A Korean research team found out the cause of the social decline in mice with autism and experimentally confirmed that it can be restored to some extent by light stimulation. If the research is further developed and applied to humans, it is expected to contribute to understanding and treating the social decline mechanisms of autistic patients in the future.
The research team, Eun-Jun Kim, head of the Synaptic Brain Disease Research Center at the Institute for Basic Science (IBS), found a condition in which the functions of brain neurons related to sociality and cognitive ability weakened through animal experiments and succeeded in restoring sociality by giving light stimulation. ‘ was introduced on the 25th (local time).
Autism is a type of brain development disorder that affects 2% of the world’s population. Decreased social and cognitive abilities are the main symptoms, and the exact pathogenesis is unknown.
According to the IBS Synaptic Brain Disease Research Center, through previous research, when the protein ‘Shank2’, which plays an important role in the creation, development, and function of synapses, is deleted, the function of ‘NMDA receptors’, which are important for synapses and neurons, is reduced and autism is induced. has been elucidated This study revealed the principle that synaptic-level problems lead to social and cognitive decline.
To find a link between brain changes and behavioral and cognitive functions, the researchers allowed autistic mice lacking the Shank2 protein to come into contact with a variety of objects, including moving objects and other mice, and observed the medial prefrontal cortex. The medial prefrontal cortex, the inner part of the frontal lobe of the brain, is primarily involved in cognitive, judgment, emotional, and thinking abilities.
As a result of the observation, neurons in normal mice responded differently to different subjects, but in autistic mice, they could not distinguish contact targets and showed similar neural activity patterns. If Shank2 is missing, it means that sociality is poor.
Schematic diagram of social decline and recovery through optogenetic stimulation in Shank2-deficient mice. Provided by IBS.
In the brain of autistic mice, the NMDA receptor function of ‘Pv neurons’ related to social and cognitive abilities among inhibitory neurons was weakened. This reduced the ‘multiple firing’ of generating multiple electrical signals at once, inhibiting the interaction between neurons. The researchers explained, “Autistic mice deficient in the Shank2 protein have abnormalities in the NMDA receptors of Pv neurons, resulting in decreased multiple firing, resulting in reduced social and cognitive abilities.”
The researchers also found that ‘electrical synapses’, which are direct pathways between neurons, were overly strengthened in Pv neurons. When a light stimulus is given to a specific Pv neuron, multiple firing occurs to nearby Pv neurons through electrical synapses, and social and cognitive abilities are restored.
Director Kim Eun-joon said, “We have succeeded in restoring sociality as well as the specific mechanism of social decline, the main symptom of autism.