak period histogram phases for low- and medium-best-frequency (BF) neurons (less than or equal to kHz) ranged from synchronous with condensation at the eardrum to 90 degrees leading it. At near-threshold (but high absolute) levels, high-BF (greater than or equal to 8 kHz) neurons responded in phase with rarefaction. At even higher levels, period histograms for responses of high-BF neurons tended to become bimodal, with one of the modes lagging rarefaction by 90 degrees. Using cochlear microphonics as an indicator of basilar membrane (BM) displacement, at threshold levels, response phase of low- and medium-BF neurons fall within a range between displacement and velocity of the BM toward scala vestibuli. High-BF neurons respond, at threshold (but high) intensities, in phase with BM displacement toward scala tympani. The rates of growth of frequency sensitivity in responses of low-BF (+ 18 dB/oct) and high-BF (+ 12 dB/oct) neurons are consistent with preferred response phases corresponding to BM SV velocity and ST displacement, respectively. At supra-threshold levels high-BF neurons may fire preferentially to both scala tympani displacement and scala vestibuli velocity. These results support the notion that, for high-intensity, low-frequency stimuli, OHC hyperpolarization can induce excitation of the dendrites innervating IHCs.
In order to ascertain whether Type II cochlear ganglion cells project to the brain, we have studied the retrograde transport of horseradish peroxidase (HRP) from the cochlear nucleus to the spiral ganglion of the chinchilla. In this animal there exist two types of ganglion neurons, which closely correspond to those previously described in guinea pigs, cats and rats. As in the guinea pig, the majority population (Type I) consists of relatively large, myelinated neurons. The minority population (Type II, 10% of the total population) consists of small, mostly unmyelinated cells, with filamentous cytoplasm and finely grained nuclear chromatin. Type II neurons tend to be clustered toward the peripheral side of Rosenthal's canal, often in close proximity to the intraganglionic spiral bundle. By 24 h after injections of HRP into the cochlear nucleus, incubation of the cochlear ganglion in diaminobenzidine/H2O2 reveals abundant HRP label in both Type I and Type II neurons. Type II neurons, however, tend to be labelled less intensely than Type I neurons. Control experiments, consisting of spillage of HRP solution over the cochlear nucleus, were carried out to determine how much HRP might be picked up by neurons after HRP diffusion. Comparison of cochleae from injected animals and from the control animals suggests that most of the label that was found in ganglion neurons after cochlear nucleus injections represents axonally transported HRP. We conclude, at least tentatively, that Type II neurons project to the brain. The fact that less label is found in Type II neurons that in Type I neurons suggests that the former have thinner axons and/or finer terminals in the cochlear nucleus.