Patterns of degeneration in the caudal cochlear nucleus of the cat after cochlear ablation

Kane, Eileen Cohen

doi:10.1002/ar.1091790106

Cited by 86 publications

(38 citation statements)

References 24 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%

“…Both auditory nerve degeneration and brainstem plasticity occur much more rapidly after cochlear ablations than after acoustic trauma. While there is some variation across species, generally degenerating fibers in the CN are seen as early as 12-48 hours after a lesion, and disappear by 10 days - 1 month (Osen, 1970, Cohen et al, 1972, Gentschev and Sotelo, 1973, Kane, 1974, Benson et al, 1997, Bilak et al, 1997, Morest et al, 1997). Sprouting and synaptogenesis after cochlear ablations occur on the same time scale as auditory nerve degeneration.…”

Section: Discussionmentioning

confidence: 99%

“…One form of denervation follows exposure to prolonged, loud sounds (acoustic trauma, AT); AT results in the death of hair cells and degeneration of the auditory nerve (reviews in Saunders et al, 1985, Kujawa and Liberman, 2009, Gold and Bajo, 2014). Axons of the acoustic nerve synapse in the three subdivisions of the cochlear nuclei (CN), the dorsal cochlear nucleus (DC), and the posterior (VCP) and anterior (VCA) subdivisions of the ventral cochlear nucleus (Cohen et al, 1972, Kane, 1974, Jones and Casseday, 1979). Noise trauma therefore removes a major input to these structures.…”

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: Discussionmentioning

confidence: 99%

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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“…The described decrease in cell density is also in accord with earlier studies that demonstrated anatomical changes related to apoptosis-inducing processes and tissue shrinkage (Aarnisalo et al, 2000), axon degeneration (Kim et al, 1997(Kim et al, , 2004, and loss of synaptic connectivity (Benson et al, 1997;Kane, 1974) in the auditory brainstem. Further, changes in synaptic connectivity at the calyx of Held synapses in the trapezoid body ( Jean-Baptiste and Morest, 1975), and a reduction of cell density in the MGB and primary auditory cortex , have also been observed.…”

supporting

confidence: 90%

Differential Impact of Temporary and Permanent Noise-Induced Hearing Loss on Neuronal Cell Density in the Mouse Central Auditory Pathway

Gröschel

Götze

Ernst

et al. 2010

Journal of Neurotrauma

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Although acoustic overstimulation has a major pathophysiological influence on the inner ear, central components of the auditory pathway can also be affected by noise-induced hearing loss (NIHL). The present study investigates the influence of a noise-induced temporary threshold shift (TTS) and/or permanent threshold shift (PTS) on neuronal cell densities in key structures of the central auditory pathway. Mice were noise-exposed (3 h, 5-20 kHz) at 115 dB sound pressure level (SPL) under anesthesia, and were investigated immediately (TTS group, n = 5) after the exposure, or 1 week later (PTS group, n = 6). Unexposed animals were used as controls (n = 7). Frequency-specific auditory brainstem responses (ABR) were recorded to examine auditory thresholds. Cell density was determined within the dorsal (DCN) and ventral (VCN) cochlear nucleus; the central nucleus of the inferior colliculus (ICC); the dorsal, ventral, and medial subdivisions of the medial geniculate body (MGBd, MGBv, and MGBm); and layer I to VI of the primary auditory cortex (AI I-VI). ABR thresholds were significantly elevated in the TTS group (52-69 dB SPL) and in the PTS group (33-42 dB SPL) compared to controls. There was a significant decrease in cell density only in the VCN of the TTS group (-10%), most likely induced by the acute overstimulation of neurons. Cell density was significantly reduced in all investigated auditory structures at 1 week post-exposure (PTS group), except in layer II of the AI (VCN: -30% and DCN: -30% (high-frequency); -39% (low-frequency); ICC: -31%; MGBd: -31%; MGBm: -28%; MGBv: -31%; AI: -10 to 14%). Thus there were dramatic changes within the neuronal cytoarchitecture of the central auditory pathway following a single noise exposure. The present findings should help clinicians to better understand the complex psychoacoustic phenomena of NIHL.

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“…The reason for this discrepancy is unknown. It may have occurred because cochlear nerve endings constitute a smaller fraction of the synaptic endings in the DCN than in the VCN (Cohen et al, 1972;Osen, 1970;Kane, 1974), reflecting the greater preponderance in the DCN of endings from both descending and intrinsic pathways (Kane and Conlee, 1979;Kane and Finn, 1977). The present methods may not reveal the loss of this smaller proportion of terminals.…”

Section: Synaptophysin Immunolabeling In the Dorsal Cnmentioning

confidence: 69%

Synaptophysin immunoreactivity in the cochlear nucleus after unilateral cochlear or ossicular removal

Benson

Gross

Suneja

et al. 1997

Synapse

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This study determined if unilateral cochlear removal in adult guinea pigs led to synaptic loss followed by synaptogenesis in the cochlear nucleus (CN) and if unilateral middle ear ossicle removal led to synaptic loss in the CN. Synaptic endings were identified immunohistochemically, using a monoclonal antibody to synaptophysin. Immunolabeling was quantified densitometrically in the CN 4-161 days after cochlear removal and 161 days after ossicle removal. Fiber degeneration was visualized with the Nauta-Rasmussen silver method. Tissue shrinkage was measured from drawings of CN sections. Compared to the contralateral side, immunolabeling density ipsilaterally was reduced by 4 days in the anterior division of the anteroventral CN (a-AVCN) and by 7 days in the anterior part of the posteroventral CN (a-PVCN). At 7 days, preterminal fiber degeneration was abundant in both areas. These findings were consistent with the loss of cochlear nerve endings and fibers. At later times, immunolabeling density recovered. In the a-AVCN, tissue shrinkage explained approximately half the recovery of staining density; the rest was attributed to synaptogenesis. In the a-PVCN, the entire recovery was attributed to tissue shrinkage. In the polymorphic layer of the dorsal CN, immunostaining density increased transiently at 4 days, while at 7 days preterminal fiber degeneration was abundant. A net loss of synaptic endings was not detected immunohistochemically. The increased immunostaining density may reflect a transient growth of immature processes or presynaptic endings. Ossicle removal produced a deficit in immunolabeling density only in the ipsilateral a-PVCN, without fiber degeneration, suggesting a loss of presynaptic endings or of synaptophysin expression.

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Patterns of degeneration in the caudal cochlear nucleus of the cat after cochlear ablation

Cited by 86 publications

References 24 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

Differential Impact of Temporary and Permanent Noise-Induced Hearing Loss on Neuronal Cell Density in the Mouse Central Auditory Pathway

Synaptophysin immunoreactivity in the cochlear nucleus after unilateral cochlear or ossicular removal

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