The hormone oxytocin can stimulate mice with autism-like symptoms to be more social, according to a new study. The research on young mice suggests a potentially critical window during early development when oxytocin can produce long-lasting benefits.
The findings are published in the 21 January issue of Science Translational Medicine.
Individuals on the autism spectrum often struggle with interacting or communicating with others. No drug for improving social behavior is currently available for this disorder. Oxytocin, known for its role in building social bond and trust in animals, has generated excitement as a possible treatment for autism, but clinical trials so far have proved disappointing.
In search of an effective drug, researchers created a mouse model of the disorder by deleting a gene responsible for a syndrome that causes a genetic form of autism spectrum disorder in humans.
"We wanted to see if we could use the mice to help inform the use of drugs in humans," said Daniel Geschwind of the University of California, Los Angeles, senior author of the study. "This study could really open a new window on how to look at this type of treatment."
Screening five drugs, the researchers found that oxytocin boosted social skills in the autistic mice, which performed better at a battery of behavioral tests and spent more time interacting with other mice than alone. Drugs that stimulated oxytocin release in the brain produced the same effect. Meanwhile, the hormone had no effect on normal mice.
"This made us think that there might be an abnormality in the actual oxytocin system in the animal," said Geschwind. Indeed, dissection revealed reduced levels of oxytocin in the brains of autistic mice, resulting from a shortage of oxytocin-producing neurons.
To see if treatment could influence brain development, the researchers gave daily doses of oxytocin to autistic mice while they were pups. Early treatment restored oxytocin to near normal levels in the mice and improved their social engagement even long after stopping treatment.
"At this point, we don't know if this [effect] will last forever or if they'll go back to their original levels," said Olga Peñagarikano, also from the University of California, Los Angeles and first author of the study.
More work needs to be done to understand this potential critical period in mice and whether it extends to people, said Geschwind. "Perhaps there'll be a possibility of measuring oxytocin in babies and children. Of course, that's very speculative. We don't know for sure," he said.
The reason clinical trials on oxytocin for autism spectrum disorders have delivered inconclusive results might have to do with the population of patients enrolled, said Geschwind. It's important to identify the subset of patients who have an oxytocin deficit and thus would respond to treatment, he said.
"We don't expect oxytocin to be able to help all autism patients," said Peñagarikano. "But we can find which patients can benefit the most from the treatment."
[Credit for associated teaser image: Flickr/ Ruud Hein]