Assistant Professor, Department of Pediatics, The Ohio State University

The research interest of my laboratory is to understand the molecular mechanism of neurodevelopmental disabilities, such as autism and mental retardation.  Dendritic spines, the small protrusions on neuronal dendrites, are the primary site of synapse formation.  Abnormalities of dendritic spines, e.g., reduced spine density or abnormal spine morphology (such as immature shape) are associated with several developmental disabilities, including autism and mental retardation.  The severity of dendritic spine abnormalities in patients is parallel to the degree of cognitive impairment.  However, the relationship between dendritic spine morphological change and behavioral impairment is still unknown. 

We recently generated secretin receptor deficient mice.  Secretin receptor deficient mice are overtly normal and fertile, however, they show abnormal social and cognitive behaviors.  Furthermore, there are fewer dendritic spines in hippocampal pyramidal cells, and synaptic plasticity in the hippocampus is impaired.  Given these findings, we hypothesize that the secretin receptor signaling pathway is required for normal synapse formation, such as dendritic spine formation, which may directly affect social and cognitive behavioral phenotypes in adults.  Therefore, we will analyze to determine the role of the secretin receptor in dendritic development, as well as examine the effects of secretin receptor on adult behavioral and neurological phenotypes.  Understanding the mechanism of dendritic spine formation will shed light on the etiology and consequently novel treatment of developmental disabilities.