Journal
HEARING RESEARCH
Volume 149, Issue 1-2, Pages 178-188Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/S0378-5955(00)00181-7
Keywords
deafferentation; nucleus magnocellularis; auditory; gliosis
Funding
- NIDCD NIH HHS [DC05189, DC02931] Funding Source: Medline
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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 'reaclive 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. (C) 2000 Elsevier Science B.V. All rights reserved.
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