The brain neural circuit that causes social decline due to autism has been identified. The research team led by Kim Eun-jun, director of the Synaptic Brain Disease Research Center at the Institute for Basic Science (IBS) (distinguished professor in the Department of Life Sciences at KAIST), presented a new perspective on ‘brain neural circuits’ as the cause of social decline, a major symptom of autism.
Autism spectrum disorder (autism) is a representative brain development disorder that causes poor social skills and repetitive behaviors and affects approximately 2.8% of the world’s population. The prevalence of autism is rapidly increasing every year, but there is no approved treatment yet as the exact pathogenesis mechanism is not known. Additionally, little was known about the link between autism and brain neural circuits. Nerve cells in various areas of the brain are complexly connected to each other to control brain function, and this is called a brain neural circuit.
Through previous research, the Synaptic Brain Disease Research Center reported that cerebral prefrontal neurons were excessively activated in an autism mouse model lacking the ‘synaptic protein IRSp53’ in the cerebral prefrontal cortex, which led to a decrease in social skills in autism patients. Through this study, it was confirmed that symptoms of reduced social skills in autistic patients are caused by overactivated prefrontal neurons damaging the reward circuits of the hypothalamus and midbrain.
The reward circuit, one of the brain’s neural circuits, makes us repeat actions essential for survival. For social animals such as mice and people, emotional communication is essential for survival, and the reward circuit plays a role in strengthening sociality by making people feel positive emotions when they engage in such behavior. When the neurotransmitter dopamine is secreted from the nerve cells that make up the reward circuit, you feel positive emotions.
Association between ‘synaptic protein IRSp53’ defect in the cerebral prefrontal cortex and reward circuit. Source: IBS
In an autism mouse model, prefrontal neurons were overactivated and the hypothalamus and midbrain reward circuits connected to them were abnormally suppressed. The reward circuit, which plays a role in strengthening social skills, is suppressed, leading to a lack of social skills. Neurons that secrete dopamine in the reward circuit were excessively suppressed compared to the normal mouse model.
In particular, the ventral tegmental area (VTA) of the midbrain is distributed with nerve cells that strengthen social skills by secreting dopamine during social interaction and causing positive emotions. In an autism mouse model, neurons in the ventral tegmental area of the midbrain were excessively suppressed, leading to decreased social skills.
Additionally, we were able to normalize the reward circuit by providing light stimulation to hypothalamic neurons. Neurons that produce dopamine were normalized, and social skills in the autism mouse model were also restored. This means that in the autism mouse model, hyperactivation of the prefrontal cortex inhibits the reward circuit, leading to a decline in social skills.
Director Kim Eun-jun said, “Through this study on autism model mice, we were able to reveal the neural circuit that regulates autism-related social skills.” He added, “Through follow-up research, we will additionally uncover brain regions and neural circuits that may be associated with autism spectrum disorders, which are the causes of autism. “It will be able to be used for understanding and treatment.”
The research results were published on September 20, 2023, in the online edition of the international academic journal ‘Molecular Psychiatry’.
논문명 : The PFC-LH-VTA pathway contributes to social deficits in IRSp53/ Molecular Psychiatry
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2023-09-30 02:20:00
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