This renewal application is focused on the study of the development of the basolateral complex and medial nucleus of the amygdala. Collectively these nuclei regulate major aspects of limbic system function. Our previous studies have identified distinct progenitor pools in the developing telencephalon that contribute to postnatal neuronal cell diversity in these amygdala subdivisions. Based on this work, in this project we will test two hypotheses. First, we will test the hypothesis that embryonic transcriptional factor expression diversity within amygdala progenitor pools underlies differential postnatal amygdala neuronal subtype fate and patterns of axonal connectivity. Second, we will test the hypothesis that key transcription factors that are expressed in these progenitor domains are required for the development and/or connectivity of postnatal amygdala neurons that are derived from these populations. Testing of these hypotheses will be accomplished using a combination cutting edge approaches including genetic fate mapping, electrophysiology, axonal tracing and conditional loss of function.
The mammalian amygdala is a central structure of the brain's limbic system, a brain circuit that coordinates appropriate behavioral responses to stimuli with emotional and motivational salience. Amygdala dysfunction is associated with numerous brain disorders including addictive behavior and developmental disorders such as autism spectrum disorders. This proposal is directed toward understanding the genetic and cellular basis of amygdala development, and thus will provide valuable insight into human disorders in which amygdala function is altered.
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