The effects of congenital deafness on auditory nerve synapses and globular bushy cells in cats

Redd, Elizabeth E.; Pongstaporn, Tan; Ryugo, David K.

doi:10.1016/s0378-5955(00)00129-5

Cited by 60 publications

(53 citation statements)

References 55 publications

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“…These changes were interpreted as a compensatory response to diminished transmitter release. Similar alterations were also reported in globular bushy cell terminals (Redd et al, 2000), whereas endings on multipolar cells showed less extensive changes (Redd et al, 2002). Significantly, the endbulbs of Held exhibited recovery of more normal synaptic structure after 3 months of electrical stimulation via a cochlear implant (Ryugo et al, 2005).…”

Section: Topography Of Auditory Nerve Projections To the Cochlear Nucsupporting

confidence: 72%

Factors influencing neurotrophic effects of electrical stimulation in the deafened developing auditory system

et al. 2008

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Research in animal models has demonstrated that electrical stimulation from a cochlear implant (CI) may help prevent degeneration of the cochlear spiral ganglion (SG) neurons after deafness. In cats deafened early in life, effective stimulation of the auditory nerve with complex signals for several months preserved a greater density of SG neurons in the stimulated cochleae as compared to the contralateral deafened ear. However, SG survival was still far from normal even with early intervention with an implant. Thus, pharmacologic agents and neurotrophic factors that might be used in combination with an implant are of great interest. Exogenous administration of GM1 ganglioside significantly reduces SG degeneration in deafened animals studied at 7-8 weeks of age, but after several months of stimulation, GM1-treated animals show only modestly better preservation of SG density compared to age-matched non-treated animals. A significant factor influencing neurotrophic effects in animal models is insertion trauma, which results in significant regional SG degeneration. Thus, an important goal is to further improve human CI electrode designs and insertion techniques to minimize trauma.Another important issue for studies of neurotrophic effects in the developing auditory system is the potential role of critical periods. Studies examining animals deafened at 30 days of age (rather than at birth) have explored whether a brief initial period of normal auditory experience affects the vulnerability of the SG or cochlear nucleus (CN) to auditory deprivation. Interestingly, SG survival in animals deafened at 30-days was not significantly different from age-matched neonatally deafened animals, but significant differences were observed in the central auditory system. CN volume was significantly closer to normal in the animals deafened at 30 days as compared to neonatally deafened animals. However, no difference was observed between the stimulated and contralateral CN volumes in either deafened group. Measurements of AVCN spherical cell somata showed that after later onset of deafness in the 30-day deafened group, mean cell size was significantly closer to normal than in the neonatally deafened group. Further, electrical stimulation elicited a significant increase in spherical cell size in the CN ipsilateral to the implant as compared to the contralateral CN in both deafened groups.Neuronal tracer studies have examined the primary afferent projections from the SG to the CN in neonatally deafened cats. CN projections exhibit a clear cochleotopic organization despite severe auditory deprivation from birth. However, when normalized for the smaller CN size after deafness, projections were 30-50% broader than normal. After unilateral electrical stimulation there was no difference between projections from the stimulated and non-stimulated ears. These findings suggest that early normal auditory experience may be essential for the normal development (or subsequent Publisher's Disclaimer: This is a PDF file of an unedited manuscript...

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Section: Topography Of Auditory Nerve Projections To the Cochlear Nucsupporting

confidence: 72%

Factors influencing neurotrophic effects of electrical stimulation in the deafened developing auditory system

et al. 2008

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“…Wave 2 is dominated by the synchronous activity of VCN globular bushy cells (GBCs: Henry 1979;Melcher and Kiang 1996). GBCs receive endbulb synapses from the auditory nerve (Fekete et al 1984;Rouiller et al 1986;Redd et al 2000;Spirou et al 2005) and respond to sound with short latency and high temporal precision (Joris and Smith 2008).…”

Section: Alterations Of Synaptic Transmission In the Auditory Nerve Amentioning

confidence: 99%

“…B The vesicular chain of the MAC in higher magnification (color fill). Redd et al 2000;Lee et al 2003). Subsequent functional assessments have confirmed irregular transmission characteristics (Oleskevich and Walmsley 2002;Oleskevich et al 2004;Manis 2005, 2006).…”

