Niparko J K
Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins University, Baltimore, Maryland 21287-0910, USA.
Laryngoscope. 1999 Nov;109(11):1721-30. doi: 10.1097/00005537-199911000-00001.
Sensorineural hearing loss may be associated with altered patterns of neuronal connections within the central auditory pathway.
The cat auditory system was used to address the relative importance of impulse traffic within the auditory nerve in maintaining central nervous system connections.
Acute, unilateral deafness was induced by tetrodotoxin intoxication of cochlear hair cells. Analysis focused on the structural patterns of contact between auditory nerve endings called end bulbs of Held and their target neurons. Specifically, end bulb morphology and target cell size within the cochlear nucleus were examined. Highly specialized synaptic contacts at this junction provide a powerful site for study.
The principal finding was that abolished activity in the auditory nerve caused nerve endings to assume a different shape, typified by more branching and smaller terminal swellings. The new shape is one typically associated with only a subpopulation of fibers in normal-hearing cats--those exhibiting a high-threshold, low-spontaneous activity profile. This result implies that abolished activity alters patterns of nerve fiber contact with second-order neurons. Tetrodotoxin produced differential effects on subpopulations of target neurons within the brainstem and is interpretable on the basis of "weighing" synaptic inputs. Second-order neurons that receive large axosomatic inputs from their parent fiber were significantly smaller than neurons that receive small, axodendritic terminals. Thus, attenuated auditory activity may produce differential effects across the auditory pathway, thereby disrupting the normal balance of inputs into synaptic stations.
Impulse traffic is a critical factor in the interaction between the ear and central auditory stations and appears necessary for the maintenance of key synapses. As hearing disorders with impaired comprehension may be modeled by studies of auditory deafferentation, these observations extend the possibility that changes in central neuronal connections underlie reduced capabilities for processing restored auditory input.
感音神经性听力损失可能与中枢听觉通路内神经元连接模式的改变有关。
利用猫的听觉系统来探讨听神经内冲动流量在维持中枢神经系统连接方面的相对重要性。
通过对耳蜗毛细胞进行河豚毒素中毒诱导急性单侧耳聋。分析重点在于听神经末梢（称为 Held 终球）与其靶神经元之间的接触结构模式。具体而言，检查了耳蜗核内终球形态和靶细胞大小。此连接处高度特化的突触接触为研究提供了有力的位点。
主要发现是听神经活动的消除导致神经末梢呈现出不同的形状，其特征为分支增多和终末肿胀变小。这种新形状通常仅与听力正常猫的一部分纤维相关——那些表现出高阈值、低自发活动特征的纤维。这一结果意味着活动的消除改变了神经纤维与二级神经元的接触模式。河豚毒素对脑干内靶神经元亚群产生了不同的影响，并且可以基于“权衡”突触输入来解释。从其母纤维接收大量轴体输入的二级神经元明显小于接收小的轴树突末梢的神经元。因此，减弱的听觉活动可能在整个听觉通路上产生不同的影响，从而破坏输入到突触部位的正常平衡。
冲动流量是耳朵与中枢听觉部位之间相互作用的关键因素，并且似乎是维持关键突触所必需的。由于对听觉传入神经切断的研究可以模拟伴有理解障碍的听力障碍，这些观察结果扩展了这样一种可能性，即中枢神经元连接的变化是处理恢复的听觉输入能力降低的基础。
