Zebrafish upregulate cortisol catabolism as a neuroprotective coping mechanism in response to waterborne cortisol exposure
The biology of chronic stress is a subject of interest due to its proposed negative consequences, including deficits to neurological welfare. To isolate the effects of chronic stress-induced elevated cortisol on neurogenesis, we developed a system that continuously exposed zebrafish to exogenous cortisol. We found that waterborne cortisol elicits small, transient increases in neurogenesis-related genes in the forebrain but no sustained effects. Though whole-body cortisol did not change, the exposure regime resulted in rapid, dose-dependent, and sustained increases in the forebrain gene expression of cortisol catabolic enzymes and whole-body levels of an inactive cortisol metabolite 20-dihydrocortisone. Differences in corticosteroid receptor expression – sequential, transient increase and decrease in both gr and mr and delayed, sustained decrease in gr – suggest differential involvement in the stress response. Overall, we provide a basis for developing a temporal map of chronic stress in zebrafish and highlight their impressive capacity for cortisol catabolism and neuroprotection in response to exogenous cortisol.