Stress in common carp, Cyprinus carpio

We characterized the endocrine stress‐axis in carp, that involves hypothalamic corticotropin releasing factor (CRF), pituitary adrenocorticotropic hormone (ACTH) and interrenal (adrenal equivalent) cortisol (F); the CRF/ACTH/F‐axis is activated during confinement. The tetraploid carp produces two CRFs that differ in a single amino acid (A 4 /P 4 ); 93% identity with human CRF is further evidence for the pressure on its evolutionary conservation. CRF signals through CRF‐receptors specific for central (CRFR1) and peripheral (CRFR2) actions. CRF is “chaperoned” by a binding protein (CRFBP), that is phylogenetically very old (>10 9 years), has an extremely well‐conserved genomic organisation, and an unique protein structure. In the hypothalamic nucleus preopticus of carp we find abundant large CRF‐neurons, and at the periphery of the nucleus and in the tuberal hypothalamus small CRFBP‐positive neurons. Both project to pars distalis ACTH‐cells; CRH induces ACTH‐release only when ACTH‐cells experience mild dopaminergic inhibition. Massive amounts of CRF and CRFBP are found in the pituitary pars intermedia meant to control melanophore stimulating hormone (MSH‐) cells and/or for peripheral circulation. In a confinement stress paradigm (F levels from 176 to 1319 nM after 24 hrs), CRF‐ and CRFBP‐gene expression is upregulated, the CRHR1 in pars distalis ACTH‐cells and the ACTH‐receptor (MC2R) in the cortisol‐producing cells are down‐regulated. Plasma MSH‐levels are elevated following stress. MSH is not corticotropic in carp (no MC5R in interrenal tissue; MC2R has too low affinity for MSH) but, conceivably, may be a lipolytic and anorexigenic signal (e.g. in addition to CRH) that explains decreased food intake during stress.