In a mouse model of autism, a single injection of a designer drug re-grew a shrunken part of the neuron and, within an hour, the mice went from antisocial and compulsive to behaving like healthy controls. That's the finding of a new study in Cell Death & Disease, written up by Eric W. Dolan at PsyPost, and the part the researchers found surprising is that the brain abnormality turned out to be reversible.
The team, led by Shimane University's Masashi Fujitani, zeroed in on the axon initial segment — the spot on a nerve cell where it decides whether to fire. In the autism-model mice, that segment was shortened in a specific layer of the prefrontal cortex, making those neurons sluggish to fire, especially along the pathway to the dorsal raphe nucleus, a major source of the brain's serotonin. Using chemogenetics — engineered receptors switched on by a drug — they reactivated exactly that circuit. The shortened segments stretched back to normal length, and the treated mice spent normal time with unfamiliar mice and buried far fewer marbles. "In a way, it seemed as if the system was simply 'switched too far' rather than fundamentally broken," Fujitani told PsyPost.
The usual caveats apply, and Fujitani is the first to state them: it's mice, it's a single autism model, and "further research is needed to determine whether the findings can be directly applied to humans."
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