Surface electrical stimulation of the auditory cortex preserves efferent medial olivocochlear neurons and reduces cochlear traits of age-related hearing loss

IF 2.5 2区 医学 Q1 AUDIOLOGY & SPEECH-LANGUAGE PATHOLOGY
V. Fuentes-Santamaría , Z. Benítez-Maicán , J.C. Alvarado , I.S. Fernández del Campo , M.C. Gabaldón-Ull , M.A. Merchán , J.M. Juiz
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引用次数: 0

Abstract

The auditory cortex is the source of descending connections providing contextual feedback for auditory signal processing at almost all levels of the lemniscal auditory pathway. Such feedback is essential for cognitive processing. It is likely that corticofugal pathways are degraded with aging, becoming important players in age-related hearing loss and, by extension, in cognitive decline. We are testing the hypothesis that surface, epidural stimulation of the auditory cortex during aging may regulate the activity of corticofugal pathways, resulting in modulation of central and peripheral traits of auditory aging. Increased auditory thresholds during ongoing age-related hearing loss in the rat are attenuated after two weeks of epidural stimulation with direct current applied to the surface of the auditory cortex for two weeks in alternate days (Fernández del Campo et al., 2024). Here we report that the same cortical electrical stimulation protocol induces structural and cytochemical changes in the aging cochlea and auditory brainstem, which may underlie recovery of age-degraded auditory sensitivity. Specifically, we found that in 18 month-old rats after two weeks of cortical electrical stimulation there is, relative to age-matched non-stimulated rats: a) a larger number of choline acetyltransferase immunoreactive neuronal cell body profiles in the ventral nucleus of the trapezoid body, originating the medial olivocochlear system.; b) a reduction of age-related dystrophic changes in the stria vascularis; c) diminished immunoreactivity for the pro-inflammatory cytokine TNFα in the stria vascularis and spiral ligament. d) diminished immunoreactivity for Iba1 and changes in the morphology of Iba1 immunoreactive cells in the lateral wall, suggesting reduced activation of macrophage/microglia; d) Increased immunoreactivity levels for calretinin in spiral ganglion neurons, suggesting excitability modulation by corticofugal stimulation. Altogether, these findings support that non-invasive neuromodulation of the auditory cortex during aging preserves the cochlear efferent system and ameliorates cochlear aging traits, including stria vascularis dystrophy, dysregulated inflammation and altered excitability in primary auditory neurons.

Abstract Image

对听皮层进行表面电刺激可保留传出内侧橄榄耳神经元并减少老年性听力损失的耳蜗特征
听觉皮层是为全脑听觉通路几乎所有层次的听觉信号处理提供上下文反馈的降序连接的源头。这种反馈对认知处理至关重要。随着年龄的增长,皮质听觉通路可能会退化,成为老年性听力损失的重要因素,进而导致认知能力下降。我们正在测试一种假设,即在衰老过程中对听觉皮层进行硬膜外表面刺激可能会调节皮质-耳蜗通路的活动,从而调节听觉衰老的中枢和外周特征。在对大鼠进行为期两周的听觉皮层表面直流电隔日硬膜外刺激后,大鼠在持续的年龄相关性听力损失过程中听觉阈值的增加会减弱(Fernández del Campo 等人,2024 年)。在此,我们报告了同样的皮层电刺激方案可诱导老化耳蜗和听觉脑干的结构和细胞化学变化,这可能是年龄退化的听觉灵敏度恢复的基础。具体来说,我们发现在对 18 个月大的大鼠进行两周的大脑皮层电刺激后,与年龄匹配的未受刺激大鼠相比:a) 在梯形体腹侧核中有更多的胆碱乙酰转移酶免疫反应神经元细胞体轮廓,这些神经元细胞体源自内侧耳蜗系统。b) 血管纹中与年龄有关的萎缩性变化减少;c) 血管纹和螺旋韧带中促炎细胞因子 TNFα 的免疫反应性降低。d) 侧壁中 Iba1 免疫活性降低,Iba1 免疫活性细胞的形态发生变化,这表明巨噬细胞/小胶质细胞的活化程度降低;d) 螺旋神经节神经元中的钙凝蛋白免疫活性水平升高,这表明皮质咽喉刺激对神经元的兴奋性有调节作用。总之,这些研究结果支持在衰老过程中对听觉皮层进行非侵入性神经调节,以保护耳蜗传出系统并改善耳蜗衰老特征,包括血管纹萎缩、炎症失调和初级听觉神经元兴奋性改变。
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来源期刊
Hearing Research
Hearing Research 医学-耳鼻喉科学
CiteScore
5.30
自引率
14.30%
发文量
163
审稿时长
75 days
期刊介绍: The aim of the journal is to provide a forum for papers concerned with basic peripheral and central auditory mechanisms. Emphasis is on experimental and clinical studies, but theoretical and methodological papers will also be considered. The journal publishes original research papers, review and mini- review articles, rapid communications, method/protocol and perspective articles. Papers submitted should deal with auditory anatomy, physiology, psychophysics, imaging, modeling and behavioural studies in animals and humans, as well as hearing aids and cochlear implants. Papers dealing with the vestibular system are also considered for publication. Papers on comparative aspects of hearing and on effects of drugs and environmental contaminants on hearing function will also be considered. Clinical papers will be accepted when they contribute to the understanding of normal and pathological hearing functions.
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