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新生期致聋猫的慢性耳蜗内电刺激:强度和刺激电极位置的影响

Chronic intracochlear electrical stimulation in neonatally deafened cats: effects of intensity and stimulating electrode location.

作者信息

Leake P A, Snyder R L, Hradek G T, Rebscher S J

机构信息

Department of Otolaryngology, University of California, San Francisco 94143.

出版信息

Hear Res. 1992 Dec;64(1):99-117. doi: 10.1016/0378-5955(92)90172-j.

Abstract

An earlier study conducted in this laboratory suggested that chronic intracochelear electrical stimulation at moderate current levels can at least partially delay or prevent the retrograde degeneration of primary auditory (spiral ganglion) neurons that otherwise is progressive after neonatal deafness induced by ototoxic drug administration. Increased survival of spiral ganglion neurons was observed within the basal cochlear region near the stimulating biopolar electrode pairs, while in more apical regions there was no significant difference between the stimulated and control cochleas. The mechanisms underlying this maintenance of spiral ganglion neurons induced by chronic electrical stimulation are uncertain, especially since increased neuronal survival was observed over broader sectors of the ganglion than would be expected to be directly activated by the bipolar electrodes and moderate stimulation intensity (6 dB above electrically evoked auditory brainstem response threshold) used. In this report, data are presented from a second series of neonatally deafened and chronically stimulated cats. The parameters for chronic electrical stimulation were manipulated in two simple ways. First, the intensity of the electrical stimulus was reduced from the earlier study, while the duration of chronic stimualtion periods was increased; and secondly, two different intracochlear positions of stimulating electrodes were employed in different experimental groups. Results indicate that elecrical stimulation of the cochlea at an extremely low intensity (2 dB above electrically evoked auditory brainstem response threshold) is sufficient to at least partially prevent or delay ganglion cell degeneration in the deafened cochlea. In addition, data suggest a differential distribution of the maintained or conserved ganglion cells, such that when the stimulating electrode pair was positioned near the base of the cochlea increased ganglion survival in a more basal cochlear sector, while stimulation at a more apical site resulted in increased neuronal survival extending to more apical regions.

摘要

本实验室早期进行的一项研究表明,在中等电流水平下进行慢性鼓室内电刺激,至少可以部分延迟或预防原发性听觉(螺旋神经节)神经元的逆行性退变,否则在耳毒性药物导致新生儿耳聋后,这种退变会持续进展。在靠近刺激双极电极对的耳蜗基部区域观察到螺旋神经节神经元的存活率增加,而在更靠近顶部的区域,刺激组和对照组的耳蜗之间没有显著差异。慢性电刺激诱导螺旋神经节神经元维持的潜在机制尚不清楚,特别是因为观察到神经节中存活增加的神经元区域比预期的由双极电极和中等刺激强度(比电诱发听觉脑干反应阈值高6分贝)直接激活的区域更广泛。在本报告中,展示了第二组新生耳聋并接受慢性刺激的猫的数据。慢性电刺激的参数通过两种简单方式进行了调整。首先,与早期研究相比,降低了电刺激的强度,同时延长了慢性刺激期的持续时间;其次,在不同实验组中采用了两个不同的鼓室内刺激电极位置。结果表明,以极低强度(比电诱发听觉脑干反应阈值高2分贝)对耳蜗进行电刺激足以至少部分预防或延迟耳聋耳蜗中神经节细胞的退变。此外,数据表明维持或保留的神经节细胞分布存在差异,即当刺激电极对位于耳蜗基部附近时,耳蜗基部区域更多的神经节存活增加,而在更靠近顶部的位置进行刺激则导致神经元存活增加并延伸到更靠近顶部的区域。

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