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HYPERACTIVE LATERAL HYPOTHALAMIC GABAERGIC NEURONS DRIVE ABNORMAL AGGRESSION IN NEUROLIGIN-3 R451C KNOCK-IN MICE
Xiaofan Liand 6 co-authors
Zhejiang University
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS07-10AM-242
Presentation
Date TBA
Board: PS07-10AM-242
Event Information
Poster Board
PS07-10AM-242
Poster
View posterAbstract
Aggressive behaviors are a common and clinically challenging comorbidity in individuals with autism spectrum disorder (ASD), yet their neural mechanisms remain poorly understood. Using the Neuroligin-3 R451C knock-in mouse model (NL3R451C) of ASD, we identified and characterized a specific neural circuit driving abnormal aggression. NL3 R451C mice exhibited heightened aggression in the resident-intruder test and aggression-seeking behavior. Following aggression, these mice showed increased neuronal activation (c-Fos+) in in multiple brain regions including the lateral hypothalamus (LH), prelimbic cortex (PrL), and ventral tegmental area (VTA). Fiber photometry revealed enhanced activity in both LH GABAergic neurons and PrL glutamatergic neurons projecting to the LH during attacks. Crucially, chemogenetic inhibition of LH GABAergic neurons projecting to either the periaqueductal gray or the VTA rescued excessive aggression, while inhibition of PrL®LH glutamatergic projections did not. Furthermore, re-expressing neuroligin-3 specifically in LH GABAergic neurons was sufficient to ameliorate the aggressive phenotype. Together, these results demonstrate that overactivation of LH GABAergic neurons due to neuroligin-3 deficiency is a critical pathological driver of abnormal aggression in this ASD model, revealing a precise circuit target for potential therapeutic intervention.
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