ELECTRON MICROSCOPIC STUDY OF THE EFFERENT AND AFFERENT INNERVATION OF THE ORGAN OF CORTI IN THE CAT.
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The purpose of this study was to determine whether patterns of phoneme identification error differ among listeners with cochlear and retrocochlear auditory disorder. Speech intelligibility performance was analyzed in 15 patients with confirmed eighth-nerve disorder and in 15 patients with cochlear disorders, matched to the retrocochlear group for age and audiometric configuration, using confusion matrices derived from responses to a monosyllabic word list. Results indicated that: (1) vowel errors were more prevalent in the retrocochlear group and varied directly with increasing stimulus presentation level; and (2) consonant errors did not differ in type or relative frequency between the two groups, nor was there a level-dependent effect for consonant errors. These results are supported by the results of closed-set vowel identification tests and thus do not appear to be an artifact of open-set testing. Vowel errors may account for a major part of the speech 'rollover' phenomenon typical of retrocochlear auditory dysfunction.
Following loss of eighth nerve input, 20-40% of neurons in the neonatal chick cochlear nucleus, nucleus magnocellularis (NM), undergo cell death. Intracellular changes that precede the death of NM neurons include increased oxidative metabolism and mitochondrial volume, decreased cytoplasmic protein synthesis, and destruction of ribosomes. Six hours following afferent deprivation, dying NM neurons demonstrate complete loss of ribosomes and cessation of protein synthesis, suggesting that the rapid destruction of ribosomes leads to neuronal death. Increased NM neuron death occurs when mitochondrial upregulation is prevented by chloramphenicol, a mitochondrial protein synthesis inhibitor. This finding suggests that increased oxidative capacity is required for neuronal survival following loss of afferent input. To study changes in the ribosomes of afferent-deprived NM neurons, we obtained a monoclonal antibody to ribosomal RNA. This monoclonal antibody, Y10B, labels ribosomes of all NM neurons receiving normal synaptic activity. Following removal of afferent input, NM neurons demonstrate a biphasic change in their pattern of Y10B label. During the initial phase, there is a uniform decrease in the density of Y10B label. In the second phase, some NM neurons recover the capacity to bind the Y10B antibody while others remain unlabeled. During this second phase, NM neurons putatively destined to die, based on their failure to synthesize protein, are unlabeled by the Y10B antibody. New gene expression is not necessary to initiate the change in ribosomal immunoreactivity that leads deafferented NM neurons toward cell death. Blocking cytoplasmic protein synthesis with cycloheximide had no effect on the biphasic change in Y10B labeling of afferent-deprived NM neurons. Treating chicks with chloramphenicol, however, prevented the recovery of Y10B immunoreactivity in NM neurons during the second phase of the response to afferent deprivation.
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The purpose of this review is to provide an overview of the central auditory nervous system (CANS). Three main relay nuclei are located between the auditory nerve and the primary auditory cerebral cortex: 1- the cochlear nucleus, 2- the contralateral inferior colliculus and 3- the contralateral medial geniculate body. Some fibers of this main ascending pathway branch off to other nuclei such as the nuclei of the superior olivary complex and the nucleus of the lateral lemniscus. Fiber tracts connect the two sides of the ascending pathway at several levels, in such a manner that each ear projects heavier to the contralateral temporal cortex. As sensory information travels within the CANS, its processing occurs not only in a serial order but also in a parallel manner resulting a highly efficient and redundant system. Finally, this review put forth a model of central auditory processing that can serve as the basis for evaluating and addressing the needs of eventual revalidation.
