Corticotropin-releasing hormone in the teleost stress response: rapid appearance of the peptide in plasma of tilapia (Oreochromis mossambicus)

Abstract

High concentrations (up to 600 pg/ml) of corticotropinreleasing hormone (CRH) were detected in plasma of the teleost fish Oreochromis mossambicus (tilapia) when screening peripheral tissues of tilapia exposed to stress. Notably, the plasma CRH response to stressors in tilapia is much more pronounced than that in higher vertebrates, such as rats. After characterisation by RIA, by spiking plasma with synthetic tilapia CRH and by methanol-acid extraction, it is concluded that the immunoreactive (ir) material in plasma represents tilapia CRH . Results indicate that a CRH-binding protein is absent in tilapia plasma.Unstressed fish had plasma CRH levels under the limit of detection (,2 pg/ml), but following capture stress plasma CRH levels (170-300 pg/ml) as well as plasma cortisol levels (120 ng/ml) increased rapidly to plateau levels, which were reached after approximately 5 min.Tilapia CRH 1-41 tested at concentrations between 10 11 and 10 7 M in vitro did not stimulate the cortisol release from interrenal tissue. Also pretreatment of interrenal tissue with 10 9 M CRH did not sensitise the cortisolproducing cells to a subsequent ACTH challenge. Fortyeight hours of net confinement or 48 h of cortisol treatment abolished the plasma CRH response and cortisol response to capture stress. The rapidity of the plasma CRH response and its inhibition after 48 h of stress or cortisol treatment point to release by central nervous tissue. Therefore the distribution of glucocorticoid receptors (GRs) in the brain and pituitary of tilapia was investigated. Main GR-ir cell clusters were found in the medial part (Dm) and posterior part of the dorsal telencephalon, in the preoptic region, in the inferior lobe of the hypothalamus and in the cerebellum.We conclude from comparison of CRH brain contents of unstressed and stressed fish that plasma CRH was released by CRH-ir cells located in the lateral part of the ventral telencephalon (Vl), and suggest that the cortisol feedback on CRH release by Vl is mainly exerted via the forebrain Dm region. We propose that CRH is mobilised during stress to fulfil peripheral functions, such as the regulation of circulating leukocytes or of cardiac output, as CRH receptors have been reported in these organs for fish species.

11-Deoxycortisol is a corticosteroid hormone in the lamprey

“…Human CRH markedly increased plasma 11-deoxycortisol concentrations in male and female lampreys 1 h after injection (Fig. 3A), a finding that is consistent with previous work showing that CRH stimulates the release of GCs in jawed vertebrates (13,14). Because CRH is known to stimulate the release of adrenocorticotropic hormone (ACTH) from the pituitary, which in turn stimulates the secretion of GC from the interrenal cells, we investigated whether sea lamprey pituitary extract would increase the secretion of 11-deoxycortisol.…”

The response of brain serotonergic and dopaminergic systems to an acute stressor in rainbow trout: a time-course study

“…However, the first sampling time was usually performed 15 min or more post-stress. Studies monitoring the activation of those markers in a more detailed fashion during the first minutes of the stress response are very scarce (Biron and Benfey, 1994;Pepels et al, 2004). In agreement with the study of Biron and Benfey (Biron and Benfey, 1994), we demonstrate here that the typical increase of plasma cortisol, glucose and lactate in response to a handling challenge takes place rapidly in rainbow trout, with all three parameters showing an increase within the initial 2 min of handling.…”

Dexamethasone modulates expression of genes involved in the innate immune system, growth and stress and increases susceptibility to bacterial disease in Senegalese sole (Solea senegalensis Kaup, 1858)

“…At hypothalamic level, high levels of circulating corticoids reduce 22e46% the number of crf mRNAs in telencephalon-preoptic area [51e53]. Also, cortisol can abolish CRF release from telencephalon to regulate plasma CRF levels [54]. In this work, we did not observed significant changes in the abundance of crf mRNAs in whole post-larvae in the short-term DXM exposure but they increased significantly after two weeks.…”