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Kristien Vandenborne, Simon A Roelens, Veerle M Darras, Eduard R Kühn, and Serge Van der Geyten

–25702. Ladram A , Bulant M, Montagne JJ & Nicolas P 1994 Distribution of TRH-potentiating peptide (Ps4) and its receptors in rat brain and peripheral tissues. Biochemical and Biophysical Research Communications 200 958

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

. European Journal of Neuroscience 10 1465 – 1478 . doi:10.1046/j.1460-9568.1998.00158.x . Heuer H Schafer MK O'Donnell D Walker P Bauer K 2000 Expression of thyrotropin-releasing hormone receptor 2 (TRH-R2) in the central nervous system of

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Edwin J W Geven, Gert Flik, and Peter H M Klaren

) axis where hypothalamic TRH stimulates the release of pituitary TSH, which stimulates the release of THs. Similarly, the hypothalamic–pituitary–interrenal (HPI) axis controls the release of cortisol from the interrenal cells in the head kidney, via

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C García-Luna, P Soberanes-Chávez, and P de Gortari

the leptin receptor ( Obrb ) and suppressor of cytokine signaling 3 (SOCS3)) and PVN mRNAs ( Trh , Crf , obrb and Socs3 ). PVN (−0.84 to −2.28 mm from bregma) and ARC (−2.28 to −3.48 mm from bregma) ( Paxinos & Watson 2005 ) were punch

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K J Oliveira, G S M Paula, R H Costa-e-Sousa, L L Souza, D C Moraes, F H Curty, and C C Pazos-Moura

and it is an agonist of receptor subtypes NPY-Y2 and NPY-Y5 ( Keire et al. 2000 ). Experimental evidence suggests that circulating PYY 3-36 inhibits appetite by acting directly on the arcuate nucleus via the Y2 receptor, a presynaptic inhibitory

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Z Zhang, P H Bisschop, E Foppen, H C van Beeren, A Kalsbeek, A Boelen, and E Fliers


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Sylvia V H Grommen, Lutgarde Arckens, Tim Theuwissen, Veerle M Darras, and Bert De Groef

hypophyseal somatostatin (SS) receptor subtypes 2 and 5 (SSTR2, SSTR5) – which mediate the inhibition of TRH- and CRH-induced TSH release by SS ( Geris et al . 2003 , De Groef et al . 2007 ). The respective decrease in TSHβ ( De Groef et al . 2006 ) and

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Maria H Warner and Geoffrey J Beckett

circulating binding proteins, modified entry of thyroid hormone into tissue, changes in thyroid hormone metabolism due to modified expression of the intracellular iodothyronine deiodinases and changes in thyroid hormone receptor (THR) expression or function

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GV Childs, G Unabia, BT Miller, and TJ Collins

There is a 2- to 3-fold increase in luteinizing hormone-beta (LHbeta) or follicle-stimulating hormone-beta (FSHbeta) antigen-bearing gonadotropes during diestrus in preparation for the peak LH or FSH secretory activity. This coincides with an increase in cells bearing LHbeta or FSHbeta mRNA. Similarly, there is a 3- to 4-fold increase in the percentage of cells that bind GnRH. In 1994, we reported that this augmentation in gonadotropes may come partially from subsets of somatotropes that transitionally express LHbeta or FSHbeta mRNA and GnRH-binding sites. The next phase of the study focused on questions relating to the somatotropes themselves. Do these putative somatogonadotropes retain a somatotrope phenotype? As a part of ongoing studies that address this question, a biotinylated analog of GHRH was produced, separated by HPLC and characterized for its ability to elicit the release of GH as well as bind to pituitary target cells. The biotinylated analog (Bio-GHRH) was detected cytochemically by the avidin-peroxidase complex technique. It could be displaced by competition with 100-1000 nM GHRH but not corticotropin-releasing hormone or GnRH. In cells from male rats exposed to 1 nM Bio-GHRH, 28+/-6% (mean+/-s.d) of pituitary cells exhibited label for Bio-GHRH (compared with 0.8+/-0.6% in the controls). There were no differences in percentages of GHRH target cells in populations from proestrous (28+/-5%) and estrous (25+/-5%) rats. Maximal percentages of labeled cells were seen following addition of 1 nM analog for 10 min. In dual-labeled fields, GHRH target cells contained all major pituitary hormones, but their expression of ACTH and TRH was very low (less than 3% of the pituitary cell population) and the expression of prolactin (PRL) and gonadotropins varied with the sex and stage of the animal. In all experimental groups, 78-80% of Bio-GHRH-reactive cells contained GH (80-91% of GH cells). In male rats, 33+/-6% of GHRH target cells contained PRL (37+/-9% of PRL cells) and less than 20% of these GHRH-receptive cells contained gonadotropins (23+/-1% of LH and 31+/-9% of FSH cells). In contrast, expression of PRL and gonadotropins was found in over half of the GHRH target cells from proestrous female rats (55+/-10% contained PRL; 56+/-8% contained FSHbeta; and 66+/-1% contained LHbeta). This reflected GHRH binding by 71+/-2% PRL cells, 85+/-5% of LH cells and 83+/-9% of FSH cells. In estrous female rats, the hormonal storage patterns in GHRH target cells were similar to those in the male rat. Because the overall percentages of cells with Bio-GHRH or GH label do not vary among the three groups, the differences seen in the proestrous group reflect internal changes within a single group of somatotropes that retain their GHRH receptor phenotype. Hence, these data correlate with earlier findings that showed that somatotropes may be converted to transitional gonadotropes just before proestrus secretory activity. The LH and FSH antigen content of the GHRH target cells from proestrous rats demonstrates that the LHbeta and FSHbeta mRNAs are indeed translated. Furthermore, the increased expression of PRL antigens by these cells signifies that these convertible somatotropes may also be somatomammotropes.

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Nadia Schoenmakers, Kyriaki S Alatzoglou, V Krishna Chatterjee, and Mehul T Dattani

Diagramatic representation of the hypothalamic–pituitary–thyroid axis with positive regulation (black) predominantly mediated by thyrotropin-releasing hormone (TRH) and negative (grey) feedback influences, predominantly mediated by thyroid hormone receptor (TR