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Results for “Cochlear nucleus degeneration”

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At least 19 recordsLinked to original sources
PubMed1978

Kainic acid injections result in degeneration of cochlear nucleus cells innervated by the auditory nerve.

When kainic acid, a putative neurotoxin for neurons with glutamatergic input, is injected into the brainstem, it produces a selective pattern of degeneration in the cochlear nucleus. The rate and extent of degeneration is correlated with the distribution of the primary auditory fibers. This evidence supports the hypothesis that glutamate is the neurotransmitter for primary auditory fibers.

Animals↗
PubMed1998

Long-term degeneration in the cochlear nerve and cochlear nucleus of the adult chinchilla following acoustic overstimulation.

Adult chinchillas were exposed once to an octave-band noise, centered at 4 kHz, and allowed to survive for 16 days or for 1, 2, 4, and 8 months. Axonal degeneration was mapped in the cochlear nucleus, using the Nauta-Rasmussen silver method, and related to hair cell damage and to loss of myelinated nerve fibers in the osseous spiral lamina of the cochlea. Axonal degeneration in the dorsal cochlear nucleus had already reached a peak by 16 days and disappeared after 1 month. Meanwhile, myelinated nerve fiber degeneration in the cochlea extended basally, followed 2 weeks to 2 months later by spread of axonal degeneration into the corresponding high-frequency region of the ventral cochlear nucleus. Axonal degeneration occurred early in the low-frequency region of the ventral cochlear nucleus, followed 2-4 weeks later by spread of myelinated fiber degeneration into more apical regions of the cochlea. New degeneration of axons in the cochlear nerve and in the ventral cochlear nucleus continued to occur for up to 8 months after stimulation. These findings imply that plastic changes in the central auditory pathways could play a role in the long-term effects of cochlear damage and acoustic overstimulation, possibly leading to a chronic neurodegenerative condition in the ear and in the brain.

Acoustic Stimulation↗
PubMedDate not supplied

Progressive degeneration in the cochlear nucleus after chemical destruction of the cochlea.

In the guinea pig, the organ of Corti and the spiral ganglion cells were destroyed by administering gentamicin into the inner ear. The antero-ventral cochlear nucleus (AVCN) was studied with electron microscopy 15 and 30 days after treatment. There does not seem to be a specific type of degeneration induced by the drug. For nerve terminals, a progressive degeneration occurred: after 15 days, clear and swollen boutons appeared and after 30 days an electron-dense type of degeneration was observed. The cell bodies of the AVCN did not seem altered infirming a rapid, direct or indirect, neurotoxic effect of the drug.

Animals↗
PubMed1993

Glial populations in the juvenile and adult Mongolian gerbil: relationship to spongiform degeneration of the ventral cochlear nucleus.

The gerbil cochlear nucleus is subject to a spongiform degeneration, the progression of which is dependent on auditory functional activity. The most affected region is the ventrolateral aspect of the caudal posterior ventral cochlear nucleus (PVCN). Lesion density and glial changes were quantified in this region for two age groups. Spongiform lesions increased significantly in area density from 4% in 60-day-old gerbils to 14% in 6-month-old gerbils. In spite of this significant increase in tissue damage, no gliosis was found. A significant age-related decrease in oligodendrocyte density was found in the PVCN.

Acoustic Stimulation↗
PubMed1997

Spongiform degeneration of the gerbil cochlear nucleus: an ultrastructural and immunohistochemical evaluation.

Observations from ultrastructural and immunohistochemical studies suggest that spongiform lesions in the gerbil cochlear nucleus are derived principally from dendrites. Almost one-fifth of the lesion profiles examined ultrastructurally exhibited synaptic contacts with axon terminals. In addition, approximately 80% of lesions are immunopositive for the dendrite-specific microtubule associated protein, MAP2. Ultrastructural studies showed a small percentage (8%) of lesions were derived from myelinated axons, although none were immunohistochemically labelled with antibodies to the tau protein. Staining with the astrocyte-specific markers GFAP, S-100 and vimentin yielded equivocal results, but did not support a major role for astrocytes in lesion formation. The histological profile matches that seen in some other well characterized types of spongiform degeneration.

