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孤独症谱系障碍(ASDs)患者常伴有痛感觉异常,部分患者对伤害性痛觉刺激(如碰撞和切割等)有更高的耐受阈值,有的甚至出现自残行为。已有研究表明,SHANK家族基因是先天性ASDs的致病基因,SHANK3基因的突变率大约为2%。本文旨在从SHANK3缺失的角度,探讨ASDs痛觉异常的发病机制。实验结果:(1)研究者建立Shank3外显子4-22敲除的小鼠(Shank3~(△e4–22)小鼠)。在本文中,纯合的Shank3~(△e4–22)小鼠称为Shank3~(-/-)小鼠
Patients with autism spectrum disorders (ASDs) often suffer from pain sensations. Some patients have higher tolerance thresholds for nociceptive pain (eg, collisions and cuts), and some even experience self-harm. Studies have shown that, SHANK family of genes is congenital ASDs pathogenic genes, SHANK3 gene mutation rate of about 2%. This article aims to explore the pathogenesis of dysarthria in ASDs from the perspective of SHANK3 deficiency. Experimental results: (1) The researchers established Shank3 exon 4-22 knockout mice (Shank3 ~ (△ e4-22) mice). In this paper, homozygous Shank3 ~ (△ e4-22) mice are called Shank3 ~ (- / -) mice