REGENERATION OF COCHLEAR EFFERENT NERVE-TERMINALS AFTER GENTAMICIN DAMAGE

Citation
Ak. Hennig et Da. Cotanche, REGENERATION OF COCHLEAR EFFERENT NERVE-TERMINALS AFTER GENTAMICIN DAMAGE, The Journal of neuroscience, 18(9), 1998, pp. 3282-3296
Citations number
59
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
0270-6474
Volume
18
Issue
9
Year of publication
1998
Pages
3282 - 3296
Database
ISI
SICI code
0270-6474(1998)18:9<3282:ROCENA>2.0.ZU;2-V
Abstract
Chickens recover auditory function after hair cell loss caused by otot oxic drug damage or acoustic overstimulation, indicating that mechanis ms exist to reestablish appropriate neuronal connections to regenerate d hair cells. However, despite similar hair cell regeneration times, h earing recovery takes substantially longer after aminoglycoside than a fter sound damage. We have therefore begun examining damage and regene ration of efferent nerve terminals by immunolabeling whole-mount cochl eae for differentially localized synaptic proteins and by visualizing the distribution of label with confocal microscopy. In undamaged cochl eae, the synaptic proteins synapsin and syntaxin show similar distribu tion patterns corresponding to the large cup-like terminals on short h air cells. After gentamycin administration, these terminals are disrup ted as hair cells are lost, leaving smaller, more numerous synapsin-re active structures in the sensory epithelium. Syntaxin reactivity remai ns associated with the extruded hair cells, indicating that the presyn aptic membrane is still attached to the postsynaptic site. In contrast , after sound damage, both synapsin and syntaxin reactivity are lost f rom the epithelium with extruded hair cells. As regenerated hair cells differentiate after gentamycin treatment, the synapsin labeling assoc iated with cup-like efferent endings reappears but is not completely r estored even after 60 d of recovery. Thus, efferent terminals are rees tablished much more slowly than after sound damage (Wang and Raphael, 1996), consistent with the prolonged loss of hearing function, This in vivo model system allows comparison of axonal reconnection after eith er complete loss (sound damage) or partial disruption (gentamycin trea tment) of axon terminals. Elucidating the differences in recovery betw een these injuries can provide insights into reinnervation mechanisms.