Animals↗
PubMed1987

Auditory experience affects degeneration of the ventral cochlear nucleus in Mongolian gerbils.

Gerbils exhibit a unique encephalopathy characterized by spongioform lesions in the neuropil of the cochlear nucleus and that others have recently described. The present results suggest that the course of this degenerative disorder is affected by acoustic experience. In gerbils in which acoustic stimulation was limited postnatally, the number and the extent of these lesions was dramatically reduced. Monaural deprivation reduced lesion number and extent only in the ipsilateral cochlear nucleus; binaural deprivation affected both cochlear nuclei. The lesions were most evident in certain portions of the cochlear nucleus, the caudal anterior ventral cochlear nucleus and the posterior ventral cochlear nucleus, sparing the rostral pole of the anterior ventral cochlear nucleus. In the affected regions the lesions were topologically restricted to the low and middle frequency regions. The apparent tonotopic distribution of lesions was associated with frequent exposure to low and middle frequency ambient noise.

Acoustic Stimulation↗
PubMed2026

Polystyrene microplastics induce auditory neurotoxicity in mammals: Integrated multi-omics profiling reveals oxidative damage and synaptic molecular dysregulation.

Microplastics (MPs) are ubiquitous environmental pollutants, yet their neurotoxic effects on the auditory system remain poorly understood. This study develops an integrated multi-level analytical framework combining auditory neurophysiology, behavioral assessment, tissue biochemistry, transcriptomics, and proteomics to investigate polystyrene (PS)-MPs-induced auditory neurotoxicity in rats. PS-MPs infiltrate the auditory system and significantly impair auditory processing, with central dysfunction emerging earlier and more prominently than peripheral alterations. Multi-omics analyses reveal coordinated suppression of glutamatergic synapse and Wnt signaling pathways in the cochlear nucleus. Mechanistically, PS-MPs perturb the crosstalk between glutamatergic synaptic and Wnt signaling, promoting AMPA receptor (AMPAR) internalization and potentially affecting synaptic plasticity-related processes and neuronal responsiveness. In parallel, PS-MPs trigger oxidative stress, apoptosis, and glial activation, reflecting pronounced neuroinflammatory and redox imbalance. In primary cochlear nucleus neurons (PCNNs), these mechanisms were further validated in vitro, where activation of Wnt signaling by Wnt3a significantly alleviated oxidative injury and reduced AMPAR internalization. Collectively, these findings provide comprehensive preclinical evidence for the neurotoxic potential of MPs and reveal a previously unrecognized PS-MPs-induced auditory neurotoxicity, although further studies are needed for human relevance. Results from the rat model further implicate Wnt-mediated signaling as a potential modulatory pathway underlying MPs-induced synaptic molecular alterations and redox dysfunction.

Animals↗
PubMed1977

Aspartic acid and glutamic acid levels in the cochlear nucleus after auditory nerve lesion.

Aspartic acid, glutamic acid and alanine were measured in the cochlear nucleus after lesioning the auditory nerve by cochlear ablation. Ultrastructural analysis of the cochlear nucleus showed that most primary auditory terminals were degenerating one day after cochlear ablation; the terminals were enlarged and the number of synaptic vesicles was reduced. Primary auditory terminals were virtually gone three days after cochlear ablation. Aspartic acid decreased after cochlear ablation in parallel with the morphological degeneration of the primary auditory terminals. The level of total aspartic acid in the cochlear nucleus had decreased more than 8% one day after cochlear ablation and more than 30% after two days, and remained at this level up to 28 days. Glutamic acid also decreased in the cochlear nucleus after cochlear ablation but not in parallel with the morphological degeneration of the primary auditory terminals. Following a slight increase one day after cochlear ablation, total glutamic acid decreased about 10% after two days and continued to decrease slowly through to day 28. Alanine dropped slowly after cochlear ablation and not in parallel with the degeneration of the primary terminals. Levels of other amino acids measured were unchanged or had increased two days after cochlear ablation. Aspartic acid and glutamic acid did not decrease in the superficial layers of the dorsal cochlear nucleus, an area receiving little or no primary innervation.

