Recovery of sensory hypersensitivity through inhibition of anterior cingulate cortex activity
The Institute for Basic Sciences (IBS, Director Noh Do-young) reported that it has found that the cause of sensory hypersensitivity in patients with autism spectrum disorders is excessive neurotransmission and increased network connectivity that occurs in specific areas of the cerebral cortex.
This is an achievement achieved by the team of Eun-Jun Kim, Director of the Synaptic Brain Disease Research Center (Professor Emeritus, Department of Life Sciences, KAIST) and Seong-Ki Kim, Director of the Neuroscience Imaging Research Center (Professor, Department of Global Biomedical Engineering, Sungkyunkwan University) using mouse model of autism.
In the case of autism spectrum disorder, hypersensitivity causes the patient to overreact to sounds, lights and touches in the everyday environment, causing considerable stress to the patient and significantly reducing the quality of life. Although it is common enough to be seen in approximately 90% of patients, its cause and mechanism are not clearly known.
The researchers first confirmed that autism-like hypersensitivity appeared in autism model mice lacking the “Grin2b” gene, one of the synapse genes.
Grin2b deletion is known to be associated with various brain diseases, including autism spectrum disorder, developmental delay, and obsessive-compulsive disorder. When researchers analyzed the responses of Grin2b-deficient autism model mice by applying mechanical and electrical stimulation and thermal stimulation, the autism model mice showed increased avoidance and hypersensitivity to sensory stimulation compared to the control group.
Next, c-fos imaging analysis, which can visualize the brain’s response to specific stimuli, was performed to identify brain regions that are abnormally hypersensitive to sensory stimulation.
Next, neural activity was monitored in real time using functional magnetic resonance imaging (fMRI) to analyze connectivity between brain regions.
As a result, it was found that in several brain regions, the anterior cingulate cortex (ACC), which is particularly related to high-level cognitive functions, was overly activated. Furthermore, hyperactivity of the anterior cingulate cortex increases excitatory neurotransmission in neurons, resulting in excessive connectivity between the anterior cingulate cortex and other brain regions.
Interestingly, when the hyperactivity of neurons in the anterior cingulate cortex was suppressed using chemical genetic methods, not only the hyperactivity of the anterior cingulate cortex but also the sensory hypersensitivity was normalized. This suggests that hyperactivation of the anterior cingulate cortex is the main cause of sensory hypersensitivity in autism spectrum disorder.
Director Kim Eun-jun, who led the research, said: “This is a new study demonstrating that excessive activity and connectivity of the anterior cingulate cortex, which is known to be closely related to high-level brain functions such as cognition and sociability, is the cause of sensory hypersensitivity in autism spectrum disorder”. “Suppressing the activity of neurons in the anterior cingulate cortex could be a way to treat sensory hypersensitivity associated with deletion of the Grin2b gene,” she said.
The results of this study were published online on May 4 (local time) in the world-renowned psychiatric journal “Molecular Psychiatry (IF 11.0)”.
Reporter Kim Young-jun kyj85@etnews.com
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