School of Neuroscience Innovators Seminar Series Presents:

Anthony LaMantia, Ph. D. Professor, Fralin Biomedical Research Institute. Director, Center for Neurobiology Research Virginia Tech.


Suckling, Feeding and Swallowing (S/F/S) is an essential innate behavior for all newborn mammals. This behavior, and the underlying circuits must be fully functional t from the moment of birth onward. Despite the essential nature of this innate behavior and its vulnerability to disruption in a broad range of genetic and clinically defined neurodevelopment disorders, very little is known about the underlying genetic architecture, developmental mechanisms and neural circuits that mediate S/F/S. This knowledge is key for understanding not only the normal behavior but also how its disruption—referred to as perinatal dysphagia—can be better diagnosed and managed. We have begun to define the relationship between genetic regulation of embryonic signaling and patterning,development of cranial nerve circuits, S/F/S biomechanics and behavior in newborn mice. We have used the mouse model of DiGeorge/22q11.2 Deletion Syndrome (22q11DS) to understand how a genetic lesion associated with multiple clinically defined neurodevelopmental  disorders (Autism, ADHD, Schizophrenia) also results in a high frequency of perinatal dysphagia. Our results indicate that the genetic lesion in 22q11DS, a heterozygous microdeletion of 1.5KB, disrupts the initial patterning of the hindbrain and neural crest at early stages of neural tube formation, and that this disruption leads to altered progenitor specification, axon and dendrite growth and synaptogenesis for cranial sensory and motor neurons. These genetic and developmental changes result in altered circuit function and S/F/S behaviors that likely underly perinatal dysphagia in 22q11DS.

For additional information contact: Dr. Michelle Olsen.