ArticleThe Journal of clinical investigation2024
Autism-associated neuroligin 3 deficiency in medial septum causes social deficits and sleep loss in mice.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Neuroligin1 in CCK-interneurons gates social memory formation via a disinhibitory microcircuit in the hippocampal CA2 in male mice.Nature communications · 2026Article
- Article
- Stress ensemble in the BNST mediates comorbid anxiety and sleep disruption.Science advances · 2026Article
- Deficiency of calretinin in prefrontal cortex causes behavioral deficits relevant to autism spectrum disorder in mice.Molecular brain · 2025Article
- Brain circuits that regulate social behavior.Molecular psychiatry · 2025Review
- Sleepless nights and social plights: medial septum GABAergic hyperactivity in a neuroligin 3-deficient autism model.The Journal of clinical investigation · 2024Article
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13 authors.
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Abstract
Patients with autism spectrum disorder (ASD) frequently experience sleep disturbance. Genetic mutations in the neuroligin 3 (NLG3) gene are highly correlative with ASD and sleep disturbance. However, the cellular and neural circuit bases of this correlation remain elusive. Here, we found that the conditional knockout of Nlg3 (Nlg3-CKO) in the medial septum (MS) impairs social memory and reduces sleep. Nlg3 CKO in the MS caused hyperactivity of MSGABA neurons during social avoidance and wakefulness. Activation of MSGABA neurons induced social memory deficits and sleep loss in C57BL/6J mice. In contrast, inactivation of these neurons ameliorated social memory deficits and sleep loss in Nlg3-CKO mice. Sleep deprivation led to social memory deficits, while social isolation caused sleep loss, both resulting in a reduction in NLG3 expression and an increase in activity of GABAergic neurons in the MS from C57BL/6J mice. Furthermore, MSGABA-innervated CA2 neurons specifically regulated social memory without impacting sleep, whereas MSGABA-innervating neurons in the preoptic area selectively controlled sleep without affecting social behavior. Together, these findings demonstrate that the hyperactive MSGABA neurons impair social memory and disrupt sleep resulting from Nlg3 CKO in the MS, and achieve the modality specificity through their divergent downstream targets.
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