MET, the gene encoding tyrosine kinase receptor for hepatocyte growth factor, is a susceptibility gene for autism spectrum disorder (ASD). Genetically altered mice with a kinase-inactive Met offer a potential model for understanding neural circuit organization changes in autism. We employed resting-state functional MRI to a kinase-inactive Met mouse model to test our hypothesis that aberrant functioning of the somatosensory-thalamocortical system is at the core of the conspicuous somatosensory behavioral phenotypes observed in autism. Results showed impaired organization of large-scale network and increased somatosensory-thalamocortical connectivity with a sex dependent manner and differences between heterozygous and homozygous Met-Emx1 mice.
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