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Autism SHANK3 Mutation and Socal Interation By Kelly Jean Sullivan





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  The  brain is like a Circuit breaker: Neurons in mice missing SHANK3 from a circuit connecting the prefrontal cortex and basolateral amygdala have fewer primary dendritic branches than those in controls do. candidate gene, disrupt a brain circuit linked to social behavior, a new study in mice finds.

 social-interaction difficulties that characterize autism arise from altered communication between different parts of the brain, past research suggests — with some findings homing in on particular circuits: Overactivity between the prefrontal cortex, which regulates social activity, and the basolateral amygdala, which plays a role in learning about rewarding or unwanted outcomes, for example, appears to decrease sociability in wildtype mice.

Neurons in the prefrontal cortex-basolateral amygdala circuit in the modified SHANK3 mice sprouted shorter, denser dendrites compared with controls. The neurons also displayed increased excitatory and decreased inhibitory activity, with the mice showing elevated neural activity in the circuit, as well as greater variability in the strength of signals in the circuit.

 Autistic people’s brains show similar overactivity in this circuit, according to resting-state functional magnetic resonance images from the Autism Brain Imaging Data Exchange dataset.

The modified male mice also showed decreased sociability in the form of reduced sniffing of other mice.

The modified female mice did not display any significant social differences, consistent with findings that suggest autism manifests differently in girls versus boys, the researchers note. 










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