Investigating the Role of 11beta-Hydroxysteroid Dehydrogenase Type 2 in Mediating the Stress-Specific Effects of Cortisol on Neurogenesis in Adult Zebrafish (Danio rerio)
Stress-induced increases in cortisol during acute and chronic stress can have biphasic effects on brain cell proliferation. The cortisol-inactivating enzyme, 11β-hydroxysteroid dehydrogenase type 2 (Hsd11b2), may modulate this differential response by buffering intracellular cortisol. Hsd11b2 is localized to known neurogenic regions of the adult zebrafish (Danio rerio) brain, but its role in regulating adult neurogenesis is unknown. My master’s thesis provides novel experimental evidence to support the hypothesis that the stressor-specific effects of cortisol on neurogenesis are mediated by the dynamic regulation of Hsd11b2. The key finding of this research is that Hsd112 gene and protein expression are induced by acute but not chronic stress, suggesting that the capacity for cortisol catabolism may underscore the context-specific effects of stress on neurogenesis. My thesis presents the differential regulation of Hsd11b2 as a newfound endogenous regulator advancing our comparative understanding of adult neurogenesis and providing ideas for future work.