Introduction The involvement of estrogens in the control of pituitary function has been extensively studied (reviewed in Seilicovich 2010 ). Initially, estradiol was described to induce lactotroph proliferation through ERα; however, apoptotic
María Andrea Camilletti, Alejandra Abeledo-Machado, Jimena Ferraris, Pablo A Pérez, Erika Y Faraoni, Daniel Pisera, Silvina Gutierrez and Graciela Díaz-Torga
Xiaoqin Fu, Shotaro Nishimura and Tom E Porter
-stimulating hormone, somatotrophs secrete growth hormone (GH) and lactotrophs secrete prolactin (PRL). Although morphological studies suggest that all of these cell types arise from a progenitor cell type in Rathke’s pouch ( Dasen & Rosenfeld 2001 ), differentiation
Emma Castrique, Marta Fernandez-Fuente, Paul Le Tissier, Andy Herman and Andy Levy
, Ahlbom et al . 1998 ), ‘massive degeneration’ ( Orgnero de Gaisan et al . 1993 ), autolytic changes ( Aoki et al . 1996 ), and bi-directional lactotroph to somatotroph transdifferentiation ( Porter et al . 1991 ) have been implicated to account for it
Ana I Arroba, Alfonso M Lechuga-Sancho, Laura M Frago, Jesús Argente and Julie A Chowen
hypoglycemia ( Kinsley et al. 1996 ). We have previously demonstrated that there is a reduction in the number of lactotrophs in the rat pituitary after 8 weeks of poorly controlled diabetes ( Arroba et al. 2003 ), which could explain the decrease in
Zhenhua Wang, Tetsuo Mitsui, Maho Ishida and Jun Arita
vectors will aid with correctly interpreting experimental data. Therefore, in this study, we used the rat pituitary lactotroph in the primary culture as a model for studying how adenovirus vector infection modulates cell proliferation. We found that the
A. I. Torres and A. Aoki
The intracellular localization of different molecular forms of prolactin was studied in various experimental models covering a wide range of secretory states.
By correlating electron microscopy, morphometry and quantification of monomeric (small) and polymeric (big) prolactin after differential extraction procedures, big prolactin was found stored in secretory granules while small prolactin was loosely associated with all organelles involved in hormone synthesis and processing. No correlation with levels of lactotrophic secretory activity was detected by either the number of secretory granules or prolactin content in lactotrophs.
J. Endocr. (1985) 105, 219–225
M. G. P. Gallardo, M. Bilinski, S. R. Chiocchio and J. H. Tramezzani
The presence of dopamine in the lactotroph cell, as well as in isolated prolactin secretory granules, was demonstrated by means of an histochemical reaction for electron microscopy. Biochemical assays further confirmed the presence of dopamine in the secretory granules.
Autoradiographic preparations examined by light microscopy showed dopamine internalization in dispersed anterior pituitary cells.
Isolated anterior pituitary lactotroph cells incorporated more [3H]dopamine than a fraction containing other anterior pituitary cells.
J. Endocr. (1985) 104, 23–28
H. A. Pasolli, A. I. Torres and A. Aoki
The relationships between the stimulation of prolactin secretion and proliferation of lactotrophs was studied from a multidisciplinary standpoint in three experimental models. Administration of both oestrogen and sulpiride resulted in a significant increase in prolactin secretion and in the lactotroph population. A single injection of 10 μg oestradiol benzoate (OB) induced a twofold increase in the proliferation of lactotrophs (morphometrically as volume density), which increased further (2·5-fold) after three OB injections. Parallel changes were observed in the net counts made on lactotrophs sectioned through the nucleus to avoid possible distortions in volume density caused by hypertrophic cytoplasms. Comparable results were obtained with the mitotic index in the same groups of rats exposed to treatment with colchicine. The effect of sulpiride on proliferation of lactotrophs was also significant (1·7-fold) but less pronounced than in rats treated with oestrogens. The treatments with oestrogen and sulpiride did not stimulate lactotrophic activity in a similar way, as judged by the levels of serum prolactin and the storage patterns of small and big prolactin in pituitary glands. Serum prolactin (mean ± s.e.m.) in control ovariectomized rats was 4·0±0·9 μg/l and one and three injections of OB raised these levels to 14·4±5·0 and 28·8±4·6 μg/l respectively. The highest levels of serum prolactin were seen in sulpiride-treated rats (467·2±28·7 μg/l). Striking differences occurred in the pituitary contents of big prolactin, the control values increasing from 5·3±0·5 to 10·2±1·3 μg/mg after one OB injection and to 14· 7 ±0·7 μg/mg after three OB injections. In contrast, the concentration of big prolactin in sulpiride-treated rats was very low (1·85 ± 0·2 μg/mg), 2·8-times smaller than the controls. Other changes were also found in the small prolactin content in pituitary tissue with higher values in all the experimental models. These differences could only be detected after differential extraction of big and small molecular forms of prolactin.
