Scientists at Stanford have found that hyperactivity in the brain’s reticular thalamic nucleus may drive autism-like behaviors:
In the new study, the researchers recorded the neural activity of this brain region in mice while observing the animals’ behavior. In mice that had been genetically modified to model autism (Cntnap2 knockout mice), the reticular thalamic nucleus showed elevated activity when the animals encountered stimuli like light or an air puff as well as during social interactions. The brain region also showed bursts of spontaneous activity, causing seizures.
Epilepsy is much more prevalent in people with autism than in the general population — 30% versus 1% — though the mechanisms are not well understood. Recognizing this connection, the researchers tested an experimental seizure drug, Z944, and found that it reversed behavioral deficits in the autism mouse model.
With a different experimental treatment that genetically modifies neurons to respond to designer drugs, known as DREADD-based neuromodulation, the researchers could suppress overactivity in the reticular thalamic nucleus and reverse behavioral deficits in the autism mouse model. They could even induce these behavioral deficits in normal mice by ramping up activity in the reticular thalamic nucleus.