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在衰老的C57BL/6J小鼠中,内毛细胞的突触改变先于螺旋神经节细胞的丧失。

Synaptic alterations at inner hair cells precede spiral ganglion cell loss in aging C57BL/6J mice.

作者信息

Stamataki Sofia, Francis Howard W, Lehar Mohamed, May Bradford J, Ryugo David K

机构信息

Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University, 720 Rutland Avenue, Baltimore, MD 21205, USA.

出版信息

Hear Res. 2006 Nov;221(1-2):104-18. doi: 10.1016/j.heares.2006.07.014. Epub 2006 Sep 26.

DOI:10.1016/j.heares.2006.07.014
PMID:17005343
Abstract

Hearing deficits have often been associated with loss of or damage to receptor hair cells and/or degeneration of spiral ganglion cells. There are, however, some physiological abnormalities that are not reliably attributed to loss of these cells. The afferent synapse between radial fibers of spiral ganglion neurons and inner hair cells (IHCs) emerges as another site that could be involved in transmission abnormalities. We tested the hypothesis that the structure of these afferent terminals would differ between young animals and older animals with significant hearing loss. Afferent endings and their synapses were examined by transmission electron microscopy at approximately 45% distance from the basal end of the cochlea in 2-3 month-old and 8-12 month-old C57BL/6J mice. The number of terminals in older animals was reduced by half compared to younger animals. In contrast, there was no difference in the density of SGCs between the age groups. Older animals featured enlarged terminals and mitochondria and enlarged postsynaptic densities and presynaptic bodies. These morphological changes may be a combination of pathologic, adaptive and compensatory responses to sensory dysfunction. Improved knowledge of these processes is necessary to understand the role of afferent connectivity in dysfunction of the aging cochlea.

摘要

听力缺陷常与受体毛细胞的丧失或损伤和/或螺旋神经节细胞的退化有关。然而,存在一些生理异常,这些异常不能可靠地归因于这些细胞的丧失。螺旋神经节神经元的放射状纤维与内毛细胞(IHC)之间的传入突触成为另一个可能参与传递异常的部位。我们检验了这样一个假设,即这些传入终末的结构在年轻动物和有明显听力损失的老年动物之间会有所不同。通过透射电子显微镜在2 - 3月龄和8 - 12月龄C57BL/6J小鼠耳蜗基部末端约45%处检查传入终末及其突触。与年轻动物相比,老年动物的终末数量减少了一半。相比之下,不同年龄组之间螺旋神经节细胞的密度没有差异。老年动物的终末、线粒体增大,突触后致密物和突触前小体增大。这些形态学变化可能是对感觉功能障碍的病理、适应性和代偿性反应的综合表现。深入了解这些过程对于理解传入连接在衰老耳蜗功能障碍中的作用是必要的。

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