Alanine↗
PubMed2000

Neuronal death, not axonal degeneration, results in significant gliosis within the cochlear nucleus of adult chickens.

Injury to the central nervous system initiates a series of events that leads to neuronal cell death and glial activation. Astrocytes respond to damage and disease by becoming hyperplastic and hypertrophied. This 'reactive gliosis' is also accompanied by the upregulation of the intermediate filament protein glial fibrillary acidic protein, the release of growth factors and the formation of the glial scar. However, the signaling cascades which regulate these events, and the molecular mechanisms that give rise to this diverse response, have not been fully elucidated. For example, the role played by degenerating neurons vs. degenerating axons in the activation of astrocytes remains to be determined. To investigate the influence of neuronal cell death vs. axonal degeneration on gliosis, the current study examines the astrocyte response to cochlea removal in two different breeds of adult chickens, one of which exhibits neuronal cell death within the brainstem nucleus magnocellularis (NM) following the lesion and one which does not. Our results indicate that degeneration of NM neurons leads to large increases in both glial proliferation and hypertrophy, while eighth nerve degeneration without NM cell death results in very small increases in glial proliferation.

Animals↗
PubMedDate not supplied

Brainstem auditory pathway degeneration associated with chronic cochlear implants in the monkey.

The form and pattern of first-order and transsynaptic degeneration in the central auditory pathway was studied in monkeys following inner ear stimulation by a cochlear implant. Multielectrode, scala tympani, and modiolar systems were implanted; in some cases, neomycin was perfused into the cochlea to destroy the organ of Corti at the time of implantation. The monkeys were maintained chronically for 5 to 120 weeks, then the cochleas and brainstems were examined histologically. The extent of spiral ganglion cell loss across animals showed variability, reflecting the different procedures and devices used. The degree and distribution of spiral ganglion cell loss was related to the degree and distribution of neural degeneration seen in the cochlear nucleus in all cases. Peripheral damage progressed toward the cochlear apex as survival time increased, and this progression was reflected in the cochlear nucleus by a ventrolateral shift in the locus of degeneration over time. In addition, evidence for transneuronal degeneration was seen at the superior olive, the lateral lemniscus and the inferior colliculus. Our findings indicate that several factors inherent in the use of a cochlear prosthesis, i.e., insertion trauma, host reaction, and/or electrical stimulation, may be associated with a long-term, continuing process of central degeneration visible at several levels of the auditory system.

Animals↗
PubMed1980

Effects of neuronal activity on kainic acid neurotoxicity in the ventral cochlear nucleus.

Kainic acid was injected into the brain stem of adult guinea pigs, and the animals were either placed in a sound reducing-chamber or stimulated with 90 dB noise. The pattern and rate of kainic acid-induced degeneration in the anteroventral cochlear nucleus (AVCN) of sound-deprived animals was similar to that in animals exposed to ambient noise [2]. The amount of degeneration was greatly increased in animals stimulated with 90 dB noise. Therefore, although decreased activity in primary auditory fibers does not protect neurons in the AVCN from kainate-induced neurotoxicity, increased auditory stimulation augments the effects of kainic acid in the cochlear nucleus.

Acoustic Stimulation↗
PubMed1997

Changes in the tonotopic map of the dorsal cochlear nucleus in hamsters with hair cell loss and radial nerve bundle degeneration.

