NSC PhD Defense Seminar: Danielle deCampo
An Extended Amygdala Path with Implications for Early Life Stress
Friday, November 1
Professor Julie Fudge, M.D.
Early life stress (ELS) carries an increased risk for the development of anxiety disorders. The goal of this thesis was to examine gene expression profiles in a novel circuit through the primate amygdala implicated in persistent anxiety, and to determine how ELS may alter gene expression in this path. The amygdala may exert effects on anxiety behaviors through inputs to the lateral bed nucleus of the stria terminalis (BSTL). In Aim 1, I used tracing techniques and found that a unique region of the amygdala, the paralaminar nucleus (PL), projects to the BSTL in primates. This suggests a novel path by which the amygdala can influence anxiety responses.
In primates, including humans, the adult PL contains a population of immature-appearing cells, suggesting capabilities for neural growth not seen in other amygdala regions. Because the PL projects to the BSTL (Aim 1), developmental changes in PL immature appearing cells may be important in BSTL regulation. In Aim 2, I used laser capture and microarray to examine whether the infant PL is enriched in genes involved in neuronal maturation.
Stress in early life can alter the developmental trajectory of maturing cells in the amygdala overall, resulting in precocious myelination, altered dendritic arborization and changes in the expression of synaptic plasticity genes. Altered neuronal maturation may be one mechanism through which ELS may alter PL structure and function, with consequences for downstream effector sites including the BSTL. In Aim 3, I used similar molecular techniques to determine whether ELS alters the expression of genes involved in neuronal maturation in the PL of stressed infant monkeys compared to controls.
Results of our gene expression studies confirm and extend previous data: cells in the PL have an increased expression of specific genes involved in neuronal maturation relative to an amygdala nucleus lacking immature appearing cells (Aim 2). Moreover, exposure to ELS decreases the expression of genes involved in neuronal maturation (Aim 3). In conclusion, ELS may affect neural development in the PL, which may ultimately alter circuitry that influences anxious behavioral responding through output channels such as the BSTL.
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