Scientists identified brain region that alters social interactions in autism model

In a mouse model, restoring the activity of a specific forebrain region reverses social traits associated with autism.


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The social deficit is a core clinical feature of autism spectrum disorder (ASD). However, the hidden neural systems remain mostly unclear.

In a new study by MIT scientists, scientists demonstrated that structural and functional impairments occur in glutamatergic synapses in the pyramidal neurons of the anterior cingulate cortex (ACC) in mice with a mutation in Shank3, a high-confidence candidate ASD gene. Mutations or deletions of the SHANK3 gene are emphatically connected with autism spectrum disorder (ASD) and a related rare disorder called Phelan-McDermid disorder.

The study provides clues to the neural circuits underlying social deficits associated with ASD. Furthermore, it found that structural and functional impairments in the anterior cingulate cortex (ACC) of SHANK3 mutant mice are linked to altered social interactions.

Guoping Feng, the James W. and Patricia T. Poitras Professor at MIT and one of the senior authors of the study said, “Neurobiological mechanisms of social deficits are very complex and involve many brain regions, even in a mouse model. These findings add another piece of the puzzle to mapping the neural circuits responsible for this social deficit in ASD models.”

Scientists focused on the ACC; a brain area noted for its job in social capacities in humans and animal models. The ACC is additionally known to assume a role in major cognitive procedures, including money-saving advantage estimation, inspiration, and decision making.

In mice lacking SHANK3, the specialists found structural and functional disruptions at the neurotransmitters, or associations, between excitatory neurons in the ACC. The analysts proceeded to demonstrate that the loss of SHANK3 in excitatory ACC neurons alone was sufficient to disturb communication between these neurons and prompted surprisingly diminished movement of these neurons during conduct tasks reflecting social interaction.

Having implicated these ACC neurons in social inclinations and interactions in SHANK3 knockout mice, scientists at that point tried in the case of initiating the same neurons could secure these practices. Utilizing optogenetics and specific drugs, Scientists actuated the ACC neurons and found improved social conduct in the SHANK3 mutant mice.

Scientists are further planning to explore brain regions downstream of the ACC that modulate social behavior in normal mice and models of autism.

Wanting Wang, a co-corresponding author of the study, said, “This will help us to better understand the neural mechanisms of social behavior, as well as social deficits in neurodevelopmental disorders.”

The study is published in Nature Neuroscience.


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