Abstract
Due to limitations of human in vivo studies, detailed computational models enable understanding the neural signaling in the degenerated auditory system and cochlear implants (CIs). Four human cochleae were used to quantify hearing levels depending on dendritic changes in diameter and myelination thickness from type I of the auditory nerve fibers (ANFs). Type I neurons transmit the auditory information as spiking pattern from the inner hair cells (IHCs) to the cochlear nucleus. The impact of dendrite diameter and degree of myelination on neural signal transmission was simulated for (1) synaptic excitation via IHCs and (2) stimulation from CI electrodes. An accurate three-dimensional human cochlear geometry, along with 30 auditory pathways, mimicked the CI environment. The excitation properties of electrical potential distribution induced by two CI were analyzed. Main findings: (1) The unimodal distribution of control dendrite diameters becomes multimodal for hearing loss cases; a group of thin dendrites with diameters between 0.3 and 1 μm with a peak at 0.5 μm appeared. (2) Postsynaptic currents from IHCs excite such thin dendrites easier and earlier than under control conditions. However, this advantage is lost as their conduction velocity decreases proportionally with the diameter and causes increased spike latency and jitter in soma and axon. Firing probability reduces through the soma passage due to the low intracellular current flow in thin dendrites during spiking. (3) Compared with dendrite diameter, variations in myelin thickness have a small impact on spiking performance. (4) Contrary to synaptic excitation, CIs cause several spike initiation sites in dendrite, soma region, and axon; moreover, fiber excitability reduces with fiber diameter. In a few cases, where weak stimuli elicit spikes of a target neuron (TN) in the axon, dendrite diameter reduction has no effect. However, in many cases, a spike in a TN is first initiated in the dendrite, and consequently, dendrite degeneration demands an increase in threshold currents. (5) Threshold currents of a TN and co-stimulation of degenerated ANFs in other frequency regions depend on the electrode position, including its distance to the outer wall, the cochlear turn, and the three-dimensional pathway of the TN.
Highlights
According to World Health Organization [WHO] (2020), nearly 466 million people worldwide have impairing hearing loss caused by hereditary, aging, disease, and injury
This study investigated the auditory nerve fiber (ANF) condition in terms of the three degeneration indicators: dendrite diameter (DD), myelination thickness (MT), and G-ratio
A small number of human subject studies were performed on the morphometry of degenerated ANFs
Summary
According to World Health Organization [WHO] (2020), nearly 466 million people worldwide have impairing hearing loss caused by hereditary, aging, disease, and injury. The ear is a vulnerable organ where sophisticated strategies were developed during evolution to transfer sound into neural signals (Figure 1) with high precision concerning frequency and loudness (Von Békésy and Wever, 1960; Mark and Rattay, 1990; Humes et al, 2010). Sensory hair cells in the cochlea convert sound into neural signals conducted along the auditory nerve fibers (ANFs) by two types of spiral ganglion neurons. The vast majority (about 95%) of spiral ganglion neurons are bipolar type I cells that connect inner hair cells (IHCs) via myelinated dendrites, large somata, and myelinated axons with the cochlear nuclei in the brain stem (Ota and Kimura, 1980). Smaller unmyelinated type II cells transmit APs from the outer hair cells (Spoendlin, 1985)
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