Neurosciences & Mental Health Program, The Hospital for Sick Children, 555 University Ave., Toronto, M5G 1X8, ON, Canada.
Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Canada.
Mol Brain. 2017 Apr 7;10(1):10. doi: 10.1186/s13041-017-0290-2.
Human studies demonstrate that sleep impairment is a concurrent comorbidity of autism spectrum disorders (ASD), but its etiology remains largely uncertain. One of the prominent theories of ASD suggests that an imbalance in synaptic excitation/inhibition may contribute to various aspects of ASD, including sleep impairments. Following the identification of Nlgn3 mutation in patients with ASD, its effects on synaptic transmission and social behaviours have been examined extensively in the mouse model. However, the contributory role of this mutation to sleep impairments in ASD remains unknown. In this study, we showed that Nlgn3 knock-in mice, an established genetic model for ASD, exhibited normal duration and distribution of sleep/wake states but significantly altered electroencephalography (EEG) power spectral profiles for wake and sleep.
人类研究表明，睡眠障碍是自闭症谱系障碍（ASD）的一种并发共病，但它的病因在很大程度上仍不确定。ASD 的一个突出理论表明，突触兴奋/抑制失衡可能导致 ASD 的各个方面，包括睡眠障碍。在鉴定出 ASD 患者的 Nlgn3 突变后，其对突触传递和社会行为的影响已在小鼠模型中得到广泛研究。然而，这种突变对 ASD 中睡眠障碍的促成作用尚不清楚。在这项研究中，我们表明，Nlgn3 敲入小鼠，即 ASD 的一种既定遗传模型，表现出正常的睡眠/觉醒状态持续时间和分布，但显著改变了觉醒和睡眠的脑电图（EEG）功率谱特征。
