J Clin Invest. 2024 Oct 1;134(19):e184795. doi: 10.1172/JCI184795.
Social deficits represent a core symptom domain of autism spectrum disorder (ASD), which is often comorbid with sleep disturbances. In this issue of the JCI, Sun et al. explored a medial septum (MS) circuit linking these behaviors in a neuroligin 3 conditional knockout model of autism. They identified GABAergic neuron hyperactivity following neuroligin 3 deletion in the MS. This hyperactivity resulted in the inhibition of the downstream preoptic area (POA) and hippocampal CA2 region, resulting in sleep loss and social memory deficits, respectively. Inactivating the hyperactive MS GABA neurons or activating the POA or CA2 rescued the behavioral deficits. Together, these findings deepen our understanding of neural circuits underlying social and sleep deficits in ASD.
社交缺陷是自闭症谱系障碍（ASD）的核心症状领域之一，常伴有睡眠障碍。在本期 JCI 中，Sun 等人在自闭症的神经连接蛋白 3 条件性敲除模型中探索了一个连接这些行为的中隔（MS）回路。他们发现神经连接蛋白 3 缺失后 MS 中的 GABA 能神经元过度活跃。这种过度活跃导致下游视前区（POA）和海马 CA2 区受到抑制，分别导致睡眠减少和社交记忆缺陷。使过度活跃的 MS GABA 神经元失活或激活 POA 或 CA2 可挽救行为缺陷。总之，这些发现加深了我们对 ASD 中社交和睡眠缺陷相关神经回路的理解。
