Synaptic dysfunctions caused by SHANK3 mutation in relation to autism-like behaviors

Yuxuan Jing

doi:10.1117/12.3012908

8 January 2024 Synaptic dysfunctions caused by SHANK3 mutation in relation to autism-like behaviors

Yuxuan Jing

Proceedings Volume 12924, Third International Conference on Biological Engineering and Medical Science (ICBioMed2023); 129240B (2024) https://doi.org/10.1117/12.3012908
Event: 3rd International Conference on Biological Engineering and Medical Science (ICBioMed2023), 2023, ONLINE, United Kingdom

Abstract

SH3 and multiple ankyrin repeat domains protein 3 (SHANK3), a multidomain protein, has been identified as one of the few proteins that directly impact synaptic activities from multiple perspectives, especially during early developmental stages. Protein interactions between SHANK3 and other postsynaptic proteins have made SHANK3 critical in the process of dendrite and spine formation, vesicle release, synaptic transmission, and synaptic plasticity. A number of SHANK3 variants have been identified in neurodevelopmental disorders, particularly in Autism spectrum disorder (ASD). The mutation or deletion of SHANK3 results in different forms of synaptic dysfunctions and can even lead to altered spine morphologies, a decline in GABA-mediated synaptic transmission, and impaired long-term potentiation (LTP). As a result, these abnormalities are associated with representative autism-like behaviors. In this review, we focus on the role of normal SHANK3 in synaptic functions and the role of its mutations in ASD conditions. SHANK3 could provide new insights for the research focuses in ASD treatments, and contribute greatly to the future clinical field.

Citation Download Citation

Yuxuan Jing "Synaptic dysfunctions caused by SHANK3 mutation in relation to autism-like behaviors", Proc. SPIE 12924, Third International Conference on Biological Engineering and Medical Science (ICBioMed2023), 129240B (8 January 2024); https://doi.org/10.1117/12.3012908

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