Meeting Abstract
Glucocorticoids (GCs) perform diverse regulatory actions in the body under baseline conditions and during stress. In the brain, GCs participate in negative feedback regulation of the hypothalamic-pituitary-adrenal axis and influence cognition, at times enhancing or inhibiting cognitive capabilities. Critically, excess GCs inhibit neurogenesis, which is widespread in the songbird brain and functionally significant for behavior. Using in vivo microdialysis, we showed that the male zebra finch brain contains detectable, fluctuating, and region-specific levels of GCs. However, while robustly elevated in the periphery, GCs did not significantly increase in the brain during and after an acute stressor. In zebra finches, regional differences in GCs correspond to expression levels of 11β hydroxysteroid dehydrogenase type 2 (11β HSD2), an enzyme that de-activates GCs, leading us to hypothesize that 11β HSD2 regulates neural GC levels. We tested this hypothesis in males and females by retrodialyzing the 11β HSD2 inhibitor carbenoxolone (CBX) during microdialysis, followed by a standard stress series. We also examined the co-expression of the GC receptors MR and GR, along with 11β HSD2, in several regions of the brain including the hippocampus and caudal medial nidopallium (NCM). These regions lie adjacent to the ventricular zone where neurogenesis occurs. The results of these experiments are expanding our understanding of the mechanisms by which the brain regulates exposure to GCs, a topic of critical importance for predicting the impact of stress on reproduction, learning, and memory, especially in the popular songbird model system.
