4.5 Article

Fine structure of degeneration in the cochlear nucleus of the chinchilla after acoustic overstimulation

Journal

JOURNAL OF NEUROSCIENCE RESEARCH
Volume 77, Issue 6, Pages 798-816

Publisher

WILEY
DOI: 10.1002/jnr.20213

Keywords

plasticity; auditory system; cochlear damage; noise; synaptic degeneration; tinnitus

Categories

Funding

  1. NIDCD NIH HHS [DC00127, DC00199, DC01366] Funding Source: Medline

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To study plastic changes in the cochlear nucleus after acoustic stimulation, adult chinchillas were exposed once to a 4-kHz octave-band noise at 108 dB SPL for 3 hr. After survival times of 1, 2, 4, 8, and 16 weeks, samples were taken for electron microscopy from a part of the cochlear nucleus, where cochlear nerve fibers degenerated after the noise exposure. Progressive changes in fine structure were characterized as early, intermediate, and late stages of degeneration. Freshly occurring synaptic degeneration appeared in each period from 1-16 weeks. Endings with large round vesicles, putative excitatory synapses of the cochlear nerve, displayed progressive increases in neurofilaments and enlarged synaptic vesicles. Compared to controls, synaptic vesicles seemed fewer, often in small clusters in the interior of endings, and smaller in the synaptic zone. These early changes progressed to mitochondrial disintegration and overt watery degeneration. Some surviving endings, however, were shrunken and displaced partially by enlarged spaces in the synaptic complex. Dense-cored vesicles gathered in these endings. In terminals with pleomorphic and flattened vesicles, presumed inhibitory endings, cytological changes appeared within 1 week and persisted for months. The synaptic endings darkened, some vesicles disintegrated, and many smaller flatter vesicles collapsed into heaps. Especially at the presynaptic membrane, vesicles were shriveled, but a few mitochondria were preserved. Without overt signs of synaptic degeneration, some of these cytological changes presumably reflect reduced synaptic activity in the inhibitory endings. These changes may contribute to a continuing process associated with abnormal auditory functions, including hyperacusis and tinnitus. (C) 2004 Wiley-Liss, Inc.

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