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reduction of hypothalamic thyrotropin-releasing hormone (TRH) content, serum thyrotropin (TSH) and thyroid hormone concentrations induced by fasting ( Ahima et al. 1996 , Seoane et al. 2000 ). Also in humans, the marked suppression of TSH secretion
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expressed in chicken pituitary ( Grommen et al . 2005 ) – it is even the most abundant isoform in rodent pituitary gland ( Bradley et al . 1989 , Hodin et al . 1989 ) – and given its role in mammalian TRH and TSH gene expression ( Langlois et al . 1997
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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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dynamic expression of selected deiodinases in specific cells. Third, deiodinases allow the homeostatic mechanism of TRH/TSH regulation to occur at physiological level by ‘manipulating’ T 4 concentrations in order to regulate TRH/TSH secretion. The
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) and decreased thyrotropin-releasing hormone (TRH) expression in the paraventricular nucleus (PVN) ( Blake et al. 1991 ). Locally produced T 3 by D2 has been proposed to contribute to the decrease in TRH expression in the PVN, which induces
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thyrotropin-releasing hormone (TRH), neurotensin and oxytocin. Internal milieu such as suckling, stress and increased levels of ovarian steroids modulate PRF and PIF activities, which transduce PRL-regulating signals ( Meites et al . 1963 , Neill 1970
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EPSRC Centre for Predictive Modelling in Healthcare, University of Exeter, Exeter, UK
Bristol Medical School, Translational Health Sciences, University of Bristol, Bristol, UK
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GHRH Unpublished data 9, 5, 2 EF1a, CAG ChR2, GCaMP6s mouse, rat PVN, LH CRH (Pomrenze et al. 2015, Füzesi et al. 2016, Romanov et al. 2017) 9, 8, 5, 2 EF1a, CAG, Syn ChR2, GCaMP6s GCaMP6m, hM3Dq mouse PVN, TRH
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Animal Reproduction and Biotechnology Laboratory, Department of Pediatrics, Department of Biomedical Sciences, Colorado State University, ARBL-Foothills Campus, Campus Delivery 1683, Fort Collins, Colorado 80-523-1683, USA
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placenta from days 35 to 55 of gestation; however, the cellular source of GH described ( Lacroix et al . 1996 , 1999 ) did not coincide with our preliminary studies (TRH Regnault & RV Anthony unpublished observations). Therefore, the first objective of
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Department of Endocrinology and Metabolism, Hypothalamic Integration Mechanisms, Laboratory of Endocrinology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
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leads to local increased bioavailabilty of T 3 concentration that suppresses thyrotrophin-releasing hormone (TRH) expression in hypophysiotropic neurons of the paraventricular nucleus of the hypothalamus ( Fekete et al . 2004 , 2010 ). In addition
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( Cocchi et al. 1999 ). Leptin also activates the hypothalamo–pituitary–thyroid axis through the thyrotropin-releasing hormone (TRH)-secreting neurons located in the paraventricular nucleus (PVN) ( Cusin et al. 2000 , Guo et al. 2004 , Huo et al
