Excess activity in reticular thalamic nucleus sparks autism traits in mice; treatments to calm it reversed sensitivity and repetition.
Researchers at Stanford Medicine have pinpointed a brain region that may drive autism-related behaviors. They report that dialing down its activity reversed symptoms in mice engineered to model autism.
The discovery highlights a new target for treatment and shows overlap with epilepsy research.The study zeroed in on the reticular thalamic nucleus, or RTN, a region that filters sensory information between the thalamus and cortex. This area had not been directly tied to autism before.Using a mouse model lacking the Cntnap2 gene, scientists recorded heightened activity in the RTN when animals faced stimuli such as light flashes or air puffs. The RTN also spiked during social encounters. In addition, bursts of spontaneous activity triggered seizures.Mice with this neural overdrive displayed traits often linked to autism. These included repetitive behaviors, heightened sensitivity, reduced social interaction, and increased motor activity. They also had greater seizure susceptibility.The findings position the RTN as a promising treatment target. John Huguenard, professor of neurology and neurological sciences, served as senior author. Lead author Sung-Soo Jang is a postdoctoral scholar in the same department.Shared pathways with epilepsyAutism and epilepsy often occur together. Roughly 30% of people with autism also experience epilepsy, compared with 1% of the general population. The connection remains poorly understood, but the new work strengthens the link.The team tested Z944, an experimental seizure drug. Administering it dampened RTN overactivity and reversed behavioral deficits in the autism mouse model. The results suggest that drugs developed for epilepsy may also hold potential for autism.Researchers also tried a method called DREADD-based neuromodulation. This approach genetically alters neurons so that they can be controlled by designer drugs. Using it, scientists suppressed RTN hyperactivity in the mice. Once again, autism-like behaviors eased.The experiments cut both ways. When researchers ramped up RTN activity in otherwise normal mice, the animals developed autism-like traits. This direct evidence strengthens the case that RTN overactivity drives the behavioral changes.A new treatment targetConnections between the thalamus and cortex have long been implicated in autism. Until now, the RTN’s specific role had remained uncertain. By identifying it as a driver of key behaviors, the Stanford team has opened a new path for intervention.The work also shows how targeting the RTN may address two conditions at once. With autism and epilepsy often appearing together, therapies that calm this region could serve both groups of patients.The authors emphasize that findings in mice do not guarantee the same results in people. Still, the study provides a clear framework for testing treatments.The research adds to a growing understanding of how disrupted brain circuits shape neurodevelopmental disorders. As the authors note in Science Advances, “Reticular thalamic hyperexcitability drives autism spectrum disorder behaviors in the Cntnap2 model of autism.”The study is published in the journal Science Advances.
Epilepsy Mouse Model Neuroscience Research Reticular Thalamic Nucleus Seizure Drug Stanford Medicine
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