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The limited dynamic range of the majority of auditory-nerve fibers represents a difficulty in accounting for normal hearing capabilities over the known psychoacoustic intensity range. The presence of noise is an additional complication because it will tend to saturate these fibers, thereby considerably reducing their dynamic range, i.e., the range of mean firing rates. In this study, simulations involving a model of auditory nerve and cochlear nucleus neurons were conducted using pure-tone stimuli in the presence of noise. The main focus is on the role of inhibition in regulating the activity of cells, improving their capability to represent signals in background noise. This concerns in particular those inhibitory neurons that receive input from a wide range of auditory-nerve fibers and respond with an onset chopper pattern. A detailed model of stellate cells is used. It allows several parameters such as the number, location, and strength of inputs to be manipulated. The fist part of this paper presents the model and its responses to pure-tone and noise stimuli presented separately. The model's capacity to generalize to tone/noise combinations is then tested. Responses to these stimuli are found to be qualitatively similar to neurophysiological findings. Model neurons exhibit appropriate shifts in their rate-level functions and their responses are inhibited or suppressed by tones outside their characteristic frequency. The model stellate cell is also found to display many of the temporal patterns reported in electrophysiological studies as a result of appropriate settings of certain parameters. Therefore, the model is sufficient to account for a larger number of findings and should serve as a basis for predicting responses to novel stimuli, or as a building block for modeling larger networks.
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A method is described in which the direct influence of anoxia and ototoxic agents on the vestibular system can be studied. After fenestration of the lateral semicircular canal in pigeons, a vestibular whole nerve action potential (VAP) could be recorded during acoustic stimulation. The cochlear whole nerve action potential (CAP) was recorded simultaneously. The influence of ototoxic agents and anoxia upon the amplitude of these action potentials was studied.
Using the in vitro isolated whole brain preparation of the guinea pig maintained at 29 degrees C, we intracellularly recorded and stained cochlear nucleus (CN) neurons and auditory nerve (AN) fibers. Discharge properties of CN cells and AN axons were tested in response to 50-ms trains of electrical pulses delivered to the AN at rates ranging from 100 to 1000 pulses per second (pps). At low stimulation rates (200-300 pps), the discharges of AN fibers and a large proportion of principal cells (bushy, octopus, stellate) in the ventral cochlear nucleus (VCN) followed with high probability each pulse in the train, resulting in synchronization of discharges within large populations of AN fibers and CN cells. In contrast, at high stimulation rates (500 pps and higher), AN fibers and many VCN cells exhibited "primary-like", "onset" and some other discharge patterns resembling those produced by natural sound stimuli. Unlike cells in the VCN, principal cells (pyramidal, giant) of the dorsal CN did not follow the stimulating pulses even at low rates. Instead, they often showed "pauser" and "build-up" patterns of activity, characteristic for these cells in conditions of normal hearing. We hypothesize that, at low stimulation rates, the response behavior of AN fibers and VCN cells is different from the patterns of neuronal activity related to normal auditory processing, whereas high stimulation rates produce more physiologically meaningful discharge patterns. The observed differences in discharge properties of AN fibers and CN cells at different stimulation rates can contribute to significant advantages of high- versus low-rate electrical stimulation of the AN used for coding sounds in modern cochlear implants.
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The aim of the present study was to examine the role of the olivocochlear system in auditory processing by examining the long-term effects of cochlear de-efferentation on auditory nerve response properties in adult chinchillas. Spontaneous rates, response thresholds, tuning curves, discharge rate-level functions, and adaptation of single auditory nerve fibers were measured in chinchillas with complete cochlear de-efferentation produced by sectioning the olivocochlear bundle in the internal auditory meatus. De-efferentation was verified as successful on the basis of acetylcholinesterase staining of surface preparations of the organ of Corti. Following chronic de-efferentation, there was a striking decrease in spontaneous rate, consistent with earlier observations in cats. In addition, the present study shows that complete de-efferentation results in: (1) increased driven discharge rates and decreased dynamic range of discharge rate-level functions, (2) larger onset-to-steady state ratio of discharge rate at moderate intensities, and (3) a hypersensitive tail of the tuning curve. These effects, largely confined to neurons that were most sensitive to frequencies between 2-8 kHz, indicate that the cochlear efferent system is important in maintaining normal function (e.g., frequency and intensity selectivity) of the auditory periphery by modulating auditory nerve fiber response properties.
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