Effects of acute handling stress on short-term central expression of orexigenic/anorexigenic genes in zebrafish
- Cortés, R., Teles, M., Oliveira, M., Fierro-Castro, C., Tort, L., Cerdá-Reverter, J.M.
- Fish physiology and biochemistry 44(1): 257-272 (Journal)
- Registered Authors
- Cerdá-Reverter, José Miguel
- Brain, Cart, Feeding behavior, Food intake, Melanocortin, Npy
- MeSH Terms
- Feeding Behavior/physiology*
- Gene Expression Regulation/physiology*
- Stress, Physiological*
- Time Factors
- 29071448 Full text @ Fish Physiol. Biochem.
Cortés, R., Teles, M., Oliveira, M., Fierro-Castro, C., Tort, L., Cerdá-Reverter, J.M. (2017) Effects of acute handling stress on short-term central expression of orexigenic/anorexigenic genes in zebrafish. Fish physiology and biochemistry. 44(1):257-272.
Physiological mechanisms driving stress response in vertebrates are evolutionarily conserved. These mechanisms involve the activation of both the hypothalamic-sympathetic-chromaffin cell (HSC) and the hypothalamic-pituitary-adrenal (HPA) axes. In fish, the reduction of food intake levels is a common feature of the behavioral response to stress but the central mechanisms coordinating the energetic response are not well understood yet. In this work, we explore the effects of acute stress on key central systems regulating food intake in fish as well as on total body cortisol and glucose levels. We show that acute stress induced a rapid increase in total body cortisol with no changes in body glucose, at the same time promoting a prompt central response by activating neuronal pathways. All three orexigenic peptides examined, i.e., neuropeptide y (npy), agouti-related protein (agrp), and ghrelin, increased their central expression level suggesting that these neuronal systems are not involved in the short-term feeding inhibitory effects of acute stress. By contrast, the anorexigenic precursors tested, i.e., cart peptides and pomc, exhibited increased expression after acute stress, suggesting their involvement in the anorexigenic effects.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes