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F Aréchiga-Ceballos, E Alvarez-Salas, G Matamoros-Trejo, M I Amaya, C García-Luna, and P de Gortari

thyroxine (T 4 ) – as well as their degrading effects on fuel reservoirs. TRH is the hypophysiotropic factor that controls HPT axis function. This peptide is synthesized in the medial PVN (mPVN) of the hypothalamus and released into the portal blood to

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Patricia Joseph-Bravo, Lorraine Jaimes-Hoy, Rosa-María Uribe, and Jean-Louis Charli

hTSH isolated from post-mortem tissues ( Weintraub & Szkudlinski 1999 ). Figure 1 Time line. Figure depicts the principal discoveries that contributed to the actual understanding of TRH neurons and regulation of the hypothalamus–pituitary–thyroid axis

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Patricia Joseph-Bravo, Lorraine Jaimes-Hoy, and Jean-Louis Charli

Introduction The tripeptide pglu-his-proNH2 was isolated from hypothalami and named according to its endocrine function: ‘thyrotrophin-releasing hormone’ (TRH; Boler et al . 1969 , Burgus et al . 1969 ). TRH is synthesized in the neuronal cell

Open access

T V Novoselova, R Larder, D Rimmington, C Lelliott, E H Wynn, R J Gorrigan, P H Tate, L Guasti, The Sanger Mouse Genetics Project, S O’Rahilly, A J L Clark, D W Logan, A P Coll, and L F Chan

the PVN ( Mrap2 +/+ n =3, Mrap2 tm1a/tm1a n =3) and in the whole hypothalamus ( Mrap2 +/+ n =4, Mrap2 tm1a/tm1a n =4) as determined by the qPCR. (C) Expression of Sim1 , Trh , Oxt , Avp , Crh and Sst in the PVN of 129/Sv wild type ( n

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Alessandro Marsili, Edith Sanchez, Praful Singru, John W Harney, Ann Marie Zavacki, Ronald M Lechan, and P R Larsen

of TSH by TRH is also required for TSH elevation during hypothyroidism, indicating that this is not simply due to the absence of negative feedback regulation on the thyrotroph TSH ( Nikrodhanond et al . 2006 ). It is well known that the conversion of

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S Harvey and L A Cogburn


Complete processing of the TRH precursor in the rat hypothalamus generates TRH and a number of other 'cryptic' peptides that flank the TRH progenitor sequences. Two of these peptides, P4 (Ser-Phe-Pro-Trp-Met-Glu-Ser-Asp-Val-Thr; present between amino acids 160 and 169 of rat prepro-TRH) and P5 (Phe-Ile-Asp-Pro-Gly-Leu-Gln-Arg-Ser-Trp-Glu-Glu-Lys-Glu-Gly-Glu-Gly-Val-Leu-Met-Pro-Glu; present between amino acids 178 and 199 of rat prepro-TRH), have recently been shown to modulate TRH-induced GH and thyrotrophin release from rat pituitary glands. The possibility that these peptides might modulate GH secretion in chickens was examined, since TRH is a physiological GH-releasing factor in birds. The administration of P4 and P5 (at doses of 10 and 100 μg/kg) consistently lowered basal plasma GH concentrations 30 and 60 min after a bolus i.v. injection. Pretreatment with P4 and P5 similarly suppressed the GH response to systemic TRH challenge. The GH-releasing activity of maximally stimulatory doses of TRH was also reduced by concomitant injections of either P4 (100 μg/kg) or P5 (100 μg/kg), which blocked the GH-releasing activity of submaximally effective doses of TRH. In marked contrast, neither P4 nor P5 significantly affected basal or TRH-induced GH release from chicken pituitary glands incubated in vitro. These results demonstrate novel actions of P4 and P5 on hypothalamic–pituitary function and, for the first time, indicate extrapituitary sites of action for these cryptic peptides in modulating anterior pituitary function.

Journal of Endocrinology (1996) 151, 359–364

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A. E. Pekary, S. Bhasin, V. Smith, M. Sugawara, R. S. Swerdloff, and J. M. Hershman


Thyrotrophin-releasing hormone (TRH) occurs in high concentrations in the rat ventral prostate and its concentration is regulated in a positive dose–response manner by testosterone in castrated rats. α-Amidation of the tetrapeptide precursor, TRH-Gly, is a rate-limiting step in TRH biosynthesis. To investigate further the hormonal regulation of TRH biosynthesis in prostatic tissue, Sprague–Dawley rats of approximately 250 g were injected s.c. with either physiological saline or 3 mg propylthiouracil (PTU) daily for 5 days. The reproductive tissues were boiled in acetic acid (1 mol/l), dried and extracted with methanol. The methanol extracts were measured for TRH immunoreactivity (TRH-IR) and TRH-Gly-IR by radioimmunoassay. Hypothyroidism induced by PTU significantly increased TRH-IR and TRH-Gly-IR levels in prostate and testis and reduced these levels in epididymis but did not affect the serum concentrations of testosterone compared with those of controls. Corresponding changes in TRH and TRH-Gly in the rat prostate were established by high-pressure liquid chromatography. To control for possible pharmacological effects of PTU on TRH biosynthesis, additional experiments were carried out on castrated rats receiving testosterone replacement and treatment with PTU plus methimazole. Treatment with thyroxine (T4) significantly reduced the increase in prostatic TRH levels due to hypothyroidism, despite the drug-induced blockade of the conversion of T4 to tri-iodothyronine. These effects parallel similar observations made in rat spinal cord and pancreas. This study demonstrates that in the male rat reproductive system the levels of TRH and its immediate biosynthetic precursor, TRH-Gly, are regulated by thyroid hormones.

