Activating the release of a mood-regulating chemical into a single brain circuit in mice that were genetically altered to exhibit autismlike symptoms can make the mice more sociable, a new Stanford study reported.
“This points to a previously understudied brain mechanism that contributes to an inability to derive pleasure from social interactions,” said Robert Malenka, MD, PhD, professor and associate chair of psychiatry and behavioral sciences, and senior author of the study published Aug. 8 in Nature.
Autism spectrum disorder is marked by severe social deficits, which researchers were able to reverse in mice by manipulating the release of serotonin, a chemical and neurotransmitter that regulates, among other things, mood and social behavior.
“Mice aren’t little human beings,” Malenka said. “We can’t ask them how they’re feeling about their social lives. But they provide insights into the human brain. They can be very useful for studying relatively primitive mechanisms governing social behavior.”
Malenka said that drugs designed to activate a particular subtype of receptor for serotonin found predominantly in the brain’s nucleus accumbens — a region that helps control reward and motivation — could improve sociability in people with autism and other disorders that lead to social withdrawal.