Section: Fig 10mentioning

confidence: 99%

The Medial Olivocochlear System Attenuates the Developmental Impact of Early Noise Exposure

Lauer

May

2011

JARO

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The early onset of peripheral deafness profoundly alters the functional maturation of the central auditory system. A prolonged exposure to an artificial acoustic environment has a similar disruptive influence. These observations establish the importance of normal patterns of sound-driven activity during the initial stages of auditory development. The present study was designed to address the role of cochlear gain control during these activity-dependent developmental processes. It was hypothesized that the regulation of auditory nerve activity by the medial olivocochlear system (MOCS) would preserve normal development when the immature auditory system was challenged by continuous background noise. To test this hypothesis, knock-out mice lacking MOCS feedback were reared in noisy or quiet environments and then evaluated with behavioral paradigms for auditory processing deficits. Relative to wild-type controls, noise-reared knock-out mice showed a decreased ability to process rapid acoustic events. Additional anatomical and physiological assessments linked these perceptual deficits to synaptic defects in the auditory brainstem that shared important features with human auditory neuropathy. Our findings offer a new perspective on the potentially damaging effects of environmental noise and how these risks are ameliorated by the protective role of MOCS feedback.

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“…Presumably, PL and AN RLFs were similar because the operating mode of these synapses is to produce a postsynaptic spike whenever there is a presynaptic spike, as demonstrated by their complex action potentials which contain both a pre-and a postsynaptic potential (Pfeiffer 1966;Bourk 1976; but see Kopp-Scheinpflug et al 2002). Bushy-cell synapses are altered in morphology following cochlear damage (Ryugo et al 1997;Redd et al 2000), but the implications for synaptic transmission of these morphological changes are not clear. In fact, some evidence suggests that AN/VCN synapses are strengthened following cochlear degeneration (Oleskovich and Walmsley 2002).…”

Section: Rate Functions Of Primary-and Non-primary-like Neurons Aftermentioning

confidence: 99%

Encoding Intensity in Ventral Cochlear Nucleus Following Acoustic Trauma: Implications for Loudness Recruitment

Cai

Young

2008

JARO

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Loudness recruitment, an abnormally rapid growth of perceived loudness with sound level, is a common symptom of sensorineural hearing loss. Following acoustic trauma, auditory-nerve rate responses are reduced, and rate grows more slowly with sound level, which seems inconsistent with recruitment (Heinz et al., J. Assoc. Res. Otolaryngol. 6:91-105, 2005). However, rate-level functions (RLFs) in the central nervous system may increase in either slope or saturation value following trauma (e.g., Salvi et al., Hear. Res. 147:261-274, 2000), suggesting that recruitment may arise from central changes. In this paper, we studied RLFs of neurons in ventral cochlear nucleus (VCN) of the cat after acoustic trauma. Trauma did not change the general properties of VCN neurons, and the usual VCN functional classifications remained valid (chopper, primary-like, onset, etc.). After trauma, non-primary-like neurons, most noticeably choppers, exhibited elevated maximum discharge rates and steeper RLFs for frequencies at and near best frequency (BF). Primary-like neurons showed the opposite changes. To relate the neurons' responses to recruitment, rate-balance functions were computed; these show the sound level required to give equal rates in a normal and a traumatized ear and are analogous to loudness balance functions that show the sound levels giving equal perceptual loudness in the two ears of a monaurally hearing-impaired person. The ratebalance functions showed recruitment-like steepening of their slopes in non-primary-like neurons in all conditions. However, primary-like neurons showed recruitment-like behavior only when rates were summated across neurons of all BFs. These results suggest that the non-primary-like, especially chopper, neurons may be the most peripheral site of the physiological changes in the brain that underlie recruitment.

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The effects of congenital deafness on auditory nerve synapses and globular bushy cells in cats

Cited by 60 publications

References 55 publications

Factors influencing neurotrophic effects of electrical stimulation in the deafened developing auditory system

Factors influencing neurotrophic effects of electrical stimulation in the deafened developing auditory system

The Medial Olivocochlear System Attenuates the Developmental Impact of Early Noise Exposure

Encoding Intensity in Ventral Cochlear Nucleus Following Acoustic Trauma: Implications for Loudness Recruitment

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