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School of Medicine and Health Sciences Poster Presentations
Amygdala Neural Development Mechanisms Are Linked to Innate Social and Non-social Behaviors During Adulthood
Poster Number
27
Document Type
Poster
Publication Date
3-2016
Abstract
Innate behaviors for fight, flight and reproduction are essential for species survival and propagation. As these innate behaviors manifest without prior training, there must be embryonic developmental mechanisms that specify these circuits. The medial amygdala (MeA), as a major target for olfactory inputs, has been implicated in the regulation of these innate behaviors. I aim to elucidate how embryonic transcription factors generate distinct neuronal subpopulations that regulate diverse social and non-social innate behaviors. During amygdala development there are at least two neuronal progenitor pools that contribute to MeA neuronal diversity. We focused on two embryonic progenitor populations that are marked by the expression of the transcription factors: Dbx1 and the autism susceptibility gene Foxp2. We found that neuronal progenitors expressing the transcription factors Dbx1 or Foxp2 will become two distinct non-overlapping adult MeA neuronal subpopulations. These two populations express different molecular markers and possess distinct intrinsic electrophysiological properties. Furthermore, Dbx1-derived and Foxp2+ MeA neurons were activated during distinct innate behaviors involved in reproduction, aggression and predator avoidance. Therefore, activation of distinct neuronal subpopulations during key social and non-social behaviors are linked to transcription factor expression during development. Thus, future research should focus on how alterations in embryonic transcription factor expression can lead to social disorders characterized by amygdala based behavioral deficits, such as autism.
Amygdala Neural Development Mechanisms Are Linked to Innate Social and Non-social Behaviors During Adulthood
Innate behaviors for fight, flight and reproduction are essential for species survival and propagation. As these innate behaviors manifest without prior training, there must be embryonic developmental mechanisms that specify these circuits. The medial amygdala (MeA), as a major target for olfactory inputs, has been implicated in the regulation of these innate behaviors. I aim to elucidate how embryonic transcription factors generate distinct neuronal subpopulations that regulate diverse social and non-social innate behaviors. During amygdala development there are at least two neuronal progenitor pools that contribute to MeA neuronal diversity. We focused on two embryonic progenitor populations that are marked by the expression of the transcription factors: Dbx1 and the autism susceptibility gene Foxp2. We found that neuronal progenitors expressing the transcription factors Dbx1 or Foxp2 will become two distinct non-overlapping adult MeA neuronal subpopulations. These two populations express different molecular markers and possess distinct intrinsic electrophysiological properties. Furthermore, Dbx1-derived and Foxp2+ MeA neurons were activated during distinct innate behaviors involved in reproduction, aggression and predator avoidance. Therefore, activation of distinct neuronal subpopulations during key social and non-social behaviors are linked to transcription factor expression during development. Thus, future research should focus on how alterations in embryonic transcription factor expression can lead to social disorders characterized by amygdala based behavioral deficits, such as autism.
Comments
Presented at: GW Research Days 2016.