Autism-risk gene mutations convergently disrupt sexually dimorphic oxytocin circuits to lower social engagement
Autism arises from diverse genetic risk factors, yet how they converge to produce core symptoms and contribute to its sex bias remains unestablished. Oxytocin increases sociability in multiple murine autism models, presenting an opportunity to identify a potentially shared mechanistic basis across etiologies. Here we show that spontaneous social investigation triggers overlapping patterns of…
Autism is believed to stem from various genetic risk factors, but the way they combine to cause the main symptoms and contribute to its gender bias is yet to be established. Oxytocin, known to boost sociability in several mouse models of autism, offers a chance to discover a possibly shared underlying mechanism shared among different causes.
This research demonstrates that triggering normal social interaction initiates similar patterns of irregular functional connections between social and sensory brain areas in two types of knockout (KO) mice. These irregular connections are subsequently corrected by administering oxytocin. The study further reveals that, during social interaction, regular mice display gender-specific oxytocin secretion and neuronal activity in the nucleus accumbens and amygdala.
However, these patterns are altered in both KO models, but can be returned to normal through targeted stimulation of the mice's natural oxytocin release, resulting in increased social interaction. The research concludes that impaired oxytocin activation of gender-specific social circuits is a common outcome of autism-risk gene mutations, potentially contributing to reduced sociability.
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