Mice with Impaired Met Tyrosine Kinase Signaling Demonstrate Characteristics Relevant to AutismJacob M. Smith1, Elizabeth M. Powell1,2,3*
- *Corresponding Author:
- Elizabeth M. Powell
HSF II S251, 20 Penn St.,Baltimore, MD 21201, USA
E-mail: [email protected]
Received date: August 30, 2012; Accepted date: September 26, 2012; Published date: October 03, 2012
Citation: Smith JM, Powell EM (2012) Mice with impaired Met Tyrosine Kinase Signaling demonstrate characteristics relevant to autism. Autism S1:002. doi:10.4172/2165-7890.S1-002
Copyright: © 2012 Smith JM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Variants of MET, a receptor tyrosine kinase which binds the ligand Hepatocyte growth factor (HGF), have been linked to elevated risk for developing autism spectrum disorders (ASD) in humans. Though best known as a proto-oncogene, MET also plays important roles during normal development, including the development of the central nervous system. Recent studies in several mouse lines have shown that mice with reduced HGF-Met signaling have altered profiles of interneurons in the cortex, striatum, and hippocampus. Alterations in neuronal development, particularly in the cerebral cortex, may contribute to the pathology of developmental disorders, including autism. Other studies have shown changes in excitatory signaling in the Met-deficient cortex. Interestingly, mice with deficient Met signaling also show behavioral alterations characteristic of autism. Here we review anatomical and behavioral findings in mice with altered HGF - Met signaling.