Distribution of thyrotrophin-releasing hormone receptor messenger RNA in rat pituitary and brain

Zabavnik, Jelka; Arbuthnott, G.W.; Eidne, Karin A.

doi:10.1016/0306-4522(93)90632-p

Cited by 36 publications

(17 citation statements)

References 33 publications

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“…However, due to an extremely low affinity of the new molecule to TRH in comparison with TRHR1 and 2, the novel receptor has not been determined to be a true cognate ligand of TRH . TRHR1 is widely distributed in the CNS and extends to several peripheral organs (Calzá et al 1992, Satoh et al 1993, 1994, Zabavnik et al 1993, Wolff et al 1996 compared with TRHR2. Therefore, the putative biological function of TRH in peripheral organs, including the effects of TRH on pancreatic cells, is probably mediated by TRHR1.…”

Section: Discussionmentioning

confidence: 99%

Expression of thyrotropin-releasing hormone receptor in immortalized beta-cell lines and rat pancreas

Luo

Yano²

2004

Journal of Endocrinology

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Thyrotropin-releasing hormone (TRH), a hypothalamic tripeptide, is expressed in pancreatic islets at peak levels during the late gestation and early neonate period. TRH increases insulin production in cultured -cells, suggesting that it might play a role in regulating pancreatic -cell function. However, there is limited information on TRH receptor expression in the pancreas. The aim of the present study was to explore the distribution of the TRH receptor in the pancreas and its function in pancreatic -cells. TRH receptor type 1 (TRHR1) gene expression was detected by RT-PCR and verified by Northern blotting and immunoblotting in the -cell lines, INS-1 and TC-6, and the rat pancreatic organ. The absence of TRH receptor type 2 expression in the tissue and cells indicated the tissue specificity of TRH receptor expression in the pancreas. The TRHR1 signals (detected by in situ hybridization) were distributed not only in islets but also in the surrounding areas of the pancreatic ductal and vasal epithelia. The apparent dissociation constant value for the affinity of [ 3 H]3-methyl-histidine TRH (MeTRH) is 4·19 in INS-1 and 3·09 nM in TC-6. In addition, TRH induced epidermal growth factor (EGF) receptor phosphorylation with a half-maximum concentration of approximately 50 nM, whereas the high affinity analogue of TRH, MeTRH, was 1 nM. This suggested that the affinity of TRH ligands for the TRH receptor influences the activation of EGF receptor phosphorylation in TC-6 cells. Our observations suggested that the biological role of TRH in pancreatic -cells is via the activation of TRHR1. Further research is required to identify the role of TRHR1 in the pancreas aside from the islets.

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Section: Discussionmentioning

confidence: 99%

Expression of thyrotropin-releasing hormone receptor in immortalized beta-cell lines and rat pancreas

Luo

Yano²

2004

Journal of Endocrinology

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“…Rat cranial and spinal motoneurons display dense TRH binding sites and express TRHR1 receptor mRNA at high levels (177, 1131,1371,1416). Expression of the TRH receptor is developmentally regulated, at least in some motoneuron pools.…”

Section: K Trhmentioning

confidence: 99%

Synaptic Control of Motoneuronal Excitability

Rekling

Funk

Bayliss

et al. 2000

Physiological Reviews

537

482

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Movement, the fundamental component of behavior and the principal extrinsic action of the brain, is produced when skeletal muscles contract and relax in response to patterns of action potentials generated by motoneurons. The processes that determine the firing behavior of motoneurons are therefore important in understanding the transformation of neural activity to motor behavior. Here, we review recent studies on the control of motoneuronal excitability, focusing on synaptic and cellular properties. We first present a background description of motoneurons: their development, anatomical organization, and membrane properties, both passive and active. We then describe the general anatomical organization of synaptic input to motoneurons, followed by a description of the major transmitter systems that affect motoneuronal excitability, including ligands, receptor distribution, pre-and postsynaptic actions, signal transduction, and functional role. Glutamate is the main excitatory, and GABA and glycine are the main inhibitory transmitters acting through ionotropic receptors. These amino acids signal the principal motor commands from peripheral, spinal, and supraspinal structures. Amines, such as serotonin and norepinephrine, and neuropeptides, as well as the glutamate and GABA acting at metabotropic receptors, modulate motoneuronal excitability through pre-and postsynaptic actions. Acting principally via second messenger systems, their actions converge on common effectors, e.g., leak K + current, cationic inward current, hyperpolarization-activated inward current, Ca 2+ channels, or presynaptic release processes. Together, these numerous inputs mediate and modify incoming motor commands, ultimately generating the coordinated firing patterns that underlie muscle contractions during motor behavior.

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“…In addition to its classical function as a releasing hormone, the distribution of TRH and its receptor indicates supplementary roles. TRH and TRH receptor (TRHR) are found distributed throughout the central and peripheral nervous systems as well as in other tissues [3][4][5][6] including thymus [6] and small intestine epithelial cells [7], consistent with its proposed role in the immune system. cDNAs encoding the highly conserved TRHR have been cloned from mouse, rat and hamster cell lines [8][9][10], from human brain [11] and from avian and bovine tissues [12,13].…”

Section: Introductionmentioning

confidence: 64%

The human neuroendocrine thyrotropin-releasing hormone receptor promoter is activated by the haematopoietic transcription factor c-Myb

Matre

Høvring

Fjeldheim

et al. 2003

Biochemical Journal

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Thyrotropin-releasing hormone (TRH) receptor (TRHR) is a G-protein-coupled receptor playing a crucial role in the anterior pituitary where it controls the synthesis and secretion of thyroidstimulating hormone and prolactin. Its widespread presence not only in the central nervous system, but also in peripheral tissues, including thymus, indicates other important, but unknown, functions. One hypothesis is that the neuropeptide TRH could play a role in the immune system. We report here that the human TRHR promoter contains 11 putative response elements for the haematopoietic transcription factor c-Myb and is highly Mybresponsive in transfection assays. Analysis of Myb binding to putative response elements revealed one preferred binding site in intron 1 of the receptor gene. Transfection studies of promoter deletions confirmed that this high-affinity element is necessary for efficient Myb-dependent transactivation of reporter plasmids in CV-1 cells. The Myb-dependent activation of the TRHR promoter was strongly suppressed by expression of a dominant negative Myb-Engrailed fusion. In line with these observations, reverse transcriptase PCR analysis of rat tissues showed that the TRHR gene is expressed both in thymocytes and bone marrow. Furthermore, specific, high-affinity TRH agonist binding to cell-surface receptors was demonstrated in thymocytes and a haematopoietic cell line. Our findings imply a novel functional link between the neuroendocrine and the immune systems at the level of promoter regulation.

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Distribution of thyrotrophin-releasing hormone receptor messenger RNA in rat pituitary and brain

Cited by 36 publications

References 33 publications

Expression of thyrotropin-releasing hormone receptor in immortalized beta-cell lines and rat pancreas

Expression of thyrotropin-releasing hormone receptor in immortalized beta-cell lines and rat pancreas

Synaptic Control of Motoneuronal Excitability

The human neuroendocrine thyrotropin-releasing hormone receptor promoter is activated by the haematopoietic transcription factor c-Myb

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