Single unit recordings in the auditory nerve of congenitally deaf white cats: Morphological correlates in the cochlea and cochlear nucleus

Abstract

It is well known that experimentally induced cochlear damage produces structural, physiological, and biochemical alterations in neurons of the cochlear nucleus. In contrast, much less is known with respect to the naturally occurring cochlear pathology presented by congenital deafness. The present study attempts to relate organ of Corti structure and auditory nerve activity to the morphology of primary synaptic endings in the cochlear nucleus of congenitally deaf white cats. Our observations reveal that the amount of sound-evoked spike activity in auditory nerve fibers influences terminal morphology and synaptic structure in the anteroventral cochlear nucleus. Some white cats had no hearing. They exhibited severely reduced spontaneous activity and no sound-evoked activity in auditory nerve fibers. They had no recognizable organ of Corti, presented >90% loss of spiral ganglion cells, and displayed marked structural abnormalities of endbulbs of Held and their synapses. Other white cats had partial hearing and possessed auditory nerve fibers with a wide range of spontaneous activity but elevated sound-evoked 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 cell loss in the base. The spatial distribution of spiral ganglion cell loss correlated with the pattern of hair cell loss. Primary neurons of hearing-impaired cats displayed structural abnormalities of their endbulbs and synapses in the cochlear nucleus which were intermediate in form compared to normal and totally deaf cats. Changes in endbulb structure appear to correspond to relative levels of deafness. These data suggest that endbulb structure is significantly influenced by sound-evoked auditory nerve activity.

Heterogeneous Ca2+ influx along the adult calyx of held: A structural and computational study

“…The complexity of calyx geometry, reported here as fractal dimension, was less than that of the largest nerve terminals of auditory-nerve fibers in the cochlear nucleus, the end bulbs of Held (Ryugo et al, 1998), but was similar to another large auditory-nerve terminal, the modified end bulbs (Redd et al, 2000). Our observation that fractal dimension was independent of calyx size corresponds to observed changes of modified end bulb size in deaf animals without a change in this parameter (Redd et al, 2000).…”

Congenital and Prolonged Adult-Onset Deafness Cause Distinct Degradations in Neural ITD Coding with Bilateral Cochlear Implants

“…Acutely deafened 9 6.4 (5-21) 7.1 (5-22) 0.4 (0.2-1.3) Long-term deafened 3 6.1 (6-10) 12.0 (12-17) 6.4 (5.9-6.4) Congenitally deaf 9 Deaf at birth 11.6 (6-36) 11.6 (5.9-35.9) Young 4 Deaf at birth 7.6 (6-11) 7.6 (5. There is significant variation among white cats with respect to cochlear pathology and degree of deafness (Heid et al 1998;Ryugo et al 1998;Ryugo et al 2003). Therefore, deafness in this group was verified in the laboratory of Dr. David Ryugo at 4 and 8 postnatal weeks using tone-and click-evoked ABR measurements .…”

“…Both congenital deafness and neonatal deafening cause structural abnormalities in the brainstem circuits that process ITD, including the endbulbs of Held in ventral cochlear nucleus (Ryugo et al 1997;Ryugo et al 1998;Lee et al 2003;Ryugo et al 2010) and inhibitory synapses onto MSO neurons (Tirko and Ryugo 2012). Chronic diotic stimulation using clinical CI processors largely reverses these changes (O'Neil et al 2010;Tirko and Ryugo 2012).…”

Restoring hearing symmetry with two cochlear implants or one cochlear implant and a contralateral hearing aid

“…Studies in the congenitally deaf white cat reveal that synapses of auditory nerve endings are abnormal, such as between end bulbs of Held and spherical bushy cells [18][19][20], as well as between modified end bulbs and globular bushy cells [21]. In addition, the synaptic abnormalities are present at an early age (6 months) in the deaf white cat.…”