Morphological changes in the cochlear nucleus of congenitally deaf white cats

Morphological changes in the cochlear nucleus of congenitally deaf white cats
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DOI:
10.1016/0006-8993(96)00719-6
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发表时间:
1996-10-14
期刊:
影响因子:
2.9
通讯作者:
Ryugo, DK
Ryugo, DK
中科院分区:
医学3区
文献类型:
--
作者:
Saada, AA;Niparko, JK;Ryugo, DK

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在动物模型和人类的研究表明,先天性耳聋产生中枢听觉通路的退行性变化。耳蜗核是接收耳蜗输入的第一个中枢结构,并且可以被认为是上行听觉通路的起源。在这种情况下,我们研究了先天性耳聋的白色猫,谁表达早发性耳蜗受体的损失,以评估耳蜗核细胞的结构变化的性质。可以想象,高级听觉结构的病理改变是通过该核团跨神经元分布的。将听力正常的非白色猫的耳蜗核与听力损失超过70 dB SPL的聋白色猫的耳蜗核进行比较。失聪的白色猫的耳蜗核体积小了大约50%,腹侧和背侧分区受到同样的影响。细胞体轮廓面积测定的前腹侧耳蜗核(AVCN),锥体细胞的背侧耳蜗核(DCN),感觉神经元的三叉神经主核,和运动神经元的面神经核的球形丛状细胞。我们发现这两组猫的非听觉神经元之间的神经元胞体大小没有统计学差异,而聋白色猫的听觉神经元比正常猫的小30.8-39.4%。这些数据表明,先天性耳聋猫的神经元变化是特定的听觉通路。虽然耳蜗核体积损失是均匀的两个部门,有一个差异的影响细胞密度:AVCN细胞密度增加了40%,而DCN细胞密度相对不受影响(增加10%)。AVCN中的星形胶质细胞密度(52%)也高于DCN中的星形胶质细胞密度(5%)。这些观察结果揭示了耳蜗核细胞对先天性耳聋的不同影响,表明在这一水平上存在选择性加工障碍。如果类似的退化模式发生在人类身上,这种病理可能是先天性耳聋成年人对人工耳蜗输入的处理减少的基础。
Investigations in animal models and humans have indicated that congenital deafness produces degenerative changes in the central auditory pathway. The cochlear nucleus is the first central structure that receives cochlear input, and may be considered the origin of ascending auditory pathways. In this context, we studied congenitally deaf white cats, who express early onset cochlear receptor loss, in order to assess the nature of structural changes in cells of the cochlear nucleus. It is conceivable that pathologic alterations in higher auditory structures are transneuronally distributed through this nucleus. The cochlear nuclei of nonwhite cats with normal hearing were compared to those of deaf white cats exhibiting hearing loss in excess of 70 dB SPL. The cochlear nuclei of the deaf white cats were smaller in volume by roughly 50%, with the ventral and dorsal divisions being equally affected. Cell body silhouette area was determined for spherical bushy cells of the anteroventral cochlear nucleus (AVCN), pyramidal cells of the dorsal cochlear nucleus (DCN), sensory neurons from the principal trigeminal nucleus, and motoneurons of the facial nucleus. We found no statistical difference in neuronal cell body size between nonauditory neurons of these two groups of cats, whereas auditory neurons of deaf white cats were 30.8-39.4% smaller than those of normal cats. These data imply that neuronal changes in congenitally deaf cats are specific to the auditory pathway. Although cochlear nucleus volume loss was uniform for both divisions, there was a differential effect on cell density: AVCN cell density increased by 40%, whereas DCN cell density was relatively unaffected (10% increase). Astrocyte density was also greater in the AVCN (52%) compared to that in the DCN (5%). These observations reveal a differential impact on cells in the cochlear nucleus to congenital deafness, suggesting selective processing impairment at this level. If similar patterns of degeneration occur in humans, such pathologies may underlie reduced processing of input from cochlear implants in congenitally deaf adults.