Disease relevance of TRH

• Transcription from the TRH promoter was regulated in a physiologically faithful manner, being significantly increased in hypothyroidism and decreased in T3-treated animals [1].
• Growth hormone response to TRH in male broiler chickens selected for body weight gain or food conversion and reared at either a moderate or a high ambient temperature [2].
• The selenium content of livers obtained following decapitation after 2 h was also increased in normal hens up to 902 +/- 42 ng/g using the highest dose of TRH (24 micrograms/kg) [3].

Psychiatry related information on TRH

• Neonatal chickens were injected intraventricularly with Ni(II), Pd(II), Cu(II) or Zn(II) complex of TRH and the potencies of stimulating locomotor activity were compared with that of TRH, Ni(II)-TRH was more potent than the ligand while Pd(II)-TRH was inert [4].
• We conclude, that food deprivation modifies the response of the hypophysis-thyroid axis to exogenous TRH in the sense that during fasting the production of rT3 is enhanced relative to T3 [5].

High impact information on TRH

• Polyethylenimine served to transfect a TRH-luciferase construct containing 554 bp of the rat TRH promoter into the hypothalami of newborn mice [1].
• We examined TR subtype effects on thyrotropin-releasing hormone (TRH) transcription and on the pituitary/thyroid axis end point: thyroid hormone secretion [1].
• Our previous studies showed that thyrotropin-releasing hormone (TRH) treatment of GH3 cells stimulated a rapid (less than 10 s) but transient (less than 60 s) association of cytosolic PKC with the membrane [6].
• In addition, increases in plasma membrane DAG in response to TRH were transient rather than sustained [6].
• Thus, the negative regulation of the TRH promoter in transiently transfected primary embryonic chick hypothalamic neurons provides a useful system for studying the molecular actions of thyroid hormone receptors [7].

Chemical compound and disease context of TRH

• At 5 weeks of age, serum T3 levels of broilers administered pituitary bGH in ovo were significantly increased as compared to controls following a challenge with 0.25 micrograms TRH/kg body weight [8].

Biological context of TRH

• In pituitary cell aggregates of 11-day-old male broiler chicks the ggPit-l * mRNA expression was significantly increased following TRH administration, indicating that the stimulatory effects of TRH on several pituitary hormones are mediated via its effect on the ggPit-l* gene expression [9].
• The number of binding sites was greater in the caudal lobe than in the cephalic lobe, although the affinity of [3H]Me-TRH binding did not differ [10].
• These results suggest that T3 inhibits GH secretion in fowl by a down-regulation of pituitary TRH receptors [11].
• This is the first report in birds of TRH up-regulation and down-regulation by testosterone and T(3) under in vitro conditions [12].
• In conclusion, the present report shows that important changes occur in the hypothalamic TRH and SRIH concentration during both embryonic development and posthatch growth of the chicken [13].

Anatomical context of TRH

• However, the molecular basis of T3 inhibition of TRH gene expression in the hypothalamus is not known [7].
• Thyrotrophin-releasing hormone (TRH)-induced growth hormone secretion in fowl: binding of TRH to pituitary membranes [10].
• Binding sites for [3H]Me-TRH were found in the cephalic lobe of the pituitary gland (the location of most lactotrophs and thyrotrophs) and in the caudal lobe (the location of most somatotrophs) [10].
• Although TRH was found in all tissues collected, it was also most abundant in brain, pituitary, thyroid and gonads [14].
• Towards hatching, TRH concentrations increased gradually in both the hypothalamic area and the brain stem [15].

Associations of TRH with chemical compounds

• Plasma growth hormone levels were reduced (P less than 0.05) 65% by dietary T3 and 33% by treatment with either T4 or TRH when compared with the CF group [16].
• GnRH and TRH increased, while testosterone and T(3) decreased, PGHalpha mRNA levels [12].
• Anterior pituitary glands from broiler fowl were incubated by themselves, with hypothalamic tissue or with thyrotrophin releasing hormone (TRH) in medium containing dopamine and its antagonist pimozide [17].
• Submaximal GH responses of conscious and anaesthetized birds to systemic TRH challenge were, however, potentiated by prior or concomitant administration of pGlu-Glu-ProNH2 [18].
• Diminished GH responses to i.v. TRH challenge occurred in birds pretreated with reserpine (a catecholamine depletor), alpha-methyl-paratyrosine (a DA synthesis inhibitor) and pimozide (a DA receptor antagonist) [19].

Regulatory relationships of TRH

• The prolactin-stimulating effects of TRH may be mediated by cyclic AMP [20].
• Growth hormone secretion induced by thyrotropin-releasing hormone in adult chickens: evidence of dose-dependent induction of either refractoriness or sensitization [21].

Other interactions of TRH

• TRH affected both the GH and TSHbeta mRNA levels [9].
• The results of this in vitro study reveal that ggPit-1 * has a role in mediating the stimulatory effects of TRH on pituitary hormones like GH and TSHbeta in the chicken pituitary [9].
• Applying this method, the effect of TRH injections on Pit-1 mRNA expression was determined in the pituitary of chick embryos and growing chicks [22].
• Next, the specificity of this response to day 16 serum was tested further by treating day 12 cells with peptides known to stimulate GH release in adult animals, GH-releasing hormone and TRH, and a GH-releasing hormone-related peptide (vasoactive intestinal peptide) [23].
• Both basal and TRH-stimulated release of prolactin from the oestrogen-primed pituitary glands was inhibited by dopamine, an effect blocked by pimozide [17].

Analytical, diagnostic and therapeutic context of TRH

• To examine their effects on T3-dependent transcription from the rat TRH promoter, we used a gene transfer technique to express TR alpha and TR beta in cultured embryonic chick hypothalamic cells [7].
• Surgical thyroidectomy increases basal and TRH-induced GH concentrations in the peripheral plasma of immature domestic fowl [24].
• The in vitro half-life of TRH was estimated to be 9.8 (by immunoassay) and 9.6 (by a biological index) min for plasma from adult male chickens and 23.9 (by immunoassay) and 20.2 (by biological index) min for plasma from 6-week-old chicks [25].
• The influence of an intravenous injection of thyrotrophin-releasing hormone (TRH) and bovine thyrotrophin (TSH) on circulating levels of thyroid hormones and the liver 5'-monodeiodination (5'-D) activity is studied in the chick embryo and the adult chicken [26].
• Thyrotrophin releasing hormone (TRH) injected intravenously after immobilization caused increases in T3 and T4 levels, suggesting that the fall in T3 and T4 during acute stress was not caused by exhaustion of hormone production by the thyroid gland but rather by inhibition of release of TRH at the hypothalamic level [27].

References