A research team at the Institute for Basic Science (IBS) research team has identified how autism spectrum disorders impair social interaction and provided clues for better understanding and treating declined social communication caused by autism.
In a previous study, the research team found that Shank2 protein deletion causes N-methyl-D-aspartate (NMDA) receptor dysfunction, which plays a key role in synaptic and neuronal function, and can lead to autism. In a recent study, the researchers revealed how synaptic-level problems lead to social and cognitive decline.
Autism spectrum disorders are a type of brain development disorder affecting about 2 percent of the world's population. Impaired social skills and cognition are considered the main symptoms, but the exact mechanism has not been explained.
The research team, led by Director Kim Eun-joon at IBS Center for Synaptic Brain Dysfunctions, put Shank2-deleted autistic mice in contact with moving objects and other mice to find a link between changes in the brain's behavioral and cognitive function.
In the brain of autistic mice, the NMDA receptor function of the Parvalbumin (Pv) neuron, related to social and cognitive ability among inhibitory neurons, was weakened. In addition, decreased NMDA receptor lowered burst firing for producing several electrical signals at once, inhibiting the interactions between neurons.
The study showed that the NMDA receptor gets problems and suppresses burst firing with Shank2 deletion, leading to impaired social and cognitive function.
Researchers also found that that electrical synapse, a direct link between neurons, was overly strengthened in Pv neurons. A specific Pv neuron with optogenetic stimulation caused burst firings in neighboring Pv neurons through electrical synapses and restored social and cognitive abilities.
"We have succeeded in improving social interaction by revealing a mechanism how autism spectrum disorders induce declined social ability, the main symptom of autism," Director Kim said. "The study results will provide a new direction for developing a treatment with a deeper understanding of autism."
The research results were published in the online international academic journal Nature Communications.