Institute for Biomedical Sciences, The George Washington University, Washington DC, United States; Center for Neuroscience Research, Children's National Medical Center, Washington, DC, United States
Katie Sokolowski
Center for Neuroscience Research, Children's National Medical Center, Washington, DC, United States
Peijun Li
Center for Neuroscience Research, Children's National Medical Center, Washington, DC, United States
Shigeyuki Esumi
Center for Neuroscience Research, Children's National Medical Center, Washington, DC, United States; Graduate School of Medical Sciences, Kumamoto-University, Kumamoto City, Japan
Yasmin Kamal
Center for Neuroscience Research, Children's National Medical Center, Washington, DC, United States
Meredith Goodrich
Center for Neuroscience Research, Children's National Medical Center, Washington, DC, United States
Livio Oboti
Center for Neuroscience Research, Children's National Medical Center, Washington, DC, United States
Timothy R Hammond
Center for Neuroscience Research, Children's National Medical Center, Washington, DC, United States
Meera Krishnamoorthy
Center for Neuroscience Research, Children's National Medical Center, Washington, DC, United States
Daniel Feldman
Center for Neuroscience Research, Children's National Medical Center, Washington, DC, United States
Molly Huntsman
Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado
Judy Liu
Center for Neuroscience Research, Children's National Medical Center, Washington, DC, United States
The medial subnucleus of the amygdala (MeA) plays a central role in processing sensory cues required for innate behaviors. However, whether there is a link between developmental programs and the emergence of inborn behaviors remains unknown. Our previous studies revealed that the telencephalic preoptic area (POA) embryonic niche is a novel source of MeA destined progenitors. Here, we show that the POA is comprised of distinct progenitor pools complementarily marked by the transcription factors Dbx1 and Foxp2. As determined by molecular and electrophysiological criteria this embryonic parcellation predicts postnatal MeA inhibitory neuronal subtype identity. We further find that Dbx1-derived and Foxp2+ cells in the MeA are differentially activated in response to innate behavioral cues in a sex-specific manner. Thus, developmental transcription factor expression is predictive of MeA neuronal identity and sex-specific neuronal responses, providing a potential developmental logic for how innate behaviors could be processed by different MeA neuronal subtypes.