Autistic Mice Go Social

Researchers from the California Institute of Technology published a study Septermber 11 in online journal Cell that has exciting implications for understanding underlying neural circuit dysfunctions in autism. Specifically, the study focused on the part of the brain called the amygdala, which processes emotions. The big discovery: antagonistic neuron populations in mouse amygdala control whether the mouse engages in social or asocial behavior. Many studies have already established that autism in mice correlates with autism in humans. 

Researchers describe the discovery as a “see-saw circuit” because the animals can’t engage in both social behavior and asocial repetitive self-grooming at the same time. Their mission was to find out why. 

The team, led by postdoctoral scholar Weizhe Hong in the laboratory of David J. Anderson, the Seymour Benzer Professor of Biology at Caltech and an investigator with the Howard Hughes Medical Institute, discovered two intermingled, yet distinct neuron populations in the amygdala. One population controls social behavior such as mating, fighting, or social grooming, while the other controlled asocial behavior such as repetitive self-grooming. The social neurons, they found, are inhibitory and release the neurotransmitter GABA, while the asocial neurons are excitatory and release the neurotransmitter glutamate, an amino acid. 

The researchers employed a technique called optogenetics to study the relationship between these two types of cells and their associated behaviors. The neurons were genetically altered to express light-sensitive proteins via microbial organisms. Then, by shining a light on the modified neurons via a tiny fiber optic cable inserted in the brain, the researchers were able to control the activity of the cells and their associated behaviors. 

The researchers were effectively able to switch different behaviors on and off. By shining the light on the social neurons, the mice exhibited social behavior. When this light was turned up, the mice became aggressive. When the light was shone on the asocial neurons, the mice spontaneously started to groom themselves. They were then able to switch off the asocial behavior by switching on the social behavior.

What really surprised the researchers was the way in which these two groups of neurons appear to interfere with each other. The activation of the social neurons inhibited the asocial behavior, while the triggering the asocial neurons inhibited the social behavior; hence the seesaw analogy.

In autism,” Anderson says, “there is a decrease in social interactions, and there is often an increase in repetitive, sometimes asocial or self-oriented, behaviors” — a phenomenon known as perseveration. “Here, by stimulating a particular set of neurons, we are both inhibiting social interactions and promoting these perseverative, persistent behaviors.” 

There have been previous studies that show how disruptions in autism-related genes can change social and asocial behavior, but this study is the first to provide the necessary link between gene activity, brain activity, and social behaviors. Obviously, the goal is not to establish a therapy where autistic people have their neurons genetically altered and then controlled via fiber optic cables, but the understanding of this seesaw circuitry will be necessary in developing future therapies. 

“All of this is very far away,” says Anderson, “but if you found the right population of neurons, it might be possible to override the genetic component of a behavioral disorder like autism, by just changing the activity of the circuits — tipping the balance of the see-saw in the other direction.”

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