The relationship between glucocorticoid levels at baseline and during an acute stress response


Meeting Abstract

P1-243  Thursday, Jan. 4 15:30 – 17:30  The relationship between glucocorticoid levels at baseline and during an acute stress response FARMER, JL*; GEDULDIG, JG; LITWA, HP; TRICOLA, GM; SISSON, ZR; HAUSSMANN, BD; PAITZ, RT; HAUSSMANN, MF; Bucknell University; Bucknell University; Bucknell University; Bucknell University; Bucknell University; Bucknell University; Illinois State University; Bucknell University jlf032@bucknell.edu

During unpredictable events, vertebrates initiate a physiological stress response, in part mediated by glucocorticoid hormones (GCs) released by the hypothalamic-pituitary-adrenal (HPA) axis. In circulation, GCs generally remain at baseline levels, with mild fluctuations reflecting predictable energetic demands. During stress, however, GC levels become elevated above baseline, which functions to mobilize glucose reserves and inhibit nonessential functions. Once the stressor has passed, homeostasis is restored and GC levels recover to baseline. An acute stress response, then, can generally be simplified to three GC levels: baseline, stress-induced rise, and homeostatic-recovery. Here, we studied Japanese quail (Coturnix japonica) using a standard bag-restraint protocol to investigate relationships between baseline GCs and either the stress-induced rise of GCs, or the homeostatic-recovery of GC levels. Specifically, we used dexamethasone, a synthetic GC that causes negative feedback on the HPA axis, to measure homeostatic-recovery. We found that GC levels at baseline correlated negatively with both the GC stress-induced rise and the GC recovery back to baseline. In other words, birds with lower baseline GC levels had a steeper increase in circulating GCs during an acute stress response and also showed a faster decrease in GCs after the stressor was removed. Our results suggest that an individual’s baseline GC level relates to their ability both to turn on, and turn off an acute stress response.

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