Auditory Dysfunction in Animal Models of Autism Spectrum Disorder
Autism spectrum disorder (ASD) is a neurodevelopmental disorder mainly characterized by social-communication impairments, repetitive behaviors and altered sensory perception. Auditory hypersensitivity is the most common sensory-perceptual abnormality in ASD, however, its underlying neurobiological m...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2022-04-01
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| Series: | Frontiers in Molecular Neuroscience |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fnmol.2022.845155/full |
| _version_ | 1818272446970593280 |
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| author | Ana Carolina Castro Ana Carolina Castro Patricia Monteiro Patricia Monteiro |
| author_facet | Ana Carolina Castro Ana Carolina Castro Patricia Monteiro Patricia Monteiro |
| author_sort | Ana Carolina Castro |
| collection | DOAJ |
| description | Autism spectrum disorder (ASD) is a neurodevelopmental disorder mainly characterized by social-communication impairments, repetitive behaviors and altered sensory perception. Auditory hypersensitivity is the most common sensory-perceptual abnormality in ASD, however, its underlying neurobiological mechanisms remain elusive. Consistently with reports in ASD patients, animal models for ASD present sensory-perception alterations, including auditory processing impairments. Here we review the current knowledge regarding auditory dysfunction in rodent models of ASD, exploring both shared and distinct features among them, mechanistic and molecular underpinnings, and potential therapeutic approaches. Overall, auditory dysfunction in ASD models seems to arise from impaired central processing. Depending on the model, impairments may arise at different steps along the auditory pathway, from auditory brainstem up to the auditory cortex. Common defects found across models encompass atypical tonotopicity in different regions of the auditory pathway, temporal and spectral processing impairments and histological differences. Imbalance between excitation and inhibition (E/I imbalance) is one of the most well-supported mechanisms explaining the auditory phenotype in the ASD models studied so far and seems to be linked to alterations in GABAergic signaling. Such E/I imbalance may have a large impact on the development of the auditory pathway, influencing the establishment of connections responsible for normal sound processing. |
| first_indexed | 2024-12-12T21:42:12Z |
| format | Article |
| id | doaj.art-7871961a59f54e13b44221e4fc6bf3ac |
| institution | Directory Open Access Journal |
| issn | 1662-5099 |
| language | English |
| last_indexed | 2024-12-12T21:42:12Z |
| publishDate | 2022-04-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Molecular Neuroscience |
| spelling | doaj.art-7871961a59f54e13b44221e4fc6bf3ac2022-12-22T00:11:00ZengFrontiers Media S.A.Frontiers in Molecular Neuroscience1662-50992022-04-011510.3389/fnmol.2022.845155845155Auditory Dysfunction in Animal Models of Autism Spectrum DisorderAna Carolina Castro0Ana Carolina Castro1Patricia Monteiro2Patricia Monteiro3Life and Health Sciences Research Institute, School of Medicine, University of Minho, Braga, PortugalICVS/3B’s–PT Government Associate Laboratory, Braga, PortugalLife and Health Sciences Research Institute, School of Medicine, University of Minho, Braga, PortugalICVS/3B’s–PT Government Associate Laboratory, Braga, PortugalAutism spectrum disorder (ASD) is a neurodevelopmental disorder mainly characterized by social-communication impairments, repetitive behaviors and altered sensory perception. Auditory hypersensitivity is the most common sensory-perceptual abnormality in ASD, however, its underlying neurobiological mechanisms remain elusive. Consistently with reports in ASD patients, animal models for ASD present sensory-perception alterations, including auditory processing impairments. Here we review the current knowledge regarding auditory dysfunction in rodent models of ASD, exploring both shared and distinct features among them, mechanistic and molecular underpinnings, and potential therapeutic approaches. Overall, auditory dysfunction in ASD models seems to arise from impaired central processing. Depending on the model, impairments may arise at different steps along the auditory pathway, from auditory brainstem up to the auditory cortex. Common defects found across models encompass atypical tonotopicity in different regions of the auditory pathway, temporal and spectral processing impairments and histological differences. Imbalance between excitation and inhibition (E/I imbalance) is one of the most well-supported mechanisms explaining the auditory phenotype in the ASD models studied so far and seems to be linked to alterations in GABAergic signaling. Such E/I imbalance may have a large impact on the development of the auditory pathway, influencing the establishment of connections responsible for normal sound processing.https://www.frontiersin.org/articles/10.3389/fnmol.2022.845155/fullautism spectrum disorder (ASD)sensory perceptionsound processingrodent modelsauditory dysfunction |
| spellingShingle | Ana Carolina Castro Ana Carolina Castro Patricia Monteiro Patricia Monteiro Auditory Dysfunction in Animal Models of Autism Spectrum Disorder Frontiers in Molecular Neuroscience autism spectrum disorder (ASD) sensory perception sound processing rodent models auditory dysfunction |
| title | Auditory Dysfunction in Animal Models of Autism Spectrum Disorder |
| title_full | Auditory Dysfunction in Animal Models of Autism Spectrum Disorder |
| title_fullStr | Auditory Dysfunction in Animal Models of Autism Spectrum Disorder |
| title_full_unstemmed | Auditory Dysfunction in Animal Models of Autism Spectrum Disorder |
| title_short | Auditory Dysfunction in Animal Models of Autism Spectrum Disorder |
| title_sort | auditory dysfunction in animal models of autism spectrum disorder |
| topic | autism spectrum disorder (ASD) sensory perception sound processing rodent models auditory dysfunction |
| url | https://www.frontiersin.org/articles/10.3389/fnmol.2022.845155/full |
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