J. Endocr. (1987) 114, 271–277

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A. E. Pekary, M. Knoble, N. H. Garcia, S. Bhasin, and J. M. Hershman


Orchidectomy has been reported to decrease concentrations of thyrotrophin (TSH) in the circulation of male rats without affecting serum levels of thyroid hormones. To understand the mechanism underlying this observation, we have measured the effect of gonadal status on the in-vitro release of TSH-releasing hormone (TRH) by male rat hypothalamic fragments. Because hormone release rates can be affected by changes in the post-translational processing of the hormonal precursors, we have also studied the corresponding changes in the concentrations of TRH and TRH-Gly, a TRH precursor peptide in hypothalamus and pituitary, by radioimmunoassay.

We observed a significant decline in the in-vitro release of TRH from incubated hypothalami 1 week after castration, which was quantitatively reversed by testosterone replacement. Concentrations of TRH and TRH-Gly in the posterior pituitary, on the other hand, which derive from neurones of hypothalamic origin, increased significantly with castration and were returned to the normal range by testosterone replacement.

We conclude that the primary effect of testosterone is the stimulation of hypothalamic TRH release, resulting in the depletion of TRH and TRH precursors from TRH-containing neurones which project into the median eminence and posterior pituitary.

Journal of Endocrinology (1990) 125, 263–270

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G Croissandeau, N Schussler, D Grouselle, P Pagesy, C Rauch, M C Bayet, F Peillon, and M Le Dafniet


TRH gene expression in the anterior pituitary has previously been reported in the human in vivo and in the rat in vitro. Until now, modulation of this synthesis with glucocorticoids and thyroid hormones has been observed in rats. The present study demonstrates for the first time that the TRH gene is also expressed, in vivo, in the rat anterior pituitary and that anterior pituitary TRH-like immunoreactivity (TRH-LI) and elongated forms of the immediate TRH progenitor sequence (TRH-elongated peptide) contents are also modulated by estrogens (E2). To investigate the presence of proTRH mRNA in the rat anterior pituitary, total RNA was reverse transcribed (RT) and the RT products were then amplified by PCR. Treatments with E2 were performed on intact and ovariectomized (OVX) rats for 2 months. TRH-LI was measured by RIA with an antibody which did not recognize the TRH-like peptide, pGlu-Glu-Pro-NH2 (<EEP-NH2) (cross-reactivity <0·1%) and was characterized further as TRH-LI by HPLC. TRH-elongated peptides were measured by EIA and characterized by Sephadex G-50 chromatography and immunoblotting (molecular mass 25–35 kDa). The plasma prolactin levels and the pituitary sizes were increased by E2 treatment in both intact and OVX rats. Anterior pituitary TRH-LI increased in intact E2-treated rats compared with intact rats (82·7 ± 19·0 versus 39·6 ± 3·6 fmol/mg protein; means ± s.e.m.; P<0·001). This increase was greater when E2 was administered to OVX rats (599·0 ± 98·4 after E2 treatment versus 58·6 ± 3·6 fmol/mg protein; P<0·001). In intact rats, anterior pituitary TRH-elongated peptide contents were not modified by E2 treatment while they were significantly decreased in OVX E2-treated rats (144·6 ±8·8 versus 223·7 ± 9·5 fmol/mg protein; P<0·001). These results demonstrate TRH gene expression in the rat anterior pituitary in vivo and suggest that E2 treatment is responsible for an increase in anterior pituitary TRH-LI, together with a decrease in TRH-elongated peptide contents.

Journal of Endocrinology (1996) 151, 87–96

Free access

SI Garcia, PI Porto, VN Martinez, AL Alvarez, S Finkielman, and CJ Pirola

The human glioblastoma-astrocytoma cell line U-373-MG shows morphological features typical of its neuroectodermal origin. Cells showed positive immunostaining for the glial fibrillary acidic protein. We used this cell culture for studying the putative production of TRH and TRH-related peptides. In a cell extract and conditioned medium, cation and anion exchange chromatography and HPLC revealed the presence of TRH and acidic TRH-like peptides which were identified, at least in part, as pGlu-Glu-ProNH(2). These findings demonstrated that U-373-MG cells are able to produce and release these peptides. Further evidence of TRH synthesis was obtained by amplification using RT-PCR of a 396 bp fragment that corresponds to the TRH precursor mRNA. Our results therefore suggest that the U-373-MG cell line may be a useful model for studying the regulation of TRH and TRH-related peptide production and the interaction of these peptides with other classical neurotransmitter systems. In fact, pilocarpine (a muscarinic cholinergic agonist) enhanced and nicotine (a nicotinic cholinergic agonist) decreased TRH and TRH-related compound production by this cell line. These data also point out that glia may produce substances with neuromodulatory action.