High impact information on CRH

• We examined by means of RT-PCR and immunostaining whether glycoprotein hormone alpha-subunit (alphaGSU) could be coexpressed with proopiomelanocortin (POMC) in vivo and under pressure of CRH in vitro [1].
• The developmental dynamics of this cell population and its response to CRH in vitro in the rat suggest a relationship of these cells with the embryonic branching of the POMC and alphaGSU cell lineages and their mutually opposite developmental course during early postnatal life [1].
• However, the known orexigenic (neuropeptide Y, agouti gene-related peptide, orexin, and orexin receptor) and anorexigenic (pro-opiomelanocortin and corticotropin-releasing hormone) neuropeptide mRNA levels remained unchanged after cerulenin treatment [2].
• We have concluded that the sensitivity of the pituitary thyrotropes to hypothalamic stimulation decreases throughout the last week of embryonic development, so that the higher expression of TSH-beta mRNA around E16-E19, and hence the increasing plasma thyroxine level, is unlikely to be the result of an increased stimulation by either TRH or CRH [3].
• However, the catabolic/anorexigenic neuropeptides namely proopiomelanocortin (POMC) and corticotropin-releasing hormone (CRH) mRNA levels remained unchanged after leptin treatment [4].

Biological context of CRH

• The results show that CRH is capable of stimulating the TSH secretion during the entire life cycle of the chicken and that SRIH may play an important role in the fine-tuning of this response by lowering the sensitivity of the thyrotropes to CRH [5].
• Despite many different modulatory endocrine and peptidergic inputs there are three main neuroendocrine 'channels' involved in osmoregulation: 1. corticotropin releasing hormone (CRH)-adrenocorticotropic hormone (ACTH)-adrenal steroids (aldosterone, corticosterone); 2. renin-angiotensin; 3. arginine-vasotocin (AVT) [6].

Anatomical context of CRH

• In four areas of the quail brain in which CRH nerve fibers and cGnRH I somata co-occurred (bed nucleus commissural pallii, nucleus preopticus medialis, nucleus septalis lateralis and nucleus accumbens), numerous instances were found of CRH-ir nerve fibers or terminals in apposition to cGnRH I cell bodies [7].

Associations of CRH with chemical compounds

• The double-label system used a sheep anti-cGnRH I primary antibody with a secondary antibody conjugated to dichlorotriazinylaminofluorescein dihydrochloride for green fluorescence and a rabbit anti-CRH antibody with a secondary conjugated to Texas Red for red fluorescence [7].
• An injection of 1 microgram of ovine CRH increased corticosterone after 0.5 h and elevated T3 and T4 after 2 h to the same extent in Dw and dw embryos [8].
• In the chicken, it was found that not only TRH, but also corticotropin-releasing hormone (CRH), the main stimulator of corticotropin release, is a potent stimulator of TSH secretion [9].
• To address this question we used double-label immunofluorescence histochemistry to determine whether corticotropin-releasing hormone (CRH)-immunoreactive (ir) neuronal elements contact chicken gonadotropin-releasing hormone I (cGnRH I)-ir somata in brains of Japanese quail [7].

Other interactions of CRH

• Possibly CRH-induced TSH secretion is mediated by a yet unknown type of CRH-R in the chicken [10].
• We also investigated the possible regulatory role of somatostatin (SRIH) in this specific endocrine function of CRH [5].

References