Role of corticotropin-releasing hormone as a thyrotropin-releasing factor in non-mammalian vertebrates

Laboratory of Comparative Endocrinology, K.U. Leuven, B3000 Leuven, Belgium.
General and Comparative Endocrinology (Impact Factor: 2.47). 04/2006; 146(1):62-8. DOI: 10.1016/j.ygcen.2005.10.014
Source: PubMed


The finding that thyrotropin-releasing hormone does not always act as a thyrotropin (TSH)-releasing factor in non-mammalian vertebrates has led researchers to believe that another hypothalamic factor may exhibit this function. In representatives of all non-mammalian vertebrate classes, corticotropin-releasing hormone (CRH) appears to be a potent stimulator of hypophyseal TSH secretion, and might therefore function as a common regulator of both the thyroidal and adrenal/interrenal axes. CRH exerts its dual hypophysiotropic action through two different types of CRH receptors. Thyrotropes express type 2 CRH receptors, while CRH-induced corticotropin (ACTH) secretion is mediated by type 1 CRH receptors on the corticotropic pituitary cells. The stimulating effect of CRH on both TSH and ACTH release has profound consequences for the peripheral action of both hormonal axes. The simultaneous stimulation of the thyroidal and adrenal/interrenal axes by CRH, possibly fine-tuned by differential regulation of the expression of the different CRH receptor isoforms, provides a potential mechanism for developmental plasticity.

Download full-text


Available from: De Groef Bert
  • Source
    • "The HPT axis plays major roles in regulating THs both in mammals and fish. In fish, the hypothalamus secretes CRF to stimulate TSH secretion and regulation of TH synthesis within the HPT axis (De Groef et al., 2006). In the present study, the transcription levels of CRF and TSH␤ were both downregulated after exposure to MC-RR, which might be explained by the negative feed-back mechanism between the hypothalamus and pituitary gland compensating for the decreased T4 levels. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Recent studies have shown that cyanobacteria-derived microcystins (MCs) have the potential to disrupt endocrine systems. However, the effects of microcystin-RR (MC-RR) and their underlying mechanisms are poorly resolved in fish. In this study, MC-RR exposure through submersion caused serious developmental toxicity, such as growth delay and depressed heart rates in zebrafish larvae. We also detected decreased levels of thyroid hormones (THs), suggesting that MC-RR-triggered thyroid endocrine disruption might contribute to the growth impairment observed in developing zebrafish. To further our understanding of mechanisms of MC-RR-induced endocrine toxicity, quantitative real-time PCR (QPCR) analysis was performed on hypothalamic-pituitary-thyroid (HPT) axis related genes, i.e., corticotropin-releasing factor (CRF), thyroid-stimulating hormone (TSH), sodium/iodide symporter (NIS), thyroglobulin (TG), thyroid receptors (TRα and TRβ) and iodothyronine deiodinases (Dio1 and Dio2), of developing zebrafish embryos exposed to 0, 0.3, 1.0 or 3.0mgL(-1) MC-RR until 96h post-fertilization. Our results showed that transcription pattern of HPT axis related genes were greatly changed by MC-RR exposure, except TG gene. Furthermore, western blot was used to validate the results of gene expression. The results showed protein synthesis of TG was not affected, while that of NIS was significantly up-regulated, which are in accordance with gene expression. The overall results indicated that exposure to MC-RR can induce developmental toxicity, which might be associated with thyroid endocrine disruption in developing zebrafish larvae. Copyright © 2015 Elsevier B.V. All rights reserved.
    Full-text · Article · Apr 2015 · Aquatic Toxicology
  • Source
    • "Also, during early development of fish, chronological correlation between ACTH and TSH production has been observed in the pituitary of European sea bass (Dicentrarchus labrax) larvae (97). Together, this data suggest that stressor-challenge drives the THs to play both fundamental and modulatory roles in the stress response [reviewed in Ref. (89, 90)]. Moreover, a reduction in basal plasma cortisol levels was observed in hyperthyroidism-induced Cyprinus carpio (98). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Besides the well-known function of thyroid hormones (THs) for regulating metabolism, it has recently been discovered that THs are also involved in testicular development in mammalian and non-mammalian species. THs, in combination with follicle stimulating hormone, lead to androgen synthesis in Danio rerio, which results in the onset of spermatogenesis in the testis, potentially relating the hypothalamic-pituitary-thyroid (HPT) gland to the hypothalamic-pituitary-gonadal (HPG) axes. Furthermore, studies in non-mammalian species have suggested that by stimulating the thyroid-stimulating hormone (TSH), THs can be induced by corticotropin-releasing hormone. This suggests that the hypothalamic-pituitary-adrenal/interrenal gland (HPA) axis might influence the HPT axis. Additionally, it was shown that hormones pertaining to both HPT and HPA could also influence the HPG endocrine axis. For example, high levels of androgens were observed in the testis in Odonthestes bonariensis during a period of stress-induced sex-determination, which suggests that stress hormones influence the gonadal fate toward masculinization. Thus, this review highlights the hormonal interactions observed between the HPT, HPA, and HPG axes using a comparative approach in order to better understand how these endocrine systems could interact with each other to influence the development of testes.
    Full-text · Article · Aug 2014 · Frontiers in Endocrinology
  • Source
    • "Intriguingly, which hypothalamic hormone drives the increasing TSH release is uncertain. In the chicken, two hypothalamic factors possess a potent TSH-releasing capacity: thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH) (reviewed by De Groef et al., 2006b). Hypothalamic TRH and CRH levels (mRNA and peptide) increase steadily toward hatching (Geris et al., 1999; Vandenborne et al., 2005; Lu et al., 2008; Ellestad et al., 2011) and the decreasing CRH peptide content of the median eminence toward E19 suggests elevated CRH secretion into the hypophyseal portal system (Vandenborne et al., 2005). "
    [Show abstract] [Hide abstract]
    ABSTRACT: A major life stage transition in birds and other oviparous sauropsids is the hatching of the cleidoic egg. Not unlike amphibian metamorphosis, hatching in these species can be regarded as a transition from a relatively well-protected "aqueous" environment to a more hazardous and terrestrial life outside the egg, a transition in which thyroid hormones (THs) (often in concert with glucocorticoids) play an important role. In precocial birds such as the chicken, the perihatch period is characterized by peak values of THs. THs are implicated in the control of muscle development, lung maturation and the switch from chorioallantoic to pulmonary respiration, yolk sac retraction, gut development and induction of hepatic genes to accommodate the change in dietary energy source, initiation of thermoregulation, and the final stages of brain maturation as well as early post-hatch imprinting behavior. There is evidence that, at least for some of these processes, THs may have similar roles in non-avian sauropsids. In altricial birds such as passerines on the other hand, THs do not rise significantly until well after hatching and peak values coincide with the development of endothermy. It is not known how hatching-associated processes are regulated by hormones in these animals or how this developmental mode evolved from TH-dependent precocial hatching.
    Full-text · Article · May 2013 · Frontiers in Endocrinology
Show more