Sleepless nights and social plights: medial septum GABAergic hyperactivity in a neuroligin 3-deficient autism model.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 39352378.
- Also identified by DOI 10.1172/JCI184795 and PMC identifier 11444191.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
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.
Medical subject headings
- Cell Adhesion Molecules, Neuronal
- GABAergic Neurons
- Disease Models, Animal
- Nerve Tissue Proteins
- Membrane Proteins