SINGLE-UNIT RECORDINGS IN THE AUDITORY-NERVE OF CONGENITALLY DEAF WHITE CATS - MORPHOLOGICAL CORRELATES IN THE COCHLEA AND COCHLEAR NUCLEUS

It is well known that experimentally induced cochlear damage produces structural, physiological, and biochemical alterations in neurons of t he cochlear nucleus. In contrast, much less is known with respect to t he naturally occurring cochlear pathology presented by congenital deaf ness. The present study attempts to relate organ of Corti structure an d auditory nerve activity to the morphology of primary synaptic ending s in the cochlear nucleus of congenitally deaf white cats. Our observa tions reveal that the amount of sound-evoked spike activity in auditor y nerve fibers influences terminal morphology and synaptic structure i n the anteroventral cochlear nucleus. Some white cats had no hearing. They exhibited severely reduced spontaneous activity and no sound-evok ed activity in auditory nerve fibers. They had no recognizable organ o f Corti, presented >90% loss of spiral ganglion cells, and displayed m arked structural abnormalities of endbulbs of Held and their synapses. Other white cats had partial hearing and possessed auditory nerve fib ers with a wide range of spontaneous activity but elevated sound-evoke d thresholds (60-70 dB SPL). They also exhibited obvious abnormalities in the tectorial membrane, supporting cells, and Reissner's membrane throughout the cochlear duct and had complete inner and outer hair cel l loss in the base. The spatial distribution of spiral ganglion cell l oss correlated with the pattern of hair cell loss. Primary neurons of hearing-impaired cats displayed structural abnormalities of their endb ulbs and synapses in the cochlear nucleus which were intermediate in f orm compared to normal and totally deaf cats. Changes in endbulb struc ture appear to correspond to relative levels of deafness. These data s uggest that endbulb structure is significantly influenced by sound-evo ked auditory nerve activity. J. Comp. Neurol. 397:532-548, 1998. (C) 1 998 Wiley-Liss, Inc.