Department of Otolaryngology-HNS, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
J Comp Neurol. 2010 Apr 1;518(7):1046-63. doi: 10.1002/cne.22262.
The effects of deafness on brain structure and function have been studied using animal models of congenital deafness that include surgical ablation of the organ of Corti, acoustic trauma, ototoxic drugs, and hereditary deafness. This report describes the morphologic plasticity of auditory nerve synapses in response to ototoxic deafening and chronic electrical stimulation of the auditory nerve. Normal kittens were deafened by neonatal administration of neomycin that eliminated auditory receptor cells. Some of these cats were raised deaf, whereas others were chronically implanted with cochlear electrodes at 2 months of age and electrically stimulated for up to 12 months. The large endings of the auditory nerve, endbulbs of Held, were studied because they hold a key position in the timing pathway for sound localization, are readily identifiable, and exhibit deafness-associated abnormalities. Compared with those of normal hearing cats, synapses of ototoxically deafened cats displayed expanded postsynaptic densities, a 35.4% decrease in synaptic vesicle (SV) density, and a reduction in the somatic size of spherical bushy cells (SBCs). In comparison with normal hearing cats, ototoxically deafened cats that received cochlear stimulation had endbulbs that expressed postsynaptic densities (PSDs) that were statistically identical in size, showed a 48.1% reduction in SV density, and whose target SBCs had a 25.5% reduction in soma area. These results demonstrate that electrical stimulation via a cochlear implant in chemically deafened cats preserves PSD size but not other aspects of synapse morphology. This determination further suggests that the effects of ototoxic deafness are not identical to those of hereditary deafness.
耳聋对大脑结构和功能的影响已经在先天性耳聋的动物模型中进行了研究，这些模型包括耳蜗组织的外科消融、声音创伤、耳毒性药物和遗传性耳聋。本报告描述了听觉神经突触对耳毒性聋和听觉神经慢性电刺激的形态可塑性。正常小猫在出生后接受新霉素治疗而耳聋，这种方法消除了听觉感受器细胞。这些猫中的一些被饲养在聋环境中，而另一些则在 2 个月大时被慢性植入耳蜗电极，并接受长达 12 个月的电刺激。听觉神经的大终末，即 Held 终球，被研究是因为它们在声音定位的时间途径中占据关键位置，易于识别，并表现出与耳聋相关的异常。与正常听力的猫相比，耳毒性聋猫的突触显示出扩张的突触后密度，突触小泡 (SV) 密度降低 35.4%，球形毛细胞 (SBC) 的体细胞大小减小。与正常听力的猫相比，接受耳蜗刺激的耳毒性聋猫的终球表达的突触后密度 (PSD) 在大小上统计学上相同，SV 密度降低 48.1%，其靶 SBC 的体细胞面积减少 25.5%。这些结果表明，在化学性耳聋的猫中通过耳蜗植入进行电刺激可以保留 PSD 的大小，但不能保留突触形态的其他方面。这一确定进一步表明，耳毒性聋的影响与遗传性聋的影响并不相同。
