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An electron microscopic study of the cerebral cortex of mutant deaf mice (Deol's dn gene) has shown differences in synaptic organisation between these mice and normally hearing ones. In the auditory cortex of the deaf mice, there are fewer synapses and these are larger than in the normally hearing, whereas there is no difference between these two categories in the visual cortex. These results are the reverse of those observed by other authors in the occipital cortex of rats raised in an enriched or impoverished environment. In humans, the functional consequences of early hearing loss have been investigated on moderately to severely deaf (60-80 db mean loss) youngsters, who have been tested for their capacity of categorical perception, auditory discrimination, and production of significant contrasts between stop consonants. Categorical perception was absent in alt but one subject. Auditory discrimination was poor for both the voiced-voiceless contrast and the place of articulation contrast. In the production experiments, the subjects had greater difficulty in producing the voiced-voiceless than the place of articulation contrasts. The possible relevance of these animal and human studies to cochlear implantation is discussed. I. ANIMAL STUDIESAuditory deprivation in animals can be obtained either by destruction of the inner ear or by restriction of auditory input.Ear destruction has been done by Levi-Montalcini (1949) and Powell & Erulkar (1961). It results in transsynaptic atrophy of the brainstem and thalamic auditory nuclei, this atrophy consisting of a reduction in size of the neurons without actual neuronal destruction, a lesion which might be reversible if proper stimulation could be restored.Complete suppression of auditory input to the intact animal cannot be achieved, because of bone conduction perception of the animal's own inner noises, so that only the results of auditory restriction are available (Wolf, 1943;Gauron & Becker, 1959). New-born rats submitted to such a restriction for several weeks or months have no difficulty in learning frequency discrimination but are less proficient than controls for discrimination of temporal sequences (Tees, 1967), and their hearing thresholds measured by electric response audiometry are elevated (Batkin et al., 1970). Webster & Webster (1977-79) observed that both postnatal auditory deprivation and experimentally produced conductive hearing loss in mice result in incomplete maturation of most brainstem auditory neurons. There is a critical period, before 45 days of age, during which acoustic stimulation has a more pronounced effect on neuronal maturation than the same stimulation given between 45 and 90 days. The changes observed were only partially reversible in animals which were submitted to auditory deprivation until 45 days of age and then placed in a normal acoustic environment. Bock et al. (1982), studying Deol's strain of deafness (dn) mutant mice, have recorded evoked potentials of normal or higher than normal amplitude at the level of the inferior colli...

An electron microscopic study of the cerebral cortex of mutant deaf mice (Deol's dn gene) has shown differences in synaptic organisation between these mice and normally hearing ones. In the auditory cortex of the deaf mice, there are fewer synapses and these are larger than in the normally hearing, whereas there is no difference between these two categories in the visual cortex. These results are the reverse of those observed by other authors in the occipital cortex of rats raised in an enriched or impoverished environment. In humans, the functional consequences of early hearing loss have been investigated on moderately to severely deaf (60-80 db mean loss) youngsters, who have been tested for their capacity of categorical perception, auditory discrimination, and production of significant contrasts between stop consonants. Categorical perception was absent in alt but one subject. Auditory discrimination was poor for both the voiced-voiceless contrast and the place of articulation contrast. In the production experiments, the subjects had greater difficulty in producing the voiced-voiceless than the place of articulation contrasts. The possible relevance of these animal and human studies to cochlear implantation is discussed. I. ANIMAL STUDIESAuditory deprivation in animals can be obtained either by destruction of the inner ear or by restriction of auditory input.Ear destruction has been done by Levi-Montalcini (1949) and Powell & Erulkar (1961). It results in transsynaptic atrophy of the brainstem and thalamic auditory nuclei, this atrophy consisting of a reduction in size of the neurons without actual neuronal destruction, a lesion which might be reversible if proper stimulation could be restored.Complete suppression of auditory input to the intact animal cannot be achieved, because of bone conduction perception of the animal's own inner noises, so that only the results of auditory restriction are available (Wolf, 1943;Gauron & Becker, 1959). New-born rats submitted to such a restriction for several weeks or months have no difficulty in learning frequency discrimination but are less proficient than controls for discrimination of temporal sequences (Tees, 1967), and their hearing thresholds measured by electric response audiometry are elevated (Batkin et al., 1970). Webster & Webster (1977-79) observed that both postnatal auditory deprivation and experimentally produced conductive hearing loss in mice result in incomplete maturation of most brainstem auditory neurons. There is a critical period, before 45 days of age, during which acoustic stimulation has a more pronounced effect on neuronal maturation than the same stimulation given between 45 and 90 days. The changes observed were only partially reversible in animals which were submitted to auditory deprivation until 45 days of age and then placed in a normal acoustic environment. Bock et al. (1982), studying Deol's strain of deafness (dn) mutant mice, have recorded evoked potentials of normal or higher than normal amplitude at the level of the inferior colli...

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