Hamsters were exposed to an intense tone (10 kHz) at levels and durations sufficient to cause hair cell loss and radial nerve bundle degeneration. A previous study reported changes in the tonotopic map of the dorsal cochlear nucleus (DCN) in hamsters with tone-induced stereocilia loss. Such changes appear similar to those observed by others in the auditory nerve following acoustic trauma, and suggest that the map alterations have a peripheral origin. However, the potential for tonotopic map reorganization after more severe lesions involving cellular degeneration in the cochlea has not yet been determined. The purpose of the present study was to determine how the tonotopic map of the DCN appears in animals with severe cochlear injury involving hair cell loss and radial nerve bundle degeneration. Neural population thresholds and tonotopic organization were mapped over the surface of the DCN in normal unexposed animals and those showing tone-induced lesions. The results indicate that cochlear lesions characterized mainly by radial bundle degeneration in a restricted portion of the organ of Corti cause changes in a corresponding region of the tonotopic map which reflect primarily changes in the shape and thresholds of neural tuning curves. In many cases the center of the lesion was represented in the DCN as a distinct characteristic frequency (CF) gap in the tonotopic map in which responses were either extremely weak or absent. In almost all cases the map area representing the center of the lesion was bordered by an expanded region of near-constant CF, a feature superficially suggestive of map reorganization (i.e., plasticity). However, these expanded map areas had abnormal tip thresholds and showed other features suggesting that their CFs had been shifted downward by distortion and deterioration of their original tips. Such changes in neural tuning following tone-induced loss of anatomical input to the central auditory pathway are similar to those observed in our previous study and by others in the auditory nerve following less severe acoustic trauma, and thus would seem to have a peripheral origin. Thus, changes in the DCN tonotopic map can be explained by peripheral modifications and do not seem to involve plastic changes (i.e., reorganization).

Acoustic Stimulation↗
PubMed1977

[Damage of the cochlea and of the cochlear nucleus after the application of aminoglycosid antibiotics--a comparative light-, transmission- and scanning electronmicroscopic study in the guinea pig (author's transl)].

Ototoxic alterations were studied in the guinea pig organ of Corti and in the cochlear nucleus after high administrations of aminoglycosid antibiotics (Gentamicin/Tobramycin, 150 mg/kg body weight/day or Amikacin 300 mg/kg body weight for 10 days). After survival times up to 22 days the animals were examined. By means of morphology degeneration was found in the cochlear nucleus before we could state it in the organ of Corti. After longer survival times, when we observed heavy degeneration in the organ of Corti we found only a few myelin figures of axons in the cochlear nerve. Cochlear nucleus: As an early sign of degeneration alterations in the mitochondria were found. Compared with the organ of Corti the damage was less widespread in the second order neurons of the afferent auditory pathways, their dendrites or nerve endings. Quantitative calculations however, were not performed. In axosomatic synapses we could observe a way of degeneration which was not reported before in damage caused by aminoglycosid antibiotics. Free postsynaptic densities were observed to be invaginated into the neuron as a probable way of sequestration. As well we could observe reoccupation of the synaptic sites by a probable sliding of neighbouring nerve endings into the free intracellular space. (Similar observations were reported first by Gentschev and Sotelo [1973] after ablation of the cochlear nerve in rats.

Aminoglycosides↗
PubMed1997

Degeneration of axons in the brainstem of the chinchilla after auditory overstimulation.

The patterns of axonal degeneration following acoustic overstimulation of the cochlea were traced in the brainstem of adult chinchillas. The Nauta-Rasmussen method for axonal degeneration was used following survivals of 1-32 days after a 105 min exposure to an octave-band noise with a center frequency of 4 kHz and a sound pressure level of 108 dB. Hair-cell and myelinated nerve-fiber loss were assessed in the cochlea. The cochleotopic pattern of terminal degeneration in the ventral cochlear nucleus correlated with the sites of myelinated fiber and inner-hair-cell loss: this correlation was less rigorous with outer-hair-cell loss, especially in the dorsal cochlear nucleus. These results are consistent with a dystrophic process with a slow time course depending on hair-cell loss and/or direct cochlear nerve-fiber damage. However, in a number of cases with no damage in the apical cochlea, fine fiber degeneration occurred with a faster course in low-frequency regions in the dorsal cochlear nucleus and, transynaptically, in a non-cochleotopic pattern in the superior olive and inferior colliculus. These findings suggest that neuronal hyperactivity plays a role in the central degeneration following acoustic overstimulation, possibly by an excitotoxic process.

Acoustic Stimulation↗