神经肽
自闭症
睡眠(系统调用)
清醒
睡眠剥夺
加巴能
自闭症谱系障碍
神经科学
心理学
精神科
昼夜节律
脑电图
计算机科学
抑制性突触后电位
兴奋性突触后电位
操作系统
作者
Haiyan Sun,Yu Shen,Pengtao Ni,Xin Liu,Yan Li,Zhihai Qiu,Jennifer Su,Yihan Wang,Miao Wu,Xiangxi Kong,Jun‐Li Cao,Wei Xie,Shuming An
摘要
Patients with autism spectrum disorder (ASD) frequently experience sleep disturbance. Genetic mutations in Neuroligin-3 (NLG3) genes are highly correlative with ASD and sleep disturbance. However, the cellular and neural circuit bases of this correlation remain elusive. Here, we find the conditional knockout of NLG3 (NLG3-CKO) in the medial septum (MS) impairs social memory and reduces sleep. NLG3 knockout in MS causes hyperactivity of MS-GABA neurons during social avoidance and wakefulness. Activation of MSGABA neurons induces social memory deficits and sleep loss in C57BL/6 mice. In contrast, inactivation of these neurons ameliorates social memory deficits and sleep loss in NLG3-CKO mice. Sleep deprivation leads to social memory deficits, while social isolation causes sleep loss, both resulting in a reduction of NLG3 expression and an increase in activity of GABAergic neurons in MS from C57BL/6 mice. Furthermore, MS-GABA-innervated CA2 neurons specifically regulate social memory without impacting sleep, whereas MSGABA-innervating neurons in the preoptic area selectively control sleep without affecting social behavior. Together, these findings demonstrate that the hyperactive MS-GABA neurons impair social memory and disrupt sleep resulting from NLG3 knockout in MS, and achieve the modality specificity through their divergent downstream targets.
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