Search Results
Neurofisiología Molecular, Escuela de Dietética y Nutrición, Dirección de Investigaciones en Neurociencias, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz (INPRFM), Calzada México-Xochimilco 101, Col. San Lorenzo Huipulco, C.P. 14370, México, Distrito Federal, México
Search for other papers by F Aréchiga-Ceballos in
Google Scholar
PubMed
Search for other papers by E Alvarez-Salas in
Google Scholar
PubMed
Search for other papers by G Matamoros-Trejo in
Google Scholar
PubMed
Search for other papers by M I Amaya in
Google Scholar
PubMed
Search for other papers by C García-Luna in
Google Scholar
PubMed
Search for other papers by P de Gortari in
Google Scholar
PubMed
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
Search for other papers by Patricia Joseph-Bravo in
Google Scholar
PubMed
Search for other papers by Lorraine Jaimes-Hoy in
Google Scholar
PubMed
Search for other papers by Rosa-María Uribe in
Google Scholar
PubMed
Search for other papers by Jean-Louis Charli in
Google Scholar
PubMed
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
Search for other papers by Patricia Joseph-Bravo in
Google Scholar
PubMed
Search for other papers by Lorraine Jaimes-Hoy in
Google Scholar
PubMed
Search for other papers by Jean-Louis Charli in
Google Scholar
PubMed
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
Search for other papers by T V Novoselova in
Google Scholar
PubMed
Search for other papers by R Larder in
Google Scholar
PubMed
Search for other papers by D Rimmington in
Google Scholar
PubMed
Search for other papers by C Lelliott in
Google Scholar
PubMed
Search for other papers by E H Wynn in
Google Scholar
PubMed
Search for other papers by R J Gorrigan in
Google Scholar
PubMed
Search for other papers by P H Tate in
Google Scholar
PubMed
Search for other papers by L Guasti in
Google Scholar
PubMed
Search for other papers by The Sanger Mouse Genetics Project in
Google Scholar
PubMed
Search for other papers by S O’Rahilly in
Google Scholar
PubMed
Search for other papers by A J L Clark in
Google Scholar
PubMed
Search for other papers by D W Logan in
Google Scholar
PubMed
Search for other papers by A P Coll in
Google Scholar
PubMed
Search for other papers by L F Chan in
Google Scholar
PubMed
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
Search for other papers by Alessandro Marsili in
Google Scholar
PubMed
Search for other papers by Edith Sanchez in
Google Scholar
PubMed
Search for other papers by Praful Singru in
Google Scholar
PubMed
Search for other papers by John W Harney in
Google Scholar
PubMed
Search for other papers by Ann Marie Zavacki in
Google Scholar
PubMed
Search for other papers by Ronald M Lechan in
Google Scholar
PubMed
Search for other papers by P R Larsen in
Google Scholar
PubMed
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
Search for other papers by SI Garcia in
Google Scholar
PubMed
Search for other papers by PI Porto in
Google Scholar
PubMed
Search for other papers by VN Martinez in
Google Scholar
PubMed
Search for other papers by AL Alvarez in
Google Scholar
PubMed
Search for other papers by S Finkielman in
Google Scholar
PubMed
Search for other papers by CJ Pirola in
Google Scholar
PubMed
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.
Search for other papers by A Boelen in
Google Scholar
PubMed
Search for other papers by J Kwakkel in
Google Scholar
PubMed
Search for other papers by W M Wiersinga in
Google Scholar
PubMed
Search for other papers by E Fliers in
Google Scholar
PubMed
in rats starvation results in decreased serum thyroid hormones and thyroid-stimulating hormone (TSH) concentrations and decreased TSH releasing hormone (TRH) mRNA expression in the hypothalamic paraventricular nucleus (PVN) associated with a modest
Search for other papers by P Fragner in
Google Scholar
PubMed
Search for other papers by SL Lee in
Google Scholar
PubMed
Search for other papers by S Aratan de Leon in
Google Scholar
PubMed
TRH was initially found in the hypothalamus and regulates TSH secretion. TRH is also produced by insulin-containing beta-cells. Endogenous TRH positively regulates glucagon secretion and attenuates pancreatic exocrine secretion. We have previously shown that triiodothyronine (T(3)) down-regulates pre-pro-TRH gene expression in vivo and in vitro. The present study was designed to determine the initial impact of T(3) on rat TRH gene promoter and to compare this effect with that of dexamethasone (Dex). Primary islet cells and neoplastic cells (HIT T-15 and RIN m5F) were transiently transfected with fragments of the 5'-flanking sequence of TRH fused to the luciferase reporter gene. The persistence of high TRH concentrations in fetal islets in culture, probably due to transactivating factors, allowed us to explore how T(3) and Dex regulate the TRH promoter activity in transfected cells and whether the hormone effect is dependent on the cell type considered. TRH gene promoter activity is inhibited by T(3) in primary but not neoplastic cells and stimulated by Dex in both primary and neoplastic cells of islets. These findings validate previous in vivo and in vitro studies and indicate the transcriptional impact of these hormones on TRH gene expression in the pancreatic islets.
Search for other papers by BH Duvilanski in
Google Scholar
PubMed
Search for other papers by D Pisera in
Google Scholar
PubMed
Search for other papers by A Seilicovich in
Google Scholar
PubMed
Search for other papers by M del Carmen Diaz in
Google Scholar
PubMed
Search for other papers by M Lasaga in
Google Scholar
PubMed
Search for other papers by E Isovich in
Google Scholar
PubMed
Search for other papers by MO Velardez in
Google Scholar
PubMed
Substance P (SP) may participate as a paracrine and/or autocrine factor in the regulation of anterior pituitary function. This project studied the effect of TRH on SP content and release from anterior pituitary and the role of SP in TRH-induced prolactin release. TRH (10(-7) M), but not vasoactive intestinal polypeptide (VIP), increased immunoreactive-SP (ir-SP) content and release from male rat anterior pituitary in vitro. An anti-prolactin serum also increased ir-SP release and content. In order to determine whether intrapituitary SP participates in TRH-induced prolactin release, anterior pituitaries were incubated with TRH (10(-7) M) and either WIN 62,577, a specific antagonist of the NK1 receptor, or a specific anti-SP serum. Both WIN 62,577 (10(-8) and 10(-7) M) and the anti-SP serum (1:250) blocked TRH-induced prolactin release. In order to study the interaction between TRH and SP on prolactin release, anterior pituitaries were incubated with either TRH (10(-7) M) or SP, or with both peptides. SP (10(-7) and 10(-6) M) by itself stimulated prolactin release. While 10(-7) M SP did not modify the TRH effect, 10(-6) M SP reduced TRH-stimulated prolactin release. SP (10(-5) M) alone failed to stimulate prolactin release and markedly decreased TRH-induced prolactin release. The present study shows that TRH stimulates ir-SP release and increases ir-SP content in the anterior pituitary. Our data also suggest that SP may act as a modulator of TRH effect on prolactin secretion by a paracrine mechanism.
Search for other papers by Patricia Joseph-Bravo in
Google Scholar
PubMed
Search for other papers by Lorraine Jaimes-Hoy in
Google Scholar
PubMed
Search for other papers by Jean-Louis Charli in
Google Scholar
PubMed
The authors and journal apologise for an error in the above paper, which appeared in volume 224 part 3, pages R139–R159 . The error relates to the legend to Figure 2 on page R141. Figure 2 Schematic representation of TRH synthesis. (A) The
