Central nervous system plasticity during hair cell loss and regeneration

被引:19
|
作者
Durham, D
Park, DL
Girod, DA
机构
[1] Univ Kansas, Med Ctr, Dept Otolaryngol, Kansas City, KS 66160 USA
[2] Univ Kansas, Med Ctr, Smith Mental Retardat & Human Dev Ctr, Kansas City, KS 66160 USA
[3] Univ Kansas, Med Ctr, Dept Speech & Hearing, Kansas City, KS 66160 USA
[4] Vet Affairs Med Ctr, Kansas City, MO USA
关键词
nucleus magnocellularis; gentamicin; deafferentation; avian; auditory;
D O I
10.1016/S0378-5955(00)00128-3
中图分类号
R36 [病理学]; R76 [耳鼻咽喉科学];
学科分类号
100104 ; 100213 ;
摘要
Following cochlear ablation, auditory neurons in the central nervous system (CNS) undergo alterations in morphology and function, including neuronal cell death. The trigger for these CNS changes is the abrupt cessation of afferent input via eighth nerve fiber activity. Gentamicin can cause ototoxic damage to cochlear hair cells responsible for high frequency hearing, which seems likely to cause a frequency-specific loss of input into the CNS. In birds, these hair cells can regenerate, presumably restoring input into the CNS. This review summarizes current knowledge of how CNS auditory neurons respond to this transient: frequency-specific loss of cochlear function. A single systemic injection of a high dose of gentamicin results in the complete loss of high frequency hair cells by 5 days, followed by the regeneration of new hair cells. Both hair cell-specific functional measures and estimates of CNS afferent activity suggest that newly regenerated hair cells restore afferent input to brainstem auditory neurons. Frequency-specific neuronal cell death and shrinkage occur following gentamicin damage to hair cells, with an unexpected recovery of neuronal cell number at longer survival times. A newly-developed method for topical, unilateral gentamicin application will allow future studies to compare neuronal changes within a given animal. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:145 / 159
页数:15
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