What comes next?
Hiroi is taking the work a step further by teaming with Jason Pugh, Ph.D., in the UT Health San Antonio Department of Cellular and Integrative Physiology, to examine excitability of a specific type of neuron in the amygdalo-piriform transition area of Tbx1-deficient mice.
They are also working on models that could initiate and restore Tbx1 heterozygosity (having two versions of the same gene) at any stage of development. When complete, Hiroi said they plan to use this model to discover the critical developmental period for amygdala shrinkage.
Amygdala volume reduction appears to originate in the embryonic phase, Hiroi said, so therapeutic intervention could target this point. Additionally, the degree of amygdala shrinkage could be a biomarker of impaired appreciation of social experiences for people with autism spectrum disorder or schizophrenia.
“This study can serve as a catalyst to translationally link basic science with human brain imaging studies and studies of patients with neurodevelopmental disorders, which are already major strengths of UT Health San Antonio,” said Hiroi.