期刊
NEUROCHEMISTRY INTERNATIONAL
卷 153, 期 -, 页码 -出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2021.105273
关键词
Axon initial segment; Ankyrin-G; Attention-deficit hyperactivity disorder; Autism spectrum disorder; Neurodevelopmental disorder
资金
- Japan Society for the Promotion of Science (JSPS) [20K06872, 17K07118, 20K06855]
- JSPS [18K14814]
- Uehara Memorial Foundation
- Takeda Science Foundation, Japan
- SENSHIN Medical Research Foundation
- Osaka Medical Research Foundation for Intractable Diseases, Japan
- Eli Lilly Japan Research Grant, Japan
- Japan Foundation for Applied Enzymology, Japan
- Grants-in-Aid for Scientific Research [20K06855, 18K14814, 17K07118, 20K06872] Funding Source: KAKEN
Researchers found that the length of the axon initial segment (AIS) is abnormally changed in rodent models of attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). These findings suggest that impairments in AIS length may be a common feature of neurodevelopmental disorders and may be conserved across species.
The axon initial segment (AIS) is a structural neuronal compartment of the proximal axon that plays key roles in sodium channel clustering, action potential initiation, and signal propagation of neuronal outputs. Mutations in constitutive genes of the AIS, such as ANK3, have been identified in patients with neurodevelopmental disorders. Nevertheless, morphological changes in the AIS in neurodevelopmental disorders have not been characterized. In this study, we investigated the length of the AIS in rodent models of attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). We observed abnormalities in AIS length in both animal models. In ADHD model rodents, we observed shorter AIS length in layer 2/3 (L2/3) neurons of the medial prefrontal cortex (mPFC) and primary somatosensory barrel field (S1BF). Further, we observed shorter AIS length in S1BF L5 neurons. In ASD model mice, we observed shorter AIS length in L2/3 and L5 neurons of the S1BF. These results suggest that impairments in AIS length are common phenomena in neurodevelopmental disorders such as ADHD and ASD and may be conserved across species. Our findings provide novel insight into the potential contribution of the AIS to the pathophysiology and pathogenesis of neurodevelopmental disorders.
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