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Abstract #2127

Kinase-inactive Met mice show altered forebrain functional connectivity: A resting state functional MRI study

Shiyu Tang1, Elizabeth M Powell2, Reha S Erzurumlu2, Wenjun Zhu1, Fu-Sun Lo2, and Su Xu1

1Diagnostic Radiology and Nuclear Medicine, University of Maryland School of Medicine, Baltimore, MD, United States, 2Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, MD, United States

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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