Fine structure of long‐term changes in the cochlear nucleus after acoustic overstimulation: Chronic degeneration and new growth of synaptic endings

Kim, J.J.; Gross, J.; Potashner, S.J.; Morest, D. Kent

doi:10.1002/jnr.20212

Cited by 42 publications

(37 citation statements)

References 17 publications

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“…Our results on the pattern of projections of the auditory nerve to the CN are in good agreement with the earlier reports showing degenerating fibers in dorsal and ventral cochlear nuclei (Cohen et al, 1972, Kane, 1974, Albright et al, 1983, Kim et al, 2004a, Kim et al, 2004c, b, Feng et al, 2012). The decrease in SV2-labeled presynaptic terminals in the VCP compared to control animals also supports the interpretation that this silver staining protocol is in fact labeling degenerating auditory nerve fibers and terminals.…”

Section: Discussionsupporting

confidence: 93%

“…There are both anatomical and electrophysiological data showing plastic reorganization in the CN after AT. Changes include the formation of new synapses and axonal sprouting (Benson et al, 1997, Bilak et al, 1997, Michler and Illing, 2002, Kim et al, 2004a, Kim et al, 2004c, b, Dong et al, 2010b). There is an increase of somatosensory input to the DC (Shore et al, 2008, Koehler et al, 2011, Dehmel et al, 2012, Zeng et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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Effects of acoustic trauma on the auditory system of the rat: The role of microglia

Baizer

Wong

Manohar³

et al. 2015

Neuroscience

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Exposure to loud, prolonged sounds (acoustic trauma, AT) leads to the death of both inner and outer hair cells (IHCs and OHCs), death of neurons of the spiral ganglion and degeneration of the auditory nerve. The auditory nerve (8cn) projects to the three subdivisions of the cochlear nuclei (CN), the dorsal cochlear nucleus (DC) and the anterior (VCA) and posterior (VCP) subdivisions of the ventral cochlear nucleus. There is both anatomical and physiological evidence for plastic reorganization in the denervated CN after AT. Anatomical findings show axonal sprouting and synaptogenesis; physiologically there is an increase in spontaneous activity suggesting reorganization of circuitry. The mechanisms underlying this plasticity are not understood. Recent data suggest that activated microglia may have a role in facilitating plastic reorganization in addition to removing trauma-induced debris. In order to investigate the roles of activated microglia in the CN subsequent to acoustic trauma we exposed animals to bilateral noise sufficient to cause massive hair cell death. We studied four groups of animals at different survival times: 30 days, 60 days, 6 months and 9 months. We used silver staining to examine the time course and pattern of auditory nerve degeneration, and immunohistochemistry to label activated microglia in the denervated CN. We found both degenerating auditory nerve fibers and activated microglia in the CN at 30 and 60 days and 6 months after AT. There was close geographic overlap between the degenerating fibers and activated microglia, consistent with a scavenger role for activated microglia. At the longest survival time, there were still silver-stained fibers but very little staining of activated microglia in overlapping regions. There were, however, activated microglia in the surrounding brainstem and cerebellar white matter.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Effects of acoustic trauma on the auditory system of the rat: The role of microglia

Baizer

Wong

Manohar³

et al. 2015

Neuroscience

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“…The principal factors that increase cell excitability are indicated. change such as those observed at the neuronal level by Kim et al (2004b). Such changes could account for the temporal forms of plasticity described in Section 1.…”

Section: Mechanism Of Temporal Plasticity and Tinnitusmentioning

confidence: 70%

Tinnitus as a plastic phenomenon and its possible neural underpinnings in the dorsal cochlear nucleus

2005

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“…Loss of OHCs following noise exposure leads to a number of plastic changes in the cochlear nucleus: widespread degeneration of fibers in the DCN was found by Kim et al [39] even in cases where there was little damage to IHCs or primary afferents. Other effects associated with OHC loss include changes in excitatory neurotransmission [40] and changes in the balance of excitatory and inhibitory synapses [41]. Removal of eighth nerve input to the cochlear nucleus can also cause changes in the expression of certain neurotransmitter (glycine) receptors [42,43], and in the biophysical properties of ion conductances [44].…”

Section: Electrical Stimulation Of the Dcn Causes Changes In The Loudmentioning

confidence: 99%

Summary of evidence pointing to a role of the dorsal cochlear nucleus in the etiology of tinnitus

Kaltenbach

2006

Acta Oto-Laryngologica

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Evidence has accumulated in the last decade that the dorsal cochlear nucleus (DCN) may be an important site in the etiology of tinnitus. This evidence comes from a combination of studies conducted in animals and humans. This paper will review the key findings, as follows. 1) Direct electrical stimulation of the DCN leads to changes in the loudness of tinnitus. This suggests that the loudness of tinnitus may be linked to changes in the level of neural activity in the DCN. 2) Exposure to tinnitus inducers, such as intense sound or cisplatin, causes neural activity in the DCN to become chronically elevated, a condition known as neuronal hyperactivity. 3) This hyperactivity is very similar to the activity that is evoked in the DCN by sound stimulation, suggesting that the hyperactivity represents a code that signals the presence of sound, even when there is no longer any sound stimulus. 4) Noise-induced hyperactivity in the DCN is correlated with tinnitus. Behavioral studies have demonstrated that animals exposed to the same intense sound that causes hyperactivity in the DCN develop tinnitus-like percepts. The correlation between the level of hyperactivity and the behavioral index of tinnitus was found to be statistically significant. 5) The DCN is a polysensory integration center, and electrophysiological studies have shown that both spontaneous activity and hyperactivity of neurons in the DCN can be modulated by stimulation of certain ipsilateral cranial nerves, such as the sensory branch of the trigeminal nerve. This ipsilateral modulation of DCN activity offers a plausible explanation of how tinnitus, when perceived on one side, can be modulated by certain manipulations of the head and neck on the side ipsilateral to the tinnitus, but rarely on the contralateral side. 6) The DCN exhibits various forms of neuronal plasticity that parallel the various forms of plasticity that characterize tinnitus. These findings collectively strengthen the view that the DCN may be a key structure that should be included as a target of anti-tinnitus treatment.

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Fine structure of long‐term changes in the cochlear nucleus after acoustic overstimulation: Chronic degeneration and new growth of synaptic endings

Cited by 42 publications

References 17 publications

Effects of acoustic trauma on the auditory system of the rat: The role of microglia

Effects of acoustic trauma on the auditory system of the rat: The role of microglia

Tinnitus as a plastic phenomenon and its possible neural underpinnings in the dorsal cochlear nucleus

Summary of evidence pointing to a role of the dorsal cochlear nucleus in the etiology of tinnitus

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