Neuroscientists at Stanford University have discovered that hyperactivity in the thalamic reticular nucleus (RTN) directly causes behaviors associated with autism, opening the door to novel therapeutic strategies.
Using mice with a deletion of the Cntnap2 gene, researchers observed heightened RTN activity in response to light, air puffs, and social interactions. These mice displayed repetitive behaviors, increased sensitivity to stimuli, and reduced social engagement, hallmarks of autism. Additionally, they showed a higher likelihood of seizures, a common biomarker in neurodevelopmental disorders.
The experimental anticonvulsant Z944 reduced RTN activity and alleviated autistic-like behaviors, highlighting shared mechanisms between autism and epilepsy. Similar results were achieved with the DREADD method, a genetic neuromodulation technique: suppressing RTN decreased symptoms, while artificially activating it in healthy mice induced them.
Lead author Sun-Su Zhang emphasized that this study provides the first direct causal evidence. He noted that targeting the RTN could serve as a dual-purpose therapy for both autism and epilepsy: “We have uncovered a mechanism that can be regulated, not just observed.”
