睡眠障碍在临床上非常普遍且患者数量巨大。睡眠障碍同样存在于患有孤独症的儿童中，但其原因一直不清楚。Neurexin/Neuroligin分子介导了突触的形成和突触的递质传递，neurexin/neuroligin基因突变与儿童孤独症的发生密切相关。我们近期报道了Neuroligin 4在睡眠中的作用。在此基础上，我们还发现neurexin突变果蝇具有睡眠维持的缺陷，但其机制不清楚。在本申请项目中，我们拟利用遗传学、分子生物学、行为学、影像学等方法研究Neurexin参与睡眠维持的分子细胞机制，并解析调控果蝇睡眠的神经环路基础。本研究的实施不仅有助于阐明儿童孤独症关联基因neurexin/neuroligin在睡眠调控中的作用机制，而且还有助于揭示控制果蝇睡眠的神经环路，为研究和治疗睡眠障碍提供借鉴和帮助。

Sleep is an essential and evolutionarily conserved behavior, but also remains one of the least understood biological phenomena. Sleep disorders are common, and are also frequently observed in the children with autism spectrum disorders (ASDs). However, the cause of those sleep disturbances is largely unknown. Neurexin/Neuroligin are synaptic adhesion molecules that function in synapse formation and synaptic transmission. Mutations of the neurexin/neuroligin genes have been strongly linked to ASDs. Recently, we reported the role of neuroligin 4 in sleep regulation. In addition, our primary data also show that Neurexin is involved in sleep homeostasis. However, the mechanism of Neurexin in sleep homeostasis is not clear. In this proposal, combination the approach in genetics, biochemistry and molecular biology, behavior study, image and electrophysiology, we plan to investigate the mechanism of Neurexin in sleep homeostasis. These studies will improve our knowledge in sleep regulation, and offers insight into the mechanism of sleep disturbances in autism patients.