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听觉剥夺引起的轴突起始段可塑性会降低人工耳蜗植入神经反应模型中的时间差敏感性。

Axon initial segment plasticity caused by auditory deprivation degrades time difference sensitivity in a model of neural responses to cochlear implants.

作者信息

Jing Anna, Xi Sylvia, Fransazov Ivan, Goldwyn Joshua H

机构信息

Department of Mathematics and Statistics, Swarthmore College, 500 College Ave, Swarthmore, PA, 19081, USA.

Courant Institute of Mathematical Sciences, New York University, 251 Mercer Street, New York, NY, 10012-1185, USA.

出版信息

J Comput Neurosci. 2025 Apr 17. doi: 10.1007/s10827-025-00902-9.

DOI:10.1007/s10827-025-00902-9
PMID:40244473
Abstract

Synaptic and neural properties can change during periods of auditory deprivation. These changes may disrupt the computations that neurons perform. In the brainstem of chickens, auditory deprivation can lead to changes in the size and biophysics of the axon initial segment (AIS) of neurons in the sound source localization circuit. This is the phenomenon of axon initial segment (AIS) plasticity. Individuals who use cochlear implants (CIs) experience periods of hearing loss, and so we ask whether AIS plasticity in neurons of the medial superior olive (MSO), a key stage of sound location processing, would impact time difference sensitivity in the scenario of hearing with cochlear implants. The biophysical changes that we implement in our model of AIS plasticity include enlargement of the AIS and replacement of low-threshold potassium conductance with the more slowly-activated M-type potassium conductance. AIS plasticity has been observed to have a homeostatic effect with respect to excitability. In our model, AIS plasticity has the additional effect of converting MSO neurons from phasic firing type to tonic firing type. Phasic firing is known to have greater temporal sensitivity to coincident inputs. Consistent with this, we find AIS plasticity degrades time difference sensitivity in the auditory deprived MSO neuron model across a range of stimulus parameters. Our study illustrates a possible mechanism of cellular plasticity in a non-peripheral stage of neural processing that could impose barriers to sound source localization by bilateral cochlear implant users.

摘要

在听觉剥夺期间,突触和神经特性会发生变化。这些变化可能会扰乱神经元执行的计算。在鸡的脑干中,听觉剥夺会导致声源定位回路中神经元轴突起始段(AIS)的大小和生物物理学发生变化。这就是轴突起始段(AIS)可塑性的现象。使用人工耳蜗(CI)的个体经历过听力损失阶段,因此我们要问,在声音定位处理的关键阶段——内侧上橄榄核(MSO)的神经元中,AIS可塑性是否会在人工耳蜗助听的情况下影响时间差敏感性。我们在AIS可塑性模型中实现的生物物理变化包括AIS的扩大以及用激活较慢的M型钾电导取代低阈值钾电导。已观察到AIS可塑性对兴奋性具有稳态作用。在我们的模型中,AIS可塑性还有将MSO神经元从相位发放类型转变为紧张性发放类型的额外作用。已知相位发放对同时输入具有更高的时间敏感性。与此一致的是,我们发现在一系列刺激参数下,AIS可塑性会降低听觉剥夺的MSO神经元模型中的时间差敏感性。我们的研究阐明了神经处理非外周阶段细胞可塑性的一种可能机制,这种机制可能会给双侧人工耳蜗使用者的声源定位带来障碍。

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