By filtering relevant sensory inputs and initiating stress responses, the brain is an essential organ in stress coping and adaptation. However, exposure to chronic or repeated stress can lead to allostatic overload, where neuroendocrinal and behavioral reactions to stress become maladaptive. This work examines forebrain mechanisms involved in allostatic processes in teleost fishes. Plasma cortisol, forebrain serotonergic (5-HTergic) neurochemistry and mRNA levels of corticotropin-releasing factor (CRF), CRF binding protein (CRFBP), CRF receptors (CRFR1 and CRFR2), mineralocorticoid receptor (MR), glucocorticoid receptors (GR1 and GR2), and 5-HT1A receptors (5-HT1Aα and 5-HT1Aβ) were investigated at 1 h before and 0, 1 and 4 h after acute stress, in two groups of rainbow trout held in densities of 25 and 140 kg m−3 for 28 days. Generally, being held at 140 kg m−3 resulted in a less pronounced cortisol response. This effect was also reflected in lower forebrain 5-HTergic turnover, but not in mRNA levels in any of the investigated genes. This lends further support to allostatic load as a situation where fish cannot mount a proper cortisol response to an acute stressor, and suggests that changes in forebrain 5-HT metabolism is involved in allostatic processes in fish. Independent of rearing densities, mRNA levels of 5-HT1Aα and MR were down regulated 4 h post stress compared to values 1 h post stress, suggesting that these receptors are under feedback control and take part in the down regulation of the hypothalamic-pituitary-interrenal (HPI) axis after an acute stressor.
- Received March 8, 2016.
- Accepted October 3, 2016.
- © 2016. Published by The Company of Biologists Ltd