In ovariectomized rats, treatment with several doses of oestrogen enhanced the proliferation observed in the lactotroph population and increased the number of mitoses. In turn, morphological data could be closely related to the higher levels of prolactin in serum and pituitary glands. A sustained stimulation of lactotrophic secretion was always followed by proliferation of lactotrophs, the number of which fluctuated in parallel with the degree of stimulation.
Journal of Endocrinology (1992) 134, 241–246
E. S. Haggi, A. I. Torres, C. A. Maldonado and A. Aoki
Regressive changes occurring in the pituitary gland of the rat after removal of litters were studied. Pituitary glands of lactating rats were characterized by the presence of numerous hypertrophied lactotrophs. Interruption of lactation caused a blockade of prolactin synthesis and secretion, followed by degeneration of lactotrophs. Morphometric analysis of pituitary glands revealed that lactotrophs accounted for about 50% of the total hypophysial cell count in lactating rats. This percentage decreased progressively and reached pre-pregnant levels 7 days after removal of litters; the decrease was inversely correlated with an increase in the number of degenerating lactotrophs which comprised 30% of all lactotrophs 72 h after removal of litters. The morphological changes found in lactotrophs were closely related to changes in the prolactin content of serum and the pituitary gland. Regression of lactotrophs appeared to be the most important cause inducing the reversal of hypophysial lactotrophic activity to pre-pregnant conditions.
J. Endocr. (1986) 111, 367–373
T Tierney and IC Robinson
The dwarf (dw/dw) rat differs from all other rodent models of GH deficiency in that its pituitary prolactin (PRL) content is normal or even increased. We have now studied this throughout postnatal development, using a combination of immunocytochemistry, RIA and fluorescence-activated cell sorting (FACS) and analysis. Compared with normal Albino Swiss (AS) rats, adult dw/dw rats showed a profound reduction in pituitary GH content accompanied by increased PRL content, significantly so in females (AS vs dw/dw; P<0.01). Somatotroph hypoplasia was evident in the adult dw/dw rats, with most GH(+ve) cells showing weak immunostaining, whereas many more strongly stained PRL cells were evident in pituitary sections from dw/dw rats. Facs analysis confirmed both somatotroph hypoplasia and relative lactotroph hyperplasia in dw/dw rats at all ages studied (9-144 days); the difference in somatotrophs increased with age whereas the difference in lactotrophs declined with age. At 9 days, the percentage of lactotrophs was 10-fold higher in dw/dw rats than in AS rats. Young dw/dw rats also had a higher proportion of mammosomatotrophs than AS rats, although this difference disappeared as the mammosomatotroph proportions increased with age in both strains. GHRH released GH from both dw/dw and as cells maintained in culture for 5 days. The sensitivity to GHRH and the amount of GH released was lower in the dw/dw cultures, mostly explained by their fewer GH cells and lower initial GH content. GHRH increased cAMP in as but not in dw/dw cultures, even when these were greatly enriched for dw/dw somatotrophs by FACS sorting prior to culture. These results suggest that GHRH-induced cAMP stimulation is required for trophic effects on GH synthesis and somatotroph proliferation, but is not required for GHRH-stimulated GH release. The inverse changes in somatotroph and lactotroph numbers suggest that the dw/dw mutation disturbs the mechanism that specifies and retains appropriate numbers of somatotrophs in their differentiated state, and results in a higher proportion of the remaining cells progressing to lactotrophs. The dw/dw phenotype is thus not confined to somatotrophs.