Adenosine Actions on Oligodendroglia and Myelination in Autism Spectrum Disorder

被引:16
|
作者
Shen, Hai-Ying [1 ,2 ]
Huang, Nanxin [3 ]
Reemmer, Jesica [1 ]
Xiao, Lan [3 ]
机构
[1] Legacy Hlth, Legacy Res Inst, Robert Stone Dow Neurobiol Dept, Portland, OR USA
[2] Washington State Univ, Dept Integrat Physiol & Neurosci, Pullman, WA 99164 USA
[3] Army Med Univ, Mil Med Univ 3, Chongqing Key Lab Neurobiol, Dept Histol & Embryol, Chongqing, Peoples R China
来源
基金
中国国家自然科学基金;
关键词
adenosine receptor; oligodendroglial differentiation; demyelination; neurotransmitter; autism; NUCLEOSIDE TRANSPORTER FAMILY; RECEPTOR-MEDIATED MODULATION; CENTRAL-NERVOUS-SYSTEM; A(2A) RECEPTOR; ACETYLCHOLINE-RELEASE; CNS MYELINATION; MOUSE MODEL; CGS; 21680; BRAIN; ACTIVATION;
D O I
10.3389/fncel.2018.00482
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Autism spectrum disorder (ASD) is the most commonly diagnosed neurodevelopmental disorder. Independent of neuronal dysfunction, ASD and its associated comorbidities have been linked to hypomyelination and oligodendroglial dysfunction. Additionally, the neuromodulator adenosine has been shown to affect certain ASD comorbidities and symptoms, such as epilepsy, impairment of cognitive function, and anxiety. Adenosine is both directly and indirectly responsible for regulating the development of oligodendroglia and myelination through its interaction with, and modulation of, several neurotransmitters, including glutamate, dopamine, and serotonin. In this review, we will focus on the recent discoveries in adenosine interaction with physiological and pathophysiological activities of oligodendroglia and myelination, as well as ASD-related aspects of adenosine actions on neuroprotection and neuroinflammation. Moreover, we will discuss the potential therapeutic value and clinical approaches of adenosine manipulation against hypomyelination in ASD.
引用
收藏
页数:12
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