Layer-specific enhancement of visual-evoked activity in the audiovisual cortex following a mild degree of hearing loss in adult rats

IF 2.5 2区 医学 Q1 AUDIOLOGY & SPEECH-LANGUAGE PATHOLOGY Hearing Research Pub Date : 2024-06-18 DOI:10.1016/j.heares.2024.109071
Ashley L. Schormans, Brian L. Allman
{"title":"Layer-specific enhancement of visual-evoked activity in the audiovisual cortex following a mild degree of hearing loss in adult rats","authors":"Ashley L. Schormans,&nbsp;Brian L. Allman","doi":"10.1016/j.heares.2024.109071","DOIUrl":null,"url":null,"abstract":"<div><p>Following adult-onset hearing impairment, crossmodal plasticity can occur within various sensory cortices, often characterized by increased neural responses to visual stimulation in not only the auditory cortex, but also in the visual and audiovisual cortices. In the present study, we used an established model of loud noise exposure in rats to examine, for the first time, whether the crossmodal plasticity in the audiovisual cortex that occurs following a relatively mild degree of hearing loss emerges solely from altered intracortical processing or if thalamocortical changes also contribute to the crossmodal effects. Using a combination of an established pharmacological ‘cortical silencing’ protocol and current source density analysis of the laminar activity recorded across the layers of the audiovisual cortex (i.e., the lateral extrastriate visual cortex, V2L), we observed layer-specific changes post-silencing in the strength of the residual visual, but not auditory, input in the noise exposed rats with mild hearing loss compared to rats with normal hearing. Furthermore, based on a comparison of the laminar profiles pre- versus post-silencing in both groups, we can conclude that noise exposure caused a re-allocation of the strength of visual inputs across the layers of the V2L cortex, including enhanced visual-evoked activity in the granular layer; findings consistent with thalamocortical plasticity. Finally, we confirmed that audiovisual integration within the V2L cortex depends on intact processing within intracortical circuits, and that this form of multisensory processing is vulnerable to disruption by noise-induced hearing loss. Ultimately, the present study furthers our understanding of the contribution of intracortical and thalamocortical processing to crossmodal plasticity as well as to audiovisual integration under both normal and mildly-impaired hearing conditions.</p></div>","PeriodicalId":12881,"journal":{"name":"Hearing Research","volume":"450 ","pages":"Article 109071"},"PeriodicalIF":2.5000,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0378595524001242/pdfft?md5=b7b80c1adb567143d0b47cde57a44d46&pid=1-s2.0-S0378595524001242-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Hearing Research","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0378595524001242","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"AUDIOLOGY & SPEECH-LANGUAGE PATHOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Following adult-onset hearing impairment, crossmodal plasticity can occur within various sensory cortices, often characterized by increased neural responses to visual stimulation in not only the auditory cortex, but also in the visual and audiovisual cortices. In the present study, we used an established model of loud noise exposure in rats to examine, for the first time, whether the crossmodal plasticity in the audiovisual cortex that occurs following a relatively mild degree of hearing loss emerges solely from altered intracortical processing or if thalamocortical changes also contribute to the crossmodal effects. Using a combination of an established pharmacological ‘cortical silencing’ protocol and current source density analysis of the laminar activity recorded across the layers of the audiovisual cortex (i.e., the lateral extrastriate visual cortex, V2L), we observed layer-specific changes post-silencing in the strength of the residual visual, but not auditory, input in the noise exposed rats with mild hearing loss compared to rats with normal hearing. Furthermore, based on a comparison of the laminar profiles pre- versus post-silencing in both groups, we can conclude that noise exposure caused a re-allocation of the strength of visual inputs across the layers of the V2L cortex, including enhanced visual-evoked activity in the granular layer; findings consistent with thalamocortical plasticity. Finally, we confirmed that audiovisual integration within the V2L cortex depends on intact processing within intracortical circuits, and that this form of multisensory processing is vulnerable to disruption by noise-induced hearing loss. Ultimately, the present study furthers our understanding of the contribution of intracortical and thalamocortical processing to crossmodal plasticity as well as to audiovisual integration under both normal and mildly-impaired hearing conditions.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
成年大鼠轻度听力损失后视听皮层视觉诱发活动的特定层增强。
成人听力受损后,各种感觉皮层会出现跨模态可塑性,其特征通常是不仅听觉皮层,而且视觉和视听皮层对视觉刺激的神经反应都会增强。在本研究中,我们利用已建立的大鼠暴露于高噪声的模型,首次研究了听力损失程度相对较轻时视听皮层中出现的跨模态可塑性是否仅源于皮层内处理过程的改变,或者丘脑皮层的变化是否也有助于产生跨模态效应。我们采用了成熟的药理学 "皮层沉默 "方案,并对视听皮层(即外侧视觉皮层,V2L)各层记录的层状活动进行了电流源密度分析,观察到与听力正常的大鼠相比,轻度听力损失的噪声暴露大鼠在沉默后残余视觉输入(而非听觉输入)的强度发生了特定层的变化。此外,根据两组大鼠消声前后的层状图比较,我们可以得出结论:噪声暴露导致视觉输入强度在 V2L 皮层各层之间重新分配,包括增强颗粒层的视觉诱发活动;这些发现与丘脑皮质可塑性一致。最后,我们证实,V2L皮层内的视听整合依赖于皮层内电路的完整处理,而这种形式的多感官处理很容易受到噪声引起的听力损失的干扰。最终,本研究加深了我们对皮层内和丘脑皮层处理对跨模态可塑性以及正常和轻度听力受损条件下视听整合的贡献的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
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.
期刊最新文献
Administration of nicotinamide mononucleotide suppresses the progression of age-related hearing loss in mice. Visualizing motions within the cochlea's organ of Corti and illuminating cochlear mechanics with optical coherence tomography. Brain activation patterns in normal hearing adults: An fNIRS Study using an adapted clinical speech comprehension task. Signal-in-noise detection across the lifespan in a mouse model of presbycusis. Why does tinnitus vary with naps? A polysomnographic prospective study exploring the somatosensory hypothesis.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1