Mechanisms underlying the cortisol response to acute warming in a freshwater teleost fish

Although acute warming is well known to increase circulating concentrations of the glucocorticoid stress hormone cortisol in fishes, the mechanisms through which fish perceive high temperatures as a stressor and activate the hypothalamic-pituitary-interrenal (HPI) axis remain poorly understood. Here, we probed these mechanisms using measurements of the cortisol response to thermal ramping, cortisol production by isolated head kidney preparations, and transcript abundances of key genes of the HPI axis. Rainbow trout mounted a significant (4.4-fold increase over baseline) cortisol response to thermal ramping at 27 °C. This 'threshold' temperature was lowered to 25 °C by 4 d of cortisol treatment and raised to 29 °C by acclimation to warmer (22 °C) water. Although transcript abundances of most HPI axis genes were unaffected by thermal ramping, expression of the steroidogenic factor (SF-1) paralogue ff1d was significantly higher (~3.1-fold) in trout exposed to thermal ramping to 27 °C. Treatment with the TRPV1 antagonist capsazepine decreased both the cortisol response to thermal ramping at 27 °C and crf transcript abundance; activation of TRPV1 using capsaicin was without effect. Together with the observation that adrenocorticotropic hormone (ACTH)-stimulated cortisol production in vitro was not affected by increasing incubation temperature, these findings demonstrate plasticity in the HPI axis response to temperature and implicate TRPV1 as a thermosensor linked to HPI axis activation. Moreover, the heightened thermal sensitivity of cortisol-treated trout suggests that fish experiencing chronic stress will be more vulnerable to climate warming